Term Paper Pwu

Case Study/Term Paper
I. INTRODUCTION ACKNOWLEDGMENT
I would like to express my deepest gratitude and sincerest appreciation to the following people who have shared their effort and time for the success of our student nurses rotation; for the untiring guidance of Dr. Alejandro Delos Santos III, the Dean of the College of Nursing of Mt. Carmel College who also stood as our clinical instructor. To the staff nurses of the Marcos Ward or Ward 2E of the National Kidney and Transplant Institute, Ms. Nerissa M. Gerial, OIC, Nursing Services; Ms. Merceditas J. Vargas-Jocson, RN, MAN, Head of the Institute of Advanced Nursing and Allied Health Professions; Ms. Darlyn DR Del Rosario, Head Nurse of Ward 2E; Ms. Glecita S. Erni, Division Chief II, Clinical and Public Nursing; the Nurses II: Ms. Hannah A. Abillano, Ms. Nadine Felice C. Aquino, Ms. Michelle M. Gutierrez, Ms. Merika G. Jimenez, and Ms. Angeline D. Salvatierra; the Nurses I: Ms. Grace F. Gayagoy, Ms. Katrina Anne D. Larios, Mr. Allan Nestor D. Fulgar, and Mr. Patrick S. Javier; JON I: Ms. Ma. Jonalyn M. Juanilio, Ms. Mariefe Jean V. Malgapo, Mr. Niel M. Udtohan, Ms. Ria Carla Labios, Ms. Eleine M. Samoro, and Ms. Franchesca C. Quitariano. And to my professor in the Graduate School of Nursing at the Philippine Womens University, Prof. Minerva De Ala, and Dean Celeste Diamculangan who inspired me to prepare this case study/term paper. To my parents, ward, mentors, and people who have
continuously supported us financially or otherwise, this case study/term paper would not have been possible without you.
Submitted by Hoser Saavedra
To Prof Minerva De Ala
DEDICATION This humble work is dedicated to the following people, who encouraged me to dream, taught me love and understanding and the value of patience : My parents, Whom I know is very proud of me and believes in me and helps me overcome doubts beyond my capacity; My Professors, Who guided me during these college years and graduate school years and encouraged me to do my best; Our friends, Who supported me in our day to day school life, put up with my memory lapses, and love me still despite all the odds; My ward, Who continuously inspire me to make the best of all I do; Dean Alejandro Delos Santos III, Prof. Minerva De Ala, and Dean Celeste Dimaculangan, Who ask questions that stimulate thought and discussion; The staff nurses and officers of IANAHP, Who gave us the opportunity to bring with us a wealth of knowledge and skills in bedside nursing and in the care of renal patients; And most importantly,
To the One Supreme Being, who is God, who has given me life, talent, knowledge and skills, and the capacity to love and care, all important characteristics of becoming a good nurse.
INTRODUCTION Excellent nursing practice reflects proficient use of the nursing process demonstrated by skillful assessment, diagnosis, planning, outcome identification, intervention, and evaluation. The nursing process provides the framework that directs nursing practice. Nursing care planning is the application of the nursing process to a specific client situation. Written nursing care plans are a means of communication among health care providers, clients, and families. They ensure that care is coordinated to achieve desired health care outcomes. Primary chronic glomerulonephritis is the most common cause of end-stage renal failure in Japan. The incidence in dialysis patients in Japan is about four times higher than in the United States for reasons which are unclear. When a nationwide survey on the natural history and treatment of primary glomerulonephritis was conducted under a program project from the Ministry of Health and Welfare of Japan entitled 'Progressive Chronic Renal Disease'. In conclusion, a high incidence of IgA nephropathy and a better renal survival of membranous nephropathy are the features of primary chronic glomerulonephritis in Japan. This high incidence of IgA nephropathy together with its poor prognosis is probably the reason for the increased incidence of primary chronic glomerulonephritis in dialysis patients in Japan. In addition, the importance of routine health examination including urinalysis is demonstrated.
In the Philippines, renal disease is now the 10th leading cause of death in the country and diabetes is now the number one cause of renal failure. Every year, there are about 7,500 deaths in the Philippines secondary to various kidney diseases and that the first four major causes of end-stage renal disease (ESRD) are diabetic nephropathy (DN) which is mainly among adults, chronic glomerulonephritis (CGN), chronic pyelonephritis (CPN) and hypertensive nephrosclerosis (HN). When a patient is diagnosed to be in the ESRD, it means that there has been a permanent damage to his/her kidney(s). These are only some of the information that Dr. Enrique T. Ona, executive director of the National Kidney and Transplant Institute (NKTI). "These diseases," he said, "are potentially preventable if diagnosed early in the course of illness thereby avoiding the need for expensive modalities of ESRD treatment, like dialysis and transplantation." "Between these two, transplantation is more recommended because it restores the quality of life of the patient. Pero napakalaki ang kakulangan natin sa mga kidney organs dahil mas marami ang nagkakasakit kaysa mga gustong mag-donate nito (But we have a very big shortage of the kidney organs since there are more persons who are sick than those who would like to donate their kidneys)," Ona remarked. Meanwhile, Dr. Remedios de Belen-Uriarte, REDCOP manager, said one of the most common causes of ESRD in the 3rd world countries, including the Philippines, is CGN, which usually afflicts children, adolescents and young adults in their productive years who belong to the low income segment of the population. In Japan and other affluent Western countries, good nutrition, clean environment, advances in medical care and early detection of the disease have resulted in the declining incidence of CGN as a major cause of renal failure. She said one of the primary reasons for progression of glomerulonephritis is failure to recognize or diagnose the disease in its early stages. Apparently asymptomatic children with subclinical glomerulonephritis can escape detection for months or years. Unless regular pediatric check-ups are done, the disease will continue unrecognized and untreated. Routine urinalysis is a simple but useful
Submitted by Hoser Saavedra To Prof Minerva De Ala
tool in the evaluation of children with asymptomatic or symptomatic renal diseases. "The very unfortunate thing about Renal Disease is that treatment is very expensive. So we really have to embark on preventive programs. In fact we should be intensifying our information dissemination and advocacy programs on REDCOP. And we can always begin by teaching the people of the following ways of preventing the Renal Disease," she further said: Drink adequate volume of water and fruit juices; Eat a balance diet; not too salty, not too sweet; For females, observe good personal hygiene; Exercise moderately; Encourage good bowel habits and prevent parasitism; Check blood pressure at least twice a year; Consult a doctor for throat and skin infections; Complete immunizations; Do not hold or play with urine; Avoid playing with your genitals; Yearly urinalysis. This study has been conducted on kidney diseases in general but focuses on the nursing care of glomerulonephritis clients particularly in children. Limitations are based on the limited hospital exposure.
II. REVIEW OF RELATED LITERATURE Local Since 1991, kidney disease has consistently ranked among the top ten causes of mortality in the governments registry of diseases. For every 100,00 population in 1998, nephritis and nephrotic syndrome accounted for 10.2 cases of 2.1% of total deaths. From January to December 1998, urinary tract infection (UTI) was the eighth leading cause of morbidity as reported by Philippine Pediatric Society accredited hospitals nationwide. In a 6-year review, the PNSP reported
a total of 5861 admissions in four accredited tertiary medical centers with fellowship programs in pediatric nephrology of these admissions. 1533 patients (26%) had postinfectious acute glomerulonephritis, 1302 (22%) had idiopathic nephrotic syndrome, 812 (14%) were in renal failure for various causes, 335% (6%) had secondary chronic glomerulonephritis, 2004 (3.5%) had bladder dysfunction, 188 (3%) had congenital or inherited renal disease, 113 (2%) had IgA nephroparty, 80 (1.5%) had urolithiasis, 79 (1.4%) had tumors, and 415 (7%) had miscellaneous disorders such as hypertension and renal tubular disease (45). (Avner, Harmon, Niaudet, WHO, 2003) The Philippines has one of the highest numbers of kidney transplantations in Asia. From 1983 to 2000, 1829 transplantations were performed at the National Kidney and Transplant Institute, 69 of which were in pediatric patients aged 5 to 18 years of age (3.78%). There were 66 first and 3 second transplantations, mostly with grafts from live donors. The most common cause of end-stage renal disease was chronic glomerulonephritis, representing 88% of cases. (RoseteLiquete, Unpublished data, 2002). There are problems in obtaining routine countrywide data reflecting the prevalence of kidney diseases. However, the mortality trends for diseases of the kidney and urinary tract are generally increasing at a slow phase. Studies indicate that around 9,500 Filipinos develop fatal diseases of the kidneys annually. Nephritis, nephrotic syndrome and nephrosis accounted for 7,963 deaths registered in 2000. This translates to a death rate of 10.4 per 100,000 population, the tenth highest among the causes of death in the country. In addition, kidney infections and calculi at any portion of the urinary tract had mortality rates of 0.8 and 0.5 per 100,000 population, respectively, during that year. A significant proportion of ESRD is secondary to the top causes of chronic illness in the country. Studies by two leading hospitals in Metro Manila indicate that the most common underlying diseases for ESRD are chronic glomerulonephritis, chronic pyelonephritis, diabetes mellitus and hypertensive nephrosclerosis. In short, deaths from renal causes are the consequences of prolonged or uncontrolled assault of infectious or metabolic agents on the kidneys and are regarded as degenerative. ESRD is expected to increase proportionately with the incidence of degenerative or lifestyle-related diseases. Unless these underlying diseases are controlled, prevalence of ESRD will remain high. Since the cost of treatment is prohibitive, deaths from ESRD will also be staggering. (Department of Health, 2006) Foreign
The results of treatment of glomerulonephritis (GN) in childhood with oral corticosteroids, immunosuppressive drugs, anticoagulants and the newer regimens of pulsed, high-dose intravenous methylprednisolone and plasma exchange are reviewed and compared with the natural history of the untreated condition. Poststreptococcal GN and the nephritis of Schnlein-Henoch purpura need no specific treatment unless extensive glomerular crescents are present. The progression of mesangiocapillary GN can probably be slowed or even reversed with long-term, alternate-day steroid therapy. As in adults, recovery of renal function in GN due to antibody to glomerular basement membrane can be achieved in some patients using plasma exchange, but only those in whom some renal function is still present when treatment is started. In rapidly progressive (extracapillary) GN with crescents, traditional therapy with oral steroids, immunosuppressive drugs and anticoagulants reduces renal mortality from 85%90% to about 50%, while pulsed methylprednisolone and plasma exchange improve the outcome further, mortality falling to about 25%. It is recommended that children with crescentic GN and deteriorating function be treated initially with pulsed methylprednisolone, followed by plasma exchange in those who fail to respond or who deteriorate following temporary response to pulse therapy. Treatment must be given early in the course of the illness if good results are to be obtained. (Haycock, 1998). According to an article in www.revolutionhealth.com, Glomerulonephritis is one disorder that can lead to kidney failure. There are many causes of glomerulonephritis. They include those related to infections, immune diseases, inflammation of the blood vessels (vasculitis) and conditions that scar the glomeruli. Often, however, the exact cause is initially unknown. Here are some of the known causes: Infections
Post-streptococcal glomerulonephritis. Glomerulonephritis may develop after a strep infection in the throat or, rarely, on your skin (impetigo). Post-infectious glomerulonephritis is becoming less common, most likely because of rapid and complete antibiotic treatment of most streptococcal infections. Bacterial endocarditis. Bacteria can occasionally spread through the bloodstream and lodge in your heart, causing an
infection of the valvular tissues inside the heart. Those at greatest risk are people with a heart defect, such as a damaged or artificial heart valve. Viral infections. Among the viral infections that may trigger glomerulonephritis are the human immunodeficiency virus (HIV), which causes AIDS, and the hepatitis B and hepatitis C viruses, which affect the liver and can become chronic infections.
New therapeutic strategies glomerulonephritis
of
molecular
intervention
in
Summary: Recent progress of genetic engineering allows us to create animal models expressing the new genetic phenotype and also indicates a sure future for clinical use of gene therapy. We applied HVJ-liposome method for manipulation of transforming growth factor (TGF)- gene expression in anti-Thy-1 experimental glomerulonephritis. Either the glomerular introduction of TGF- antisense oligodeoxynucleotides or transfection of gene for decorin, a natural inhibitor of TGF-, into the skeletal muscle could suppress the extracellular matrix (ECM) expansion in glomerulonephritis. Thus, these results may suggest the potential of gene therapy as a novel treatment for fibrotic diseases caused by TGF-. Proteinuria is too much protein in your urine, causing foamy urine and swelling. Generally, if your kidneys are physically healthy, proteins do not typically filter into your urine because of their large size. In the circumstances of glumeruli (filters) damage in your kidney, proteins have less difficulty making it through. The protein most likely to show up in a urine test is albumin, whats referred to as albuminuria. Inflammation in the glomeruli (glomerulonephritis or nephritis) leads to proteinuria and many diseases can damage the glomeruli, causing proteinuria. Highest risk factors are:

diabetes hypertension family member with kidney disease
Proteinuria is also associated with cardiovascular disease, as damaged blood vessels may lead to kidney failure.
A couple of signs or symptoms of protenuria include:

foamy urine hands, feet, abdomen, face swelling
A urine test is the way to determine unhealthy protein passage. Additionally, a blood test for creatinine and urea nitrogen levels indicate impaired kidney function. Obviously, if you have diabetes and/or hypertension, your health objective needs to be getting blood glucose and blood pressure under your control. Reducing intake of dietary salt and protein may also be a recommended form of treatment.
Glomerulonephritis, Poststreptococcal Background Acute glomerulonephritis is characterized by the sudden appearance of hematuria, proteinuria and red blood cell casts in the urine, edema, and hypertension with or without oliguria. It can follow streptococcal infections. This illness was first recognized as a complication of the convalescence period of scarlet fever in the 18th century. A link between hemolytic streptococci and acute glomerulonephritis was recognized in the 20th century. Although the incidence of poststreptococcal glomerulonephritis has declined in the United States, it continues to have high incidence in other parts of the world, especially in areas with tropical climates where skin infections are common. Pathophysiology Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci designated as nephritogenic. The offending organisms are virtually always group A streptococci. Acute poststreptococcal glomerulonephritis (APSGN) follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.
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Although many morphologic, clinical, and serologic features suggest that APSGN is an immune complex disorder, the precise nature of the antigen-antibody interaction is undefined. ASPGN is believed to be an immune-mediated disease, in which an immune complex containing a streptococcal antigen is deposited in the affected glomeruli. The size of glomerular basement membrane (GBM) pores and the molecular size of the streptococcus-Ig complex are also important determinants. The molecular size of the streptococcus-Ig complex is about 15 nm (10 nm for streptococcus group A and 5 nm for immunoglobulin). The GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm, respectively. Therefore, the immune complex molecule can be more easily rodded into the glomerulus in children than in adults and, thus, may explain the increased frequency of ASPGN in children compared to that in adults. The 2 antigens isolated from nephritogenic streptococci are under investigation in APSGN. These include the cationic cysteine protease exotoxin B and glyceraldehyde phosphate dehydrogenase (also known as presorbing antigen or PA-Ag). These fractions have an affinity for glomeruli and have been shown to induce specific, long-lasting antibody responses in biopsy specimens from patients with APSGN. The relevance of exotoxin B and glyceraldehyde phosphate dehydrogenase was recently evaluated in the same renal biopsy and serum samples of patients with well-defined APSGN. Glomerular deposits of and antibody response to exotoxin B was more consistently present in APSGN than deposits of and antibody response to glyceraldehyde phosphate dehydrogenase. Antibodies to exotoxin B and PA-Ag are elevated in the majority of patients with APSGN. Intravenous injections of PA-Ag produce acute glomerulonephritis in animals. Antibodies to PA-Ag are found in 30 of 31 patients with APSGN but are low or absent in those with uncomplicated streptococcal infection or in patients with rheumatic fever. PA-Ag is also known to activate the alternate pathway of the complement cascade, which happens to be preferentially activated in persons with APSGN. The observation that some patients may only have C3 deposition may relate to this mechanism. In addition to streptococcal antigens, rheumatoid factor, cryoglobulins, and antineutrophil cytoplasmic serum antibodies are present in some
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of these patients. The pathogenic significance of this autoimmune response is not defined. Frequency International APSGN can occur sporadically or epidemically.
Incidence seems to be decreasing in the United States and Europe, but sporadic cases of the disease continue to be reported from all over the world. The prevalence of nephritis varies considerably among persons with sporadic infections with nephritogenic streptococci. The reason for this variability is not known. Epidemic poststreptococcal glomerulonephritis occurs mainly in developing countries in areas such as Africa, the West Indies, and the Middle East. Reasons for this changing epidemiology relate to the nutritional status of the community, the more liberal use of antibiotic prophylaxis, and, possibly, the change in the nephritogenic potential of streptococci. Among epidemic infections with nephritogenic streptococci, the apparent clinical attack rate is 10-12%.
Mortality/Morbidity Early death is extremely rare in children (<1%) but is significantly more common in adults (25%). This is secondary to congestive heart failure and azotemia.

Congestive heart failure is more common in adults (43%) than in children (<5%). Nephrotic-range proteinuria is more common in adults (20%) than in children (4-10%). Approximately 83% of adults have azotemia, compared to 2540% of children.
Race No racial predilection is recognized. Sex
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Clinical cases of APSGN are twice as common in males compared to females. If subclinical disease is considered, both sexes are affected equally. The familial incidence rate is nearly 40%, but no genetic marker has been identified. Age This condition typically affects children aged 2-12 years. A large series reported that 5% are younger than 2 years and 10% are older than 40 years. History A history suggestive of preceding streptococcal infection may include a preceding infective episode such as pharyngitis, tonsillitis, or pyoderma. This is the sine qua non for the diagnosis of APSGN.
Latent period
A latent period always occurs between the streptococcal infection and the onset of signs and symptoms of acute glomerulonephritis. o In general, the latent period is 1-2 weeks after a throat infection and 3-6 weeks after a skin infection. o The onset of signs and symptoms at the same time as pharyngitis (also called synpharyngitic nephritis) is more likely to be immunoglobulin A (IgA) nephropathy rather than APSGN. Dark urine (brown-, tea-, or cola-colored)
o
This is often the first clinical symptom. o Dark urine is caused by hemolysis of red blood cells that have penetrated the glomerular basement membrane and have passed into the tubular system. Periorbital edema
o o
o o
The onset of puffiness of the face or eyelids is sudden. It is usually prominent upon awakening and, if the patient is active, tends to subside at the end of the day. In some cases, generalized edema and other features of circulatory congestion, such as dyspnea, may be present. Edema is a result of a defect in renal excretion of salt and water.

o
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The severity of edema is often disproportionate to the degree of renal impairment. Nonspecific symptoms
o o
These can include general malaise, weakness, and anorexia and are present in 50% of patients. Approximately 15% of patients complain of nausea and vomiting.
Physical
Acute nephritic syndrome
Acute nephritic syndrome presenting as edema, hematuria, and hypertension with or without oliguria is the most frequent presentation of APSGN. o Approximately 95% of clinical cases have at least 2 manifestations, and 40% have the full-blown acute nephritic syndrome. Edema
o
Edema is present in 80-90% of cases, and it is the presenting complaint in 60% of cases. o Compromised intraglomerular blood flow due to glomerular hypercellularity results in progressive encroachment on the cross-sectional area of the glomerular capillaries. o This leads to reduced blood flow that manifests as low fractional excretion of sodium and concentrated urine. This salt and water retention leads to edema. Hypertension
o o o
Hypertension occurs in 60-80% of cases and is more common among elderly individuals. In 50% of cases, the hypertension can be severe; however, more often it is transient, with normalization of blood pressure upon restoration of the glomerular filtration rate, loss of edema, and normalization of plasma volume. If hypertension persists, it is more indicative of the progression to a more chronic stage or that the disease is not poststreptococcal glomerulonephritis. Hypertension is thought to be the result of excessive salt and water retention.

o
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Despite excessive sodium retention, the plasma levels of atrial natriuretic peptide are increased. In this condition, this suggests that the kidneys are unresponsive to atrial natriuretic peptide. o Plasma renin activity is usually low, and studies by Parra et al have shown that an inhibition of angiotensin-converting enzyme could be an effective short-term treatment for this low-renin hypertension. o Hypertensive encephalopathy occurs in no more than 510% of patients. Usually, clinical improvement occurs without any neurological sequelae. Oliguria
This is present in 10-50% of cases, and, in 15%, urine output is less than 200 mL. o Oliguria is indicative of the severe crescentic form of the disease. o It is often transient, with diuresis occurring within 1-2 weeks. Hematuria
o
This is present universally. o In 30% of cases, gross hematuria is present. Left ventricular dysfunction o Left ventricular dysfunction with or without hypertension or pericardial effusion may be present during the acute congestive and convalescent phases. o In rare cases, persons with APSGN can show signs of pulmonary hemorrhage.
o
Causes

Poststreptococcal glomerulonephritis follows infection with only certain strains of streptococci designated as nephritogenic. The offending organisms are virtually always group A streptococci. APSGN follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.
DIFFERENTIALS Other Problems to be Considered

15 endocarditis cryoglobulinemia nephropathy polyarteritis nephritis
Bacterial Essential IgA Microscopic Shunt Visceral abscess WORKUP Lab Studies
Evidence of preceding streptococcal infection
Antibody titers to extracellular products of streptococci are positive in more than 95% of patients with pharyngitis and 80% of patients with skin infections. o The antistreptolysin (ASO), antinicotinamide adenine dinucleotidase (anti-NAD), antihyaluronidase (AHase), and antiDNAse B are commonly positive after pharyngitis, and antiDNAse B and AHase titers are more often positive following skin infections. o ASO titers are frequently used to document streptococcal infection, but a more sensitive test is the streptozyme test, which tests antibodies to ASO, antiDNAse B, AHase, and anti-NAD. o Recent studies suggest that the relatively unavailable antizymogen titer test is superior to both antiDNAse B and ASO titers. o Antizymogen titers that are 2 dilutions higher than the mean in healthy controls are reported to have a sensitivity of 88% and a specificity of 85% in the diagnosis of streptococcal infection in patients with glomerulonephritis. antibody titers to glyceraldehyde phosphate o High dehydrogenase are also found in persons with APSGN. o In general, the antibody titers are elevated at 1 week, peak at 1 month, and fall toward preinfection levels after several months. Elevated BUN and creatinine values
o o o
This reflects the decrease in the glomerular filtration rate that occurs in the acute phase. The elevations are usually transient.

o
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Their failure to normalize within several weeks or months indicates that the patient may not have a true APSGN and suggests seeking an alternative diagnosis. who have the crescentic form of o Patients glomerulonephritis have rapid deterioration and, often, incomplete recovery of renal function. Serologic findings
Low serum complement levels indicative of an antigenantibody interaction are a universal finding in the acute phase of APSGN. o Most patients have marked depression of serum hemolytic component CH50 and serum concentrations of C3. o The activation of the alternative pathway of the complement system is thought to be responsible for the hypocomplementemia. o In some patients, the levels of C2 and C4 may also be decreased, but to a lesser extent, suggesting that both classic and alternate pathways of the complement system are activated. o In most uncomplicated cases, the complement levels return to normal in 6-8 weeks. Prolonged hypocomplementemia suggests an alternative diagnosis. o Occasionally, low complement levels persist for 3 months. o The level of reduction of serum complement levels does not have any prognostic significance. o Circulating immune complexes and cryoglobulins are found in 60% of cases, and rheumatoid factor is found in 43% of cases. Urinalysis o Results are always abnormal. o Hematuria and proteinuria are present in all cases. o Urine sediment has red blood cells, red blood cell casts, white blood cells, granular casts, and, rarely, white blood cell casts. o Dysmorphic red blood cells indicative of glomerular hematuria can usually be detected by performing phasecontrast microscopy. o Red blood cell casts are best detected in first, earlymorning urine specimens examined by the physician immediately after the patient voids.
o

o o o o o
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Hematuria usually resolves within 3-6 months but may persist as long as 18 months. Microscopic hematuria may be present in patients in whom the disease has otherwise clinically resolved. Proteinuria may be mild or so severe that it causes nephrotic syndrome. Approximately 5-10% of patients with APSGN have nephrotic-range proteinuria. Proteinuria usually disappears in 6 months. A mild increase in urinary protein excretion is present in 15% at 3 years and 2% at 10 years. Patients with nephrotic-range proteinuria in the acute phase or persistent heavy proteinuria have a worse prognosis. This is often associated with an evolution to a garlandlike pattern of immune deposits as the disease progresses.
Imaging Studies

Chest radiographs may show findings of congestive heart failure. Renal ultrasound images usually reveal normal-sized kidneys bilaterally.
Procedures
APSGN is often a clinical diagnosis and requires the detection of glomerulonephritis and evidence of preceding streptococcal infection. Atypical features in the early phase that suggest the need for renal biopsy include the following:
Absence of the latent period between streptococcal infection and acute glomerulonephritis o Anuria o Rapidly deteriorating renal function o Normal serum complement levels o No rise in antistreptococcal antibodies o Extrarenal manifestations of systemic disease o No improvement or continued decrease in the glomerular filtration rate at 2 weeks o Persistence of hypertension beyond 2 weeks Atypical features in the recovery phase that mandate a renal biopsy include the following:
o To Prof Minerva De Ala

o o o o
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Failure of glomerular filtration rate to normalize by 4 weeks Persistent hypocomplementemia beyond 6 weeks Persistent microscopic hematuria beyond 18 months Persistent proteinuria beyond 6 months
Histologic Findings
Pathologic findings of changes in gross appearance o The kidneys are symmetrically enlarged to approximately 25-50% of normal. o They are pale in appearance, and the cut surfaces bulge because of interstitial edema. o The glomeruli may stand out as reddish or gray translucent dots. o The cut surfaces may have tiny red speckles caused by red blood cells in the lumen of the Bowman space and tubules. Light microscopy o The most striking finding is hypercellularity of the glomeruli. All glomeruli are affected (diffuse) and usually to an approximately equal degree. The glomerular tufts are larger than normal, and the cells are more numerous. o The cell types typically present include endothelial and mesangial cells and migrant inflammatory cells, which include polymorphonuclear leukocytes and monocytes. o Polymorphonuclear leukocytes are present in large numbers, hence the term exudative glomerulonephritis. o Necrosis in the glomerular tuft is not typically found. o The individual lobules are wider than usual and may have a clubbed appearance. o Generally, the glomerular capillary walls are not thick. o In some patients, crescent formation may be found, but usually, only a small percentage of glomeruli are affected by crescents. o The tubules are normal in the majority of cases. o When proteinuria is present, hyaline droplets (protein reabsorption droplets) may be present in the proximal convoluted tubules. o In patients with severe exudative glomerulonephritis, polymorphonuclear leukocytes may be present in the lumen.

o
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The degree of interstitial involvement is variable. The interstitial areas show edema and infiltration with polymorphonuclear leukocytes and mononuclear cells. The arteries and arterioles are normal. Immunofluorescence o In biopsy samples taken in the first 2-3 weeks of illness, deposits of immunoglobulin G and C3 in a diffuse granular pattern are present along the glomerular capillary wall and mesangium. o Immunoglobulin M may be present in small amounts. Significant amounts of IgA suggest an alternative diagnosis. o Sorger et al have described 3 different patterns of immunofluorescence called the garland pattern, the starry sky pattern, and the mesangial pattern. o The starry sky pattern is an irregular, finely granular pattern with small deposits often situated on the glomerular basement membrane overlying the mesangium. This pattern is often seen in the early phase of the disease. o The starry sky pattern may turn into the mesangial pattern, which is characterized by granular deposition of C3 with or without immunoglobulin G. It seems to be most closely related to a resolving pattern. o In approximately 25% of patients, the deposits are large and densely packed and aggregate into a ropelike or garlandlike pattern. These correspond to the humps on the subepithelial side of the glomerular capillary wall seen with electron microscopy. These types of deposits may persist for months and may be associated with the persistence of proteinuria and the development of glomerulosclerosis. Electron microscopy o Many of the ultrastructural changes confirm the findings from light microscopy evaluations. o The number of endothelial, mesangial, and infiltrating inflammatory cells is increased. o The glomerular basement membrane is usually normal in thickness and contour, although occasionally patchy thickening may be noted. o The most consistent and classic diagnostic finding is the presence of glomerular subepithelial electron-dense immune-type deposits, often referred to as humps. The deposits are discrete and are commonly found on the part
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of the glomerular basement membrane overlying the mesangium. TREATMENT Medical Care Symptomatic therapy is recommended for patients with APSGN, and it should be based on the clinical severity of the illness. The major goal is to control edema and blood pressure.
During the acute phase of the disease, restrict salt and water.
If significant edema or hypertension develops, administer diuretics. o Loop diuretics increase urinary output and consequently improve cardiovascular congestion and hypertension. For hypertension not controlled by diuretics, usually calcium channel blockers or angiotensin-converting enzyme inhibitors are useful. For malignant hypertension, intravenous nitroprusside or other parenteral agents are used. Indications for dialysis include life-threatening hyperkalemia and clinical manifestations of uremia. Restricting physical activity is appropriate in the first few days of the illness but is unnecessary once the patient feels well. Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated. A renal biopsy is indicated for patients with rapidly progressive renal failure. If the biopsy findings show evidence of crescentic glomerulonephritis with more than 30% of the glomeruli involved, a short course of intravenous pulse steroid therapy is recommended (500 mg to 1 g/1.73 m2 of methylprednisone qd for 3-5 d). However, no controlled clinical trials have evaluated such therapy. Long-term treatment with steroids or immunosuppressives is not recommended. Specific therapy for streptococcal infection is an important part of the therapeutic regimen.
o o o
Treat patients, family members, and any close personal contacts who are infected. Throat cultures should be performed on all these individuals. Treat with oral penicillin G (250 mg qid for 7-10
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d) or with erythromycin (250 mg qid for 7-10 d) for patients allergic to penicillin. o This helps prevent nephritis in carriers and helps prevent the spread of nephritogenic strains to others. Patients with skin infections must practice good personal hygiene. This is essential. During epidemics, recommend that high-risk individuals, including close contacts and family members, receive empirical prophylactic treatment.
Surgical Care Surgical care is not indicated. Consultations

Nutritionist or dietitian Nephrologist
Diet

Low-salt diet - Two grams of sodium per day Fluid restriction - One liter per day
Activity
Restricting physical activity is appropriate in the first few days of the illness but is not necessary once the patient feels well.
MEDICATION Therapy for patients with APSGN is symptomatic in nature and depends on the clinical severity of the illness. The major aims are to control the edema and blood pressure. During the acute phase of the disease, salt and water should be restricted. If significant edema or hypertension develops, diuretics should be administered. Loop diuretics increase urinary output and consequently improve cardiovascular congestion and hypertension. For hypertension not controlled by diuretics, calcium channel blockers or angiotensin-converting enzyme inhibitors are generally useful. For
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malignant hypertension, intravenous nitroprusside or other parenteral agents are used. The indications for dialysis include life-threatening hyperkalemia and clinical manifestations of uremia. Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated. In patients with rapidly progressive renal failure, a renal biopsy is indicated. If the biopsy findings show evidence of crescentic glomerulonephritis with more than 30% of the glomeruli involved, a short course of intravenous pulse steroid therapy is recommended (500 mg to 1 g/1.73 m2 of methylprednisone qd for 3-5 d). However, no controlled clinical trials have evaluated such therapy. Long-term treatment with steroids or immunosuppressives is not recommended. Drug Category: Diuretics Used to control edema and circulatory congestion. Drug Name Furosemide (Lasix) Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on Description response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with increments of 1 mg/kg/dose until a satisfactory effect is achieved. 20-40 mg PO/IV q6-8h initial; maximum dose can be Adult Dose titrated carefully to 600 mg/d Pediatric Dose 1-2 mg/kg PO/IV; doses > 6 mg/kg not recommended Contraindicatio Documented hypersensitivity; hepatic coma, anuria, ns and state of severe electrolyte depletion Interactions Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are
23
Pregnancy
Precautions
possible when taken concurrently C - Safety for use during pregnancy has not been established. Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter
Drug Category: Calcium channel blockers In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. Calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity. Drug Name Amlodipine (Norvasc) Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Benefits nonpregnant Description patients with systolic dysfunction, hypertension, or arrhythmias. Can be used during pregnancy if clinically indicated. Adult Dose 5-20 mg PO qd Pediatric Dose Not established Contraindicatio Documented hypersensitivity ns Fentanyl may increase hypotensive effects; may Interactions increase cyclosporin levels; H2 blockers (cimetidine) may increase toxicity C - Safety for use during pregnancy has not been Pregnancy established. Adjust dose in renal/hepatic impairment; may cause Precautions lower extremity edema; allergic hepatitis has occurred but is rare
Drug Category: Angiotensin-converting enzyme inhibitors Decrease aldosterone secretion.
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Drug Name
Captopril (Capoten) Prevents conversion of angiotensin I to angiotensin II, Description a potent vasoconstrictor, resulting in lower aldosterone secretion. Adult Dose 25 mg PO bid/tid; not to exceed 150 mg tid Not established; use only if other measures to control Pediatric Dose blood pressure have not been effective Contraindicatio Documented hypersensitivity; renal impairment ns NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; Interactions rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when given concurrently with diuretics C - Safety for use during pregnancy has not been Pregnancy established. Category D in second and third trimester of Precautions pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure Drug Name Enalapril (Vasotec) Competitive inhibitor of angiotensin-converting enzyme. Reduces angiotensin II levels, decreasing Description aldosterone secretion. Clinical response usually observed within 15 min of administration. 10-40 mg PO qd in 1-2 divided doses Adult Dose Hypertensive emergencies: 1.25 mg IV q6h; can increase to 5 mg q6h Pediatric Dose Not established Contraindicatio Documented hypersensitivity ns NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; Interactions rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when given concurrently with diuretics C - Safety for use during pregnancy has not been Pregnancy established. Category D in second and third trimester of Precautions pregnancy; caution in renal impairment, valvular stenosis, or severe congestive heart failure
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Drug Category: Vasodilators Used to treat hypertensive emergencies. Vasodilators reduce SVR, which, in turn, may allow forward flow, improving cardiac output. Drug Name Nitroprusside (Nitropress) Produces vasodilation and increases inotropic activity of heart. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate. Should not be used to treat compensatory hypertension (arteriovenous shunt or coarctation of aorta). 0.25-10 mcg/kg/min IV infusion 1-8 mol/kg/min IV Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic and atrial fibrillation or flutter Effects are additive when administered with other hypotensive agents C - Safety for use during pregnancy has not been established. Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, levels may increase and can cause cyanide toxicity; sodium nitroprusside has the ability to lower blood pressure and thus should be used only in patients with mean arterial pressures >70 mm Hg Hydralazine (Apresoline) Decreases systemic resistance through direct vasodilation of arterioles. 10-20 mg IV q4-6h 0.1-0.2 mg/kg IV q4-6h Documented hypersensitivity; mitral valve rheumatic heart disease MAOIs and beta-blockers may increase toxicity; pharmacologic effects may be decreased by indomethacin B - Usually safe but benefits must outweigh the risks. Has been implicated in myocardial infarction; caution in possible coronary artery disease; caution in slow acetylators for fear of causing drug-induced lupus
Description
Adult Dose Pediatric Dose Contraindicatio ns Interactions Pregnancy
Precautions
Drug Name Description Adult Dose Pediatric Dose Contraindicatio ns Interactions Pregnancy Precautions
26
FOLLOW-UP Further Inpatient Care

In the acute phase, admit for observation and treatment of hypertension and congestive heart failure. Admit for monitoring and to initiate dialysis (when indicated) if renal function progressively worsens.
Further Outpatient Care

Monitor blood pressure every month for 6 months and then every 6 months thereafter. Monitor BUN and serum creatinine levels every 3 months after the acute phase for 1 year and then yearly after that. Check serum complement levels at 6-8 weeks to make sure they have returned to normal. Check urine for hematuria and proteinuria every 3-6 months.
In/Out Patient Meds

Most patients do not require any medications after the acute phase. In the acute phase, diuretics may be needed to control edema and congestive heart failure. Antihypertensives may be needed in the chronic phase if the patient's blood pressure remains high.
Transfer
Transfer may be necessary if renal biopsy facilities are not available and the diagnosis is in doubt or if rapidly progressive renal failure develops. Transfer may be necessary if azotemia worsens and dialysis facilities are not available on site.
Deterrence/Prevention

The patient and any family member or close personal contact should have a throat culture. Treatment with penicillin G or erythromycin (if allergic to penicillin) helps prevent nephritis in carriers and helps prevent the spread of nephritogenic strains to others.

27
Patients with skin infections must pay close attention to personal hygiene. Epidemics should prompt empirical prophylactic treatment for high-risk individuals (family and close personal contacts).
Complications
Complications in the acute phase include the following:
Congestive heart failure o Azotemia o Early death secondary to congestive heart failure and azotemia Complications in the chronic phase include the following:
o o o
Nephrotic-range proteinuria Chronic renal insufficiency and end-stage renal disease
Prognosis

In children, the immediate prognosis is excellent. In elderly patients who have congestive heart failure or azotemia in the early phase, early mortality rates can be as high as 25%. The long-term prognosis is debatable.
o o
Fewer than 1% of children have elevated serum creatinine values after 10-15 years of follow-up. Adults who develop massive proteinuria often have the garlandlike pattern of immune deposits. Their prognosis is worse; approximately 25% progress to chronic renal failure.
Patient Education

Patients with skin infections should know the importance of personal hygiene. In epidemics, all close personal contacts and family members should be told to seek medical attention for prophylactic treatment of streptococcal infections. For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center and Ear, Nose, and Throat Center. Also, see eMedicine's patient education articles Blood in the Urine and Strep Throat.
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Medical/Legal Pitfalls
Failure to follow up on the natural course of the disease
Make sure serum complement levels have returned to normal at 6-8 weeks. o Make sure hematuria and proteinuria resolve or improve and do not get worse. Failure to make the correct diagnosis
o o o
A risk of missing alternative diagnoses in atypical cases exists if a renal biopsy is not performed. See Procedures for details on indications for renal biopsy.
Special Concerns
Patients with subclinical nephritis outnumber those with overt nephritis by a ratio ranging from 4-10:1. Careful evaluation of abnormal urinalysis results may help reveal a diagnosis of poststreptococcal glomerulonephritis.
Renal Anemia in the news Mycophenolate mofetil glomerulonephritis ineffective for membranous
NEW YORK (Reuters Health) - Mycophenolate mofetil does not increase remissions or decrease proteinuria in patients with membranous glomerulonephritis, according to a report in the October issue of the American Journal of Kidney Diseases. Although mycophenolate mofetil has been shown to prevent glomerular lesions in experimental models of glomerulonephritis, the authors explain, trials evaluating immunosuppressive treatments have yielded inconsistent results. Dr. Bertrand Dussol from Hopital de la Conception, Marseille, France, and colleagues evaluated the efficacy and safety of mycophenolate mofetil monotherapy in a randomized controlled trial of 36 patients with biopsy-proven membranous glomerulonephritis. Mean proteinuria-to-creatinine ratios remained stable in the control group and in the mycophenolate mofetil group, the authors report, and
29
there was no significant difference between the groups in the number of patients experiencing complete or partial remission. Similarly, kidney function, as measured by estimated glomerular filtration rate, remained stable in both groups. Four patients in the mycophenolate mofetil group failed to complete the trial because of serious adverse events, though one event was likely related to long-term tobacco use rather than to treatment with mycophenolate mofetil, the researchers note. The investigators conclude that a 12-month course of mycophenolate mofetil in adults with idiopathic membranous glomerulonephritis and nephritic syndrome does not reduce proteinuria or achieve remission. In addition, there are some concerns regarding the safety of this drug in these patients. Treatment of Glomerulonephritis CME The American Society of Nephrology Renal Week 2002 is a setting in which experts from throughout the world assemble to discuss and evaluate the most recent advances in the evaluation and treatment of kidney disease. One of the sessions addressed the latest advances in the treatment of glomerulonephritis. Glomerulonephritis is a condition characterized by inflammation that attacks the glomeruli, the filter in the kidney that produces the urine. A number of types of glomerulonephritis exist, each of which has different causes, outcomes if not treated, and responses to treatments. Some types of glomerulonephritis lead to kidney failure, which is treated with either kidney transplantation or dialysis. Other types of glomerulonephritis lead to protein loss in the urine, which can cause edema formation, cholesterol disorders, malnutrition, and increased susceptibility to infection. Because many types of glomerulonephritis respond poorly to existing treatment regimens, new and improved treatment options are needed. A new treatment option receiving increased attention worldwide, and particularly at this meeting, is mycophenolate mofetil (MMF). MMF is widely used by people with an organ transplant because it is very effective in preventing rejection of the transplanted organ. Because of high levels of efficacy and relatively low rates of side effects, MMF is receiving increased attention as a therapy for glomerulonephritis.
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MMF is an oral medication that is converted by the body to an active compound, mycophenolic acid (MPA). MPA has specific effects on lymphocytes, white blood cells that mediate many of the effects of glomerulonephritis on the kidney. MPA also has beneficial effects on blood vessel cells, other inflammatory cells such as monocytes, and on scar tissue-forming fibroblasts. Each of these effects predicts MMF might be very effective in treating glomerulonephritis. MMF for the Treatment of IgA Nephropathy One of the reports at this meeting addressed the treatment of IgA nephropathy.[1] IgA nephropathy is the most common form of glomerulonephritis in the world, causing as many as 40% of all cases of glomerulonephritis. IgA nephropathy is characterized by blood in the urine, loss of protein into the urine, and, frequently, a slowly progressive course. As many as 20% to 30% of people with IgA nephropathy develop renal failure over an approximate 20-year period. Standard treatment options for IgA nephropathy include glucocorticoid steroids, fish oil supplements, angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers, and, for severe conditions, cyclophosphamide. Each of these treatment options has limitations, and some patients do not respond to any of these options. Chen and colleagues[1] reported the results of a large study evaluating the role of MMF. They examined patients with severe IgA nephropathy, as evidenced by the degree of inflammation and scar tissue on kidney biopsy (Lee classification grade IV-V) and amount of protein in the urine (> 2 g/day), who did not have severe renal failure (serum creatinine < 4 mg/dL). They observed that MMF decreased urine protein excretion significantly at 12 and 18 months. This was accompanied by improvements in cholesterol and triglyceride levels. After 18 months, a significantly higher number of people treated with MMF had either complete remission or an effective response compared with those treated with standard glucocorticoids. The major limitations to MMF were an increased risk of herpes zoster infection ("shingles") and gastrointestinal (GI) side effects, such as nausea and diarrhea. These results suggest that patients with severe IgA nephropathy may benefit from using MMF. Rituximab for the Nephropathy (IMN) Treatment of Idiopathic Membranous
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Another major cause of glomerulonephritis is IMN. IMN is associated with loss of large amounts of protein into the urine, and approximately one third of patients experience progressive loss of renal function and, ultimately, renal failure. More effective treatment options for IMN are needed. A newly developed medication is rituximab. Rituximab is an antibody that destroys specific immune cells that are thought to underlie the development of IMN. Remuzzi and colleagues[2] reported the results from a study in Italy, in which 8 patients with IMN that had not responded to standard therapies were treated with rituximab. They observed that 1 of the 8 patients had essentially a complete response of disease, and 3 others had substantial improvements in their disease, as evidenced by decreased urinary protein losses. When the authors of this study compared the responses of these 8 patients with those of control patients chosen who had similar baseline conditions, but who were not treated with rituximab, they suggested that treatment with rituximab significantly decreased urine protein losses and improved renal function. Several side effects were seen with rituximab, including laryngeal spasm, chills, and skin rash. While these results are very preliminary and need to be repeated by future studies, they suggest the potential for rituximab to be added to the armamentarium of therapeutic options for IMN. ACE-I for the Treatment of Glomerulonephritis An exciting report examining a novel mechanism by which a common class of medications, ACE-I, are effective in the treatment of glomerulonephritis was provided by Lods and colleagues.[3] ACE-I were originally designed as blood pressure-lowering agents, and for this they are extremely effective. They also have been shown to be effective in preventing myocardial infarction and stroke, in addition to slowing the progression of renal disease. For the latter, these effects are substantially greater than their effect on lowering blood pressure. Lods and colleagues showed that ACE-I specifically inhibit the effects of enzymes involved in extracellular matrix degradation and cellular proliferation, which helps to explain the effectiveness of ACE-I in the treatment of glomerulonephritis. Thus, ACE-I have gained another reason for their use to treat glomerulonephritis. Treatment of Lupus Nephritis
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Systemic lupus erythematosus (SLE) is a systemic disease in which the body's immune system reacts against specific organs. Some patients are afflicted by severe kidney involvement; when this is severe, it can be identified by kidney biopsy as proliferative lupus nephritis, World Health Organization (WHO) class III, IV, or V+. The standard treatment for proliferative lupus nephritis includes intravenous (IV) cyclophosphamide and glucocorticoids; the identification that cyclophosphamide is effective in this condition revolutionized the treatment of this condition in the 1980s. However, cyclophosphamide has significant long-term side effects, leading many to desire new, more effective, and less-toxic treatment options. Ligtenberg and colleagues[4] reported the initial results of a trial comparing IV cyclophosphamide plus glucocorticoids with the combination treatment of the immunosuppressive agent azathioprine plus IV pulses of glucocorticoids and oral glucocorticoids. After 32 weeks of treatment, the responses to treatment were essentially identical in the 2 treatment groups. The only major difference in complications between the 2 groups was an increased risk of herpes zoster (ie, shingles) infection in the glucocorticoid-azathioprine group. While further studies are needed to determine the exact role of glucocorticoids-azathioprine treatment, these results suggest that additional treatment options for proliferative lupus nephritis may become available. A report by Stephany and colleagues[5] supported the findings of Ligtenberg and colleagues. They summarized their experience with MMF in 31 patients with SLE and renal disease, approximately half of whom had previously received IV cyclophosphamide and half of whom had not. Similar results, including stable renal function and protein excretion rates, were seen in these 2 groups. One patient developed significant worsening of disease, and 6 patients discontinued MMF -- 3 because of side effects (infection, anemia, and GI intolerance), 2 due to a desire to have a planned pregnancy (MMF use is contraindicated during pregnancy), and 1 for unknown reasons. These results, while preliminary, suggest that MMF may play a role in treatment of lupus nephritis in the future. A second important issue in the treatment of people with SLE and renal involvement is how to prevent recurrence of the disease. Previous studies show that aggressive treatment can lead to resolution of the renal disease. However, disease recurs in a large proportion of people shortly after discontinuing the initial treatment, unless additional
33
treatment, termed maintenance therapy, is provided. The standard maintenance therapy, IV cyclophosphamide every 3 months, is associated with a number of side effects. Contreras and colleagues[6] reported a comparison of 3 maintenance treatment regimens: IV cyclophosphamide every 3 months, daily MMF, and daily azathioprine. People receiving MMF were significantly less likely to have recurrence of their lupus nephritis than people treated with IV cyclophosphamide, and tended to do better than those treated with azathioprine. Both MMF and azathioprine were associated with fewer hospital days, less amenorrhea in women, and fewer infections than were seen in people treated with IV cyclophosphamide. While the numbers of people treated with each of these 3 options were relatively small (approximately 20 per group) and additional studies are needed, these results raise the possibility of more effective treatment options with fewer side effects than are available with current treatment plans. Lupus Nephritis in Children Another group of patients of particular concern is children with lupus nephritis. At the University of Miami, children with proliferative lupus nephritis who had WHO class III, IV, or V+ lupus nephritis and who had been treated with IV cyclophosphamide in the past had only an approximately 28% chance of having still-functioning kidneys 5 years after their initial diagnosis. Although these results are discouraging, they are significantly better than the results seen before cyclophosphamide was first used, when essentially no patients still had functioning kidneys at that time. Nevertheless, more effective longterm therapies are needed. Gesteira and colleagues[7] reported their experience using MMF as maintenance therapy for children with lupus nephritis after the disease was controlled with IV cyclophosphamide. Relatively low doses of MMF, 300-600 mg/m2, were used. Thirteen children have been treated with this regimen for at least 2 years. They observed that urine protein losses were improved after 18 months and that renal function, which typically worsened over time in patients not treated with MMF, tended to stabilize. In contrast to their previous findings, which indicated that only about 25% to 30% of children still had functioning kidneys after 5 years, approximately 75% of children treated with MMF had functioning kidneys after 5 years. In the University of Miami experience, MMF appears to be beneficial in the treatment of children with proliferative lupus nephritis. However, other centers treating children with lupus nephritis, but who do not use MMF, have reported outcomes similar to
34
this University of Miami experience. Clearly, additional studies are needed to define the role of MMF in the treatment armamentarium of children with lupus nephritis.
MMF for Treatment of Glomerulonephritis: A Review of the Literature Daniel Cattran, MD,[8] an international expert in the treatment of glomerulonephritis, reviewed the world's literature on the use of MMF to treat glomerulonephritis. He noted that MMF has multiple potentially beneficial effects. These include inhibiting proliferation of immune cells involved in glomerulonephritis, specifically B and T lymphocytes; inhibiting adhesion and migration of inflammatory cells to blood vessels; and induction of programmed cell death of inflammatory cells. Furthermore, MMF is likely to be highly specific for immune cells, thereby limiting its side effects. The published literature testing MMF's effects in several published and unpublished clinical studies was reviewed. Dr. Cattran emphasized that numerous studies suggest that MMF may be effective in treating a wide variety of renal diseases. However, he also reminded the audience that side effects can be significant, with many studies reporting infectious complications, most commonly herpes zoster, affecting approximately 20% of patients receiving MMF. GI side effects are also common. Thus, although MMF may become an important new addition to the treatment of patients with glomerulonephritis, it should be used by those who are experienced with its indications, effectiveness, and side effects. Glomerulonephritis (GN) Glomerulonephritis includes a range of immune-mediated disorders that cause inflammation within the glomerulus and other compartments of the kidney.1 Glomerulonephritis results from a variety of immune and inflammatory mechanisms. It is often described as primary, when there is no associated disease elsewhere, or secondary, when glomerular involvement is part of a systemic disease, e.g. systemic lupus erythematosus, polyarteritis nodosa. Primary glomerulonephritis may be classified according to the clinical syndrome produced, the histopathological appearance or the underlying aetiology. There is no direct correlation between the clinical syndrome produced and the pathological description. Glomerulonephritides may be:

35
Minimal change Diffuse: affects all glomeruli Focal: affects only some of the glomeruli Segmental: only parts of an affected glomeruli are affected.
Many cases of glomerulonephritis result in a mild, asymptomatic illness that remains undiagnosed.1 Histological patterns The commonly used pathological classification depends on light microscopy, but immunofluorescence and electron microscopy provide additional information and may give clues as to the aetiology. Minimal change disease Light microscopy is virtually normal, but electron microscopy shows widespread fusion of the epithelial cell foot processes on the outside of the glomerular basement membrane. Immunofluorescence is usually negative. Most often presents in children aged between two and four years. Accounts for 90% of cases of nephrotic syndrome in children, and about 20% of cases in adults.
Clinical features: nephrotic syndrome with selective proteinuria; normal renal function, normal blood pressure, normal complement levels; increased risk of infections, especially urinary tract infections and pneumococcal peritonitis (therefore give prophylactic penicillin if oedematous).
Associated with atopy in children, especially those who are HLA-DR7 positive.

May also be related to underlying Hodgkin's disease in adults. Usually responds to a course prednisolone, but relapse is frequent. of high-dose
Relapsing disease may go into remission following treatment with prednisolone and cyclophosphamide or cyclosporin. One third of patients have one episode, one third develop occasional relapses and one third have frequent relapses which stop before adulthood.
36
Minimal change disease does not progress to endstage renal failure. Focal segmental glomerulosclerosis Some of the glomeruli show segmental scarring, together with foot process fusion as in minimal change disease. Common cause of nephrotic syndrome in older children and younger adults; it may be associated with haematuria, hypertension and impaired renal function.
About 50% of patients may respond to a course of high-dose prednisolone, although treatment for up to 4 months is often required in adults. If this is unsuccessful, some patients may respond to the addition of cyclophosphamide, and cyclosporin can be used to reduce proteinuria.
Progresses to end-stage renal failure over several years in up to 50% of patients, but progression may be halted by treatment with corticosteroids.
A variant known as 'collapsing glomerulopathy' is associated with HIV infection.
Membranous nephropathy Widespread thickening of the glomerular basement membrane occurs. Immunofluorescence reveals granular deposits of immunoglobulin and complement.

Although most cases are idiopathic, it may also be secondary to SLE, hepatitis B, malignancy, or the use of gold or penicillamine.

More common in men.
Most common cause of nephrotic syndrome in adults. May present with proteinuria or nephritic syndrome, hypertension. Haematuria is rare. The idiopathic form may respond to a treatment regimen involving alternate months of corticosteroids with chlorambucil or cyclophosphamide, or to cyclosporin.
It progresses to end-stage renal failure in 30-50% of patients. The remainder with idiopathic membranous nephropathy have a complete or partial spontaneous remission of nephrotic syndrome with stable renal function.
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Mesangiocapillary glomerulonephritis (MCGN) Also known as glomerulonephritis.
membranoproliferative
Proliferation of mesangial cells, an increase in mesangial matrix and thickening of the glomerular basement membrane. Can be subdivided according to the appearance on electron microscopy.

Uncommon. May present with nephrotic syndrome or nephritic syndrome in children and young adults. Associated with low levels of C3. Secondary forms of the disease are associated with hepatitis C with or without cryoglobulins, other chronic infections and SLE. Nephrotic patients are often treated with corticosteroids but there is no treatment of proven benefit.

Approximately 50% of patients will develop endstage renal failure within ten years. Mesangial proliferative nephritis Mesangial cell proliferation combined with matrix expansion occurs. It is most often seen in the context of IgA deposition, when it is known as IgA nephropathy. Other immunoglobulins and complement components may also be present. IgA nephropathy (Berger's disease) often presents with macroscopic haematuria, which may be precipitated within a few days by an upper respiratory tract infection. It is also detected as asymptomatic haematuria and/or proteinuria, and can present with nephrotic syndrome.

More common in males.
Association with HLA B35 and D4, Coeliac disease, alcoholic liver disease and HIV. Some studies suggest that a course of high-dose prednisolone can reduce proteinuria and delay renal impairment. In patients with deteriorating renal function, immunosuppressive drugs are also often used. Although progression is slow, 20-30% of patients (unusual in children but more common in adults) may eventually develop end-stage renal failure.
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The renal lesion of Henoch-Schonlein purpura is similar to that of IgA nephropathy, and this may be a variant of the same disease. 20% develop impaired renal failure and 5% develop end-stage renal failure. Diffuse proliferative glomerulonephritis Widespread hypercellularity occurs, caused by both infiltrating inflammatory cells and proliferation of endothelial and mesangial cells. There is generally deposition of immunoglobulins and complement around the capillary loops. Generally presents with an acute nephritic syndrome two or more weeks after an infection.

Classically caused by streptococcal infection.
Rare in developed countries, but post-streptococcal glomerulonephritis remains common in the developing world. Many other bacterial and viral causes have now been described and is also associated with SLE.

Almost all children will recover without treatment (other than antibiotics for the infection), but a small proportion of adults may develop renal impairment. Focal segmental proliferative glomerulonephritis Usually occurs secondary to systemic disease, e.g. SLE, Alport's syndrome. There is often associated segmental necrosis of the capillary loops, which is followed by crescent formation.

The term crescentic glomerulonephritis is used when there is an accumulation of cells outside the capillary loops, but within Bowman's capsule. Crescentic glomerulonephritis May occur as part of the evolution of certain forms of primary glomerulonephritis (e.g. IgA nephropathy or mesangiocapillary glomerulonephritis), but is more often seen in conditions such as Goodpasture's syndrome and systemic vasculitis. Idiopathic crescentic glomerulonephritis is now regarded as a form of anti-neutrophil cytoplasm antibody (ANCA)-positive vasculitis limited to the kidney.

39
It presents with the clinical syndrome of rapidly progressive glomerulonephritis. Without treatment, the disease progresses to endstage renal failure within a few months Prednisolone and cyclophosphamide are generally effective in patients before severe renal damage occurs. Plasma exchange is recommended in patients with advanced renal disease.
Goodpasture's syndrome: Due to autoantibodies directed against the alpha 3 chain of type IV collagen, which is a major structural component of the glomerular basement membrane.
o
50% of patients haemorrhage.

o o
also
have
pulmonary
The syndrome presents with rapidly progressive glomerulonephritis, usually leading to renal failure within 6 months if untreated. Treatment with prednisolone, cyclophosphamide and plasma exchange is generally effective as long as it is started before renal disease is advanced.
o
It is very rare for patients to relapse, and the long-term outcome is good following successful treatment.
o
Presentation There is a spectrum of disease, from asymptomatic abnormalities to the nephritic and nephrotic syndromes.2

urinary
Asymptomatic haematuria and/or proteinuria.
Nephrotic syndrome: heavy proteinuria, hypoalbuminemia and fluid retention. Nephritic syndrome: haematuria (sometimes macroscopic), proteinuria, a fall in glomerular filtration rate, salt and water retention, and hypertension. Rapidly progressive glomerulonephritis: rapid loss of renal function, such that the patient will be in end-stage renal failure within weeks or months.
40
Chronic glomerulonephritis involves a much slower deterioration in renal function, usually over several years, accompanied by haematuria, proteinuria and hypertension. Investigations The investigations consist of an assessment of the severity of glomerular injury, together with a search for the cause: Urine dipstick and microscopy: haematuria and/or proteinuria will be found and, in some forms, red-cell casts.

Urine protein quantification: measured in 24-hour urine sample or by protein:creatinine ratio. Glomerular filtration rate: can be calculated by 24-hour creatinine clearance or from the serum creatinine by the Cockcroft and Gault formula: Male: GFR = (140 - age) x (weight) / (serum creatinine x 72)
o o
Female: GFR = (140 - age) x (weight) x 0.85 / (serum creatinine x 72) Full blood count, ESR, CRP. Biochemistry: renal function, electrolytes, liver function; serum albumin low in nephrotic syndrome; high potassium, low bicarbonate and high phosphate in renal failure.

Glucose: to exclude diabetes. and urine protein
Serum immunoglobulins, serum electrophoresis: to exclude myeloma.
Serum complement: low in systemic lupus erythematosus and cryoglobulinaemia and some forms of primary glomerulonephritis. Autoantibodies: ANA, anti-double stranded DNA, Antineutrophil cytoplasm antibody (ANCA), anti-glomerular basement membrane antibodies.

HBsAg; anti-HCV; anti-streptolysin O titre (ASOT). Radiology: renal ultrasound, chest x-ray.
Renal biopsy: except in the mildest cases, or in nephrotic syndrome in children. Management
41
Management will depend on type, severity and complications of glomerulonephritis. General Measures Monitoring of haematuria and proteinuria. Treatment of oedema with diuretics and potassium supplementation.

Blood pressure management: establishing target blood pressures and treatment of hypertension with angiotensin-converting enzyme inhibitor or angiotensin II receptor antagonists. Diet: advice on protein content will depend on presence and degree of nephrotic syndrome or renal failure.

Lipid-lowering therapy.
Specific Management Measures Dependent on the type and degree of histological changes but include: Immunosuppressive therapies including corticosteroids, alkylating agents (e.g., cyclophosphamide, chlorambucil), other cytotoxics (e.g., azathioprine, mizoribine), levamisole, and cyclosporin A.
Antithrombotics, such as dipyridamole, warfarin, and aspirin therapy.

Intravenous immunoglobulin. Dialysis.
Complications Hypertension may accelerate the decline in renal function so tight blood pressure control is an essential part of the management of all forms of glomerulonephritis. Nephrotic syndrome: pneumococcal infection.

e.g.
thrombotic
episodes,
End-stage renal failure.
Prognosis Depends on the type of glomerulonephritis but treatments for glomerulonephritis remain non-specific, often leading to side-effects, and only partly successful.
Glomerulonephritis is a common cause of end-stage chronic renal failure.
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Glomerular diseases are classified as those that present predominantly with hematuria (nephritic syndrome), high-level proteinuria (nephrotic syndrome), or both (see Appendix A: Glomerular Diseases: Glomerular Diseases by Age and Presentation). The diseases may be primary or have secondary causes (see Appendix B: Glomerular Diseases: Causes of Glomerulonephritis and Appendix C: Glomerular Diseases: Causes of Nephrotic Syndrome). The pathophysiology of nephritic and nephrotic diseases differs substantially, but their clinical overlap is considerableeg, several diseases may present with the same clinical pictureand the presence of hematuria or proteinuria does not itself predict response to treatment and prognosis. The diagnosis of glomerular disease is usually made when screening or diagnostic testing reveals elevated serum creatinine and abnormal urinalysis (hematuria with or without casts, proteinuria, or both). Approach to the patient involves distinguishing predominant-nephritic from predominant-nephrotic features and identifying likely causes by patient age (see Table 1: Glomerular Diseases: Glomerular Diseases by Age and Presentation), accompanying illness (see Table 2: Glomerular Diseases: Causes of Glomerulonephritis and Table 3: Glomerular Diseases: Causes of Nephrotic Syndrome), and other elements of the history (eg, time course, systemic manifestations, family history). Renal biopsy is indicated when diagnosis is unclear from history or when histology influences choice of treatment and outcomes (eg, lupus nephritis). Glomerulonephritis Definition Your kidneys are complex organs whose primary task is to remove wastes, excess fluid and unneeded electrolytes from your body. Any condition that interferes with kidney function can lead to a potentially dangerous buildup of waste products in your bloodstream. Glomerulonephritis (glo-mer-u-lo-nuh-FRI-tis) is a type of kidney disease that hampers your kidneys' ability to remove waste and excess fluids. Also called glomerular disease, glomerulonephritis can be acute,
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referring to a sudden attack of inflammation, or chronic, which comes on gradually. Glomerular disease can be part of a systemic disease, such as lupus or diabetes, or it can be a disease by itself primary glomerulonephritis. Treatment depends on the type of glomerulonephritis you have. Symptoms Signs and symptoms of glomerulonephritis may depend on whether you have the acute or chronic form, and the cause. Your first indication that something is wrong may come from symptoms or from the results of a routine urinalysis. Signs and symptoms may include:

Cola-colored or diluted iced-tea-colored urine from red blood cells in your urine (hematuria) Foam in the toilet water from protein in your urine (proteinuria) High blood pressure (hypertension) Fluid retention (edema) with swelling evident in your face, hands, feet and abdomen Fatigue from anemia or kidney failure Less frequent urination than usual Causes
Your kidneys are two bean-shaped, fist-sized organs situated at the small of your back, just below your rib cage, one on each side of your spine. Blood enters your kidneys through arteries from your aorta, the large artery that carries blood away from your heart. Each kidney contains approximately 1 million tiny filters (glomeruli), each of which is attached to the opening of a small fluid-collecting tube (tubule). Each glomerulus and tubule form a nephron, the functional unit of the kidneys. The glomeruli filter your blood as it passes through your kidneys. After being filtered by the glomeruli, blood travels through veins in the kidneys back to your bloodstream. The waste, after being modified by the tubules, goes to your bladder as urine through a tube from each kidney (ureter) and passes out of your body when you urinate. Every day about 1.5 to 2 quarts of extra water with waste products leave your body as urine. When your kidneys lose their filtering ability,
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dangerous levels of fluid and waste accumulate in your body, a condition known as kidney failure.
Many causes of glomerulonephritis Glomerulonephritis is one disorder that can lead to kidney failure. There are many causes of glomerulonephritis. They include those related to infections, immune diseases, inflammation of the blood vessels (vasculitis) and conditions that scar the glomeruli. Often, however, the exact cause is initially unknown. Here are some of the known causes: Infections
Post-streptococcal glomerulonephritis. Glomerulonephritis may develop after a strep infection in your throat or, rarely, on your skin (impetigo). Post-infectious glomerulonephritis is becoming less common, most likely because of rapid and complete antibiotic treatment of most streptococcal infections. Bacterial endocarditis. Bacteria can occasionally spread through your bloodstream and lodge in your heart, causing an infection of the valvular tissues inside the heart. Those at greatest risk are people with a heart defect, such as a damaged or artificial heart valve. Viral infections. Among the viral infections that may trigger glomerulonephritis are the human immunodeficiency virus (HIV), which causes AIDS, and the hepatitis B and hepatitis C viruses, which affect the liver and can become chronic infections.
Immune diseases
Lupus. A chronic inflammatory disease, lupus can affect many parts of your body, including your skin, joints, kidneys, blood cells, heart and lungs. Goodpasture's syndrome. A rare immune lung disorder that may mimic pneumonia, Goodpasture's syndrome causes bleeding (hemorrhage) into your lungs as well as glomerulonephritis. IgA nephropathy. Characterized by recurrent episodes of blood in the urine, this condition results from deposits of immunoglobulin A (IgA) in the glomeruli. IgA nephropathy can
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progress for years with no noticeable symptoms. The disorder seems to be more common in men than in women. Vasculitis
Polyarteritis. This form of vasculitis affects small and medium blood vessels in many parts of your body, such as your heart, kidneys and intestines. Wegener's granulomatosis. This form of vasculitis affects small and medium blood vessels in your lungs, upper airways and kidneys.
Conditions that cause scarring of the glomeruli
High blood pressure. Damage to your kidneys and their ability to perform their normal functions can occur as a result of high blood pressure. Glomerulonephritis can also cause high blood pressure because it reduces kidney function. Diabetic kidney disease. Possibly the most common cause of end-stage kidney disease in the United States, diabetic kidney disease (diabetic nephropathy) can affect anyone with diabetes. Diabetic nephropathy usually takes years to develop, and maintaining good control of blood sugar levels and controlling blood pressure may prevent or slow the kidney damage. Focal segmental glomerulosclerosis. Characterized by scattered scarring of some of the glomeruli, this condition may result from another disease or occur for no known reason.
Chronic glomerulonephritis sometimes develops after a bout of acute glomerulonephritis. In some people there's no history of kidney disease at all, and the first indication of chronic glomerulonephritis is chronic kidney failure. Infrequently, chronic glomerulonephritis runs in families. In many cases, no one knows the cause. Tests and diagnosis Specific signs and symptoms may suggest glomerulonephritis, but the condition often comes to light when a routine urinalysis is abnormal. The urinalysis may show red blood cells, an indicator of possible damage to
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the glomeruli; white blood cells, a common indicator of infection; or increased protein, which may indicate nephron damage. Other indicators, such as increased blood levels of creatinine or urea, also are red flags. Or, your hard-to-control high blood pressure may cause your doctor to suspect glomerulonephritis. If your doctor suspects glomerulonephritis, you may undergo one or more of the following diagnostic procedures, in addition to urine testing:
Blood tests. These can provide information about kidney damage and impairment of the filtering mechanisms by measuring levels of waste products, such as creatinine and blood urea nitrogen. Imaging tests. If your doctor detects evidence of damage, he or she may recommend diagnostic studies that allow visualization of your kidneys, such as a kidney X-ray, an ultrasound examination or a computerized tomography (CT) scan. Kidney biopsy. This procedure involves using a special needle to extract small pieces of kidney tissue for microscopic examination to help determine the cause of the inflammation. A kidney biopsy is almost always necessary to confirm a diagnosis of glomerulonephritis. Complications
Complications of glomerulonephritis may include:
Acute kidney failure. Loss of function in the filtering part of the nephron may cause waste products to accumulate rapidly. This condition may require emergency dialysis, an artificial means of removing extra fluids and waste from your blood, typically by an artificial kidney machine (dialyzer). Chronic kidney failure. In this extremely serious complication, the kidneys gradually lose function. Kidney function at less than 10 percent of normal capacity indicates end-stage kidney disease, which usually requires dialysis or a kidney transplant to sustain life. High blood pressure. Damage to your kidneys and the resultant buildup of wastes in the bloodstream can raise your blood pressure. Nephrotic syndrome. This is a group of signs and symptoms that may accompany glomerulonephritis and other conditions that affect the filtering ability of the glomeruli. Nephrotic
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syndrome is characterized by high protein levels in the urine, resulting in low protein levels in the blood, high serum cholesterol, and swelling of the eyelids, feet and abdomen. Treatments and drugs Treatment and outcome of glomerulonephritis depend on whether you have an acute or chronic form of the disease, on the underlying cause, and on the type and severity of your signs and symptoms. Some cases of acute glomerulonephritis, especially those that follow a strep infection, often improve on their own and require no specific treatment. To control your high blood pressure and slow the decline in kidney function, your doctor may prescribe one of several medications, including:

Diuretics Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor agonists Calcium channel blockers Beta blockers
Your doctor also may prescribe drugs to treat the underlying cause of glomerulonephritis:

Strep or other bacterial infection. Your doctor likely will prescribe an appropriate antibiotic. Lupus or vasculitis. Doctors often prescribe corticosteroids and immune-suppressing drugs. IgA nephropathy. Fish oil supplements have been successful in some people with IgA nephropathy and are under study. Goodpasture's syndrome. Plasmapheresis is sometimes used to treat people with Goodpasture's syndrome. Plasmapheresis is a mechanical process that removes antibodies from your blood by taking the plasma out of your blood and replacing it with fluid or donated plasma.
Therapies for associated kidney failure For acute glomerulonephritis and acute kidney failure, temporary dialysis can help remove excess fluid and control high blood pressure. The only long-term therapies for end-stage kidney failure are kidney
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dialysis and kidney transplantation. When a transplant isn't possible, often because of poor general health, dialysis becomes the only option. Glomerulonephritis Prevention There's no way to prevent most forms of glomerulonephritis. However, you can seek prompt treatment of a strep infection causing a sore throat or impetigo. To prevent infections, such as HIV and hepatitis, that can lead to some forms of glomerulonephritis, follow safe sex guidelines and avoid intravenous drug use. Controlling your blood sugar may prevent diabetic nephropathy, and controlling your blood pressure makes damage to your kidneys caused by hypertension less likely. Lifestyle and home remedies Your doctor may recommend changes in your diet, including restricting salt intake to prevent or minimize fluid retention, swelling and hypertension. Cutting back on protein and potassium consumption may slow the buildup of wastes in your blood. If you have diabetes, maintaining a healthy weight and controlling your blood sugar levels and blood pressure may help slow kidney damage. Coping and support Living with chronic glomerulonephritis and chronic kidney failure can tax your emotional resources. Talk with your doctor to be sure you know your treatment options. Also, you might benefit from joining a support group. Such a group can provide both sympathetic listening and useful information. To find out about support groups in your area that deal with kidney disease, Primary Glomerulonephritis Contents: Primary Glomerulonephritis Introduction: Primary Glomerulonephritis Is a kidney inflammation due to autoimmune causes and not associated with any other disease. Primary glomerulonephritis is one of the main causes of end-stage renal failure in people under 45. Approximately 0.02% of the US population suffer from primary glomerulonephritis.
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Misdiagnosis and Primary Glomerulonephritis Interstitial cystitis an under-diagnosed bladder condition: The medical condition of interstitial cystitic is a bladder condition that can be misdiagnosed as various conditions such as overactive bladder or other causes of pelvic pain. This condition can cause chronic pelvic pain or symptoms of urinary incontinence, similar to overactive bladder. Millions of patients may be misdiagnosed - an estimated third of the 9 million women with chronic pelvic pain (CPP) or 4.5 million of the 17 million women with overactive bladder syndrome do not respond well to treatment, and may have interstitial cystitis rather than their given diagnosis. In other words, about 6 million US women may have misdiagnosed interstitial cystitis. Autoimmune diseases: The word "auto" is the Greek word for self. The immune system is a complicated network of cells and cell components (called molecules) that normally work to ... Autoimmune diseases: A group of disorders in which the primary cause is the an inflammatory reaction caused by the body's own immune system attacking tissues. More detailed information about the symptoms, causes, and treatments of Autoimmune diseases is available below. Hematuria: Differential Diagnosis Signs and Symptoms
Transient hematuria Urinary tract infection/pyelonephritis Nephrolithiasis (kidney or bladder stones) Exercise Trauma, instrumentation, catheterization, or foreign bodies Endometriosis Transient unexplained Henoch-Schnlein purpura/HUS Coagulopathy and excess anticoagulation Prostatitis, epididymitis Persistent hematuria Sickle cell anemia Cancer (prostate, bladder, kidney) Benign prostatic hypertrophy Polycystic kidney disease Intrinsic glomerular disease Other causes of red or brown urine (pseudohematuria) Beeturia (14% population are susceptible after eating beets): Due
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to excretion of betalaine, a reddish pigment Myoglobinuria: Rapidly filtered and excreted; source is usually due to rhabdomyolysis; look for increased elevation of plasma CPK levels Hemoglobinuria: Occurs when the filtered load of unbound dimer exceeds resorptive capacity of the proximal tubules, generally at serum levels >100150 mg/dL Urethral carbuncle Urethritis (e.g., Chlamydia) Porphyria Phenazopyridine (bladder analgesic): Produces an orange color in urine Postinfectious glomerulonephropathy Hereditary (Alport's syndrome) IgA nephropathy (Berger's disease): Often see gross hematuria without positive family history of disease Loin pain hematuria syndrome Thin basement membrane disease (benign familial hematuria): Usually see microscopic hematuria; gross hematuria or renal failure is rare Hypercalciuria or hyperuricuria Arteriovenous malformation Fistula Others include food dyes, phenolphthalein, rifampin, and porphyrins Excessive anticoagulation Trauma Hematuria: Differential Diagnosis (Pediatric Signs and Symptoms)
Transient (fever, dehydration, exercise) Urinary tract infection Most common cause of gross hematuria Hypercalciuria (common) Primary glomerulonephritis (GN) Acute poststreptococcal GN: Gross hematuria hypertension, oliguria; 5 days to several weeks after Group A strep pharyngitis or pyoderma; can also occur after other infections IgA nephropathy (Berger disease): recurrent gross hematuria occurs at or near onset of a URI Membranoproliferative GN GN associated with systemic disease HSP
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SLE Other vasculitis (rare) e.g.,Wegener Other glomerular disease Benign familial hematuria Alport syndrome: Usually X linked, high- frequency deafness, progression to renal failure Glomerular disease (e.g., FSGS) usually presents as nephrotic syndrome Tubulointerstitial disease Polycystic kidney disease, interstitial nephritis, papillary necrosis, ATN Urinary pelvic junction obstruction Urolithiasis/nephrolithiasis Painless in up to 50% of children Urethrorrhagia Recurrent gross hematuria (spotting on the underwear) Most common in peripubertal males Malignancies (e.g., Wilms tumor) Vascular (e.g., renal vein thrombosis) Trauma Non-urinary tract blood Menses, perineal irritation, pinworms, masturbation, STDs, sexual abuse Munchausen/Munchausen by proxy (rare) Hematuria: Medical causes (Handbook of Signs & Symptoms (Third Edition)) Bladder cancer
A primary cause of gross hematuria in men, bladder cancer may also produce pain in the bladder, rectum, pelvis, flank, back, or leg Other common features are nocturia, dysuria, urinary frequency and urgency, vomiting, diarrhea, and insomnia. Bladder trauma Gross hematuria is characteristic in traumatic rupture or perforation of the bladder Typically, hematuria is accompanied by lower abdominal pain and, occasionally, anuria despite a strong urge to void The patient may also develop swelling of the scrotum, buttocks, or perineum and signs of shock, such as tachycardia and hypotension. Calculi Bladder and renal calculi produce hematuria, which may be associated with signs of a urinary tract infection (UTI), such as dysuria and urinary
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frequency and urgency Bladder calculi usually cause gross hematuria, referred pain to the lower back or penile or vulvar area and, in some patients, bladder distention. Renal calculi may produce microscopic or gross hematuria The cardinal symptom, however, is colicky pain that travels from the CVA to the flank, suprapubic region, and external genitalia when a calculus is passed. The pain may be excruciating at its peak. Other signs and symptoms may include nausea and vomiting, restlessness, a fever, chills, abdominal distention and, possibly, decreased bowel sounds. Coagulation disorders Macroscopic hematuria is usually the first sign of hemorrhage in coagulation disorders, such as thrombocytopenia or disseminated intravascular coagulation Other features include epistaxis, purpura (petechiae and ecchymoses), and signs of GI bleeding. Cortical necrosis (acute) Accompanying gross hematuria in acute cortical necrosis are intense flank pain, anuria, leukocytosis, and a fever. Cystitis Hematuria is a telling sign in all types of cystitis Bacterial cystitis usually produces macroscopic hematuria with urinary urgency and frequency, dysuria, nocturia, and tenesmus. The patient complains of perineal and lumbar pain, suprapubic discomfort, and fatigue and occasionally has a low-grade fever. More common in women, chronic interstitial cystitis occasionally causes grossly bloody hematuria. Associated features include urinary frequency, dysuria, nocturia, and tenesmus. Microscopic and macroscopic hematuria may occur with tubercular cystitis, which may also cause urinary urgency and frequency, dysuria, tenesmus, flank pain, fatigue, and anorexia. Viral cystitis usually produces hematuria, urinary urgency and frequency, dysuria, nocturia, tenesmus, and a fever. Diverticulitis When diverticulitis involves the bladder, it usually causes microscopic hematuria, urinary frequency and urgency, dysuria, and nocturia Characteristic findings include left lower quadrant pain, abdominal tenderness, constipation or diarrhea and, at times, a palpable, firm,
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fixed, and tender abdominal mass The patient may also develop mild nausea, flatulence, and a low-grade fever. Glomerulonephritis Acute glomerulonephritis usually begins with gross hematuria that tapers off to microscopic hematuria and red cell casts, which may persist for months It may also produce oliguria or anuria, proteinuria, a mild fever, fatigue, flank and abdominal pain, generalized edema, increased blood pressure, nausea, vomiting, and signs of lung congestion, such as crackles and a productive cough. Chronic glomerulonephritis usually causes microscopic hematuria accompanied by proteinuria, generalized edema, and increased blood pressure Signs and symptoms of uremia may also occur in advanced disease. Nephritis (interstitial) Typically, nephritis causes microscopic hematuria However, the patient with acute interstitial nephritis may develop gross hematuria. Other findings are a fever, a maculopapular rash, and oliguria or anuria. In chronic interstitial nephritis, the patient has dilute almost colorless urine that may be accompanied by polyuria and increased blood pressure. Nephropathy (obstructive) Obstructive nephropathy may cause microscopic or macroscopic hematuria, but urine is rarely grossly bloody The patient may report colicky flank and abdominal pain, CVA tenderness, and anuria or oliguria that alternates with polyuria. Polycystic kidney disease Polycystic kidney disease is a hereditary disorder that may cause recurrent microscopic or gross hematuria Although commonly asymptomatic before age 40, it may cause increased blood pressure, polyuria, dull flank pain, and signs of a UTI, such as dysuria and urinary frequency and urgency Later, the patient develops a swollen, tender abdomen and lumbar pain thats aggravated by exertion and relieved by lying down He may also have proteinuria and colicky abdominal pain from the ureteral passage of clots or stones.
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Prostatitis Whether acute or chronic, prostatitis may cause macroscopic hematuria, usually at the end of urination It may also produce urinary frequency and urgency and dysuria followed by visible bladder distention. Acute prostatitis also produces fatigue, malaise, myalgia, polyarthralgia, a fever with chills, nausea, vomiting, perineal and low back pain, and a decreased libido Rectal palpation reveals a tender, swollen, boggy, firm prostate. Chronic prostatitis commonly follows an acute attack. It may cause persistent urethral discharge, dull perineal pain, ejaculatory pain, and a decreased libido. Pyelonephritis (acute) Acute pyelonephritis typically produces microscopic or macroscopic hematuria that progresses to grossly bloody hematuria After the infection resolves, microscopic hematuria may persist for a few months. Related signs and symptoms include a persistent high fever, unilateral or bilateral flank pain, CVA tenderness, shaking chills, weakness, fatigue, dysuria, urinary frequency and urgency, nocturia, and tenesmus. The patient may also exhibit nausea, anorexia, vomiting, and signs of paralytic ileus, such as hypoactive or absent bowel sounds and abdominal distention. Renal cancer The classic triad of signs and symptoms includes grossly bloody hematuria; dull, aching flank pain; and a smooth, firm, palpable flank mass Colicky pain may accompany the passage of clots Other findings include a fever, CVA tenderness, and increased blood pressure In advanced disease, the patient may develop weight loss, nausea and vomiting, and leg edema with varicoceles. Renal infarction Typically, renal infarction produces gross hematuria The patient may complain of constant, severe flank and upper abdominal pain accompanied by CVA tenderness, anorexia, and nausea and vomiting Other findings include oliguria or anuria, proteinuria, hypoactive bowel sounds and, a day or two after infarction, a fever and increased blood pressure.
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Renal papillary necrosis (acute) Acute renal papillary necrosis usually produces grossly bloody hematuria, which may be accompanied by intense flank pain, CVA tenderness, abdominal rigidity and colicky pain, oliguria or anuria, pyuria, fever, chills, vomiting, and hypoactive bowel sounds Arthralgia and hypertension are common. Renal trauma About 80% of patients with renal trauma have microscopic or gross hematuria Accompanying signs and symptoms may include flank pain, a palpable flank mass, oliguria, hematoma or ecchymoses over the upper abdomen or flank, nausea and vomiting, and hypoactive bowel sounds Severe trauma may precipitate signs of shock, such as tachycardia and hypotension. Renal tuberculosis Gross hematuria is commonly the first sign of renal tuberculosis It may be accompanied by urinary frequency, dysuria, pyuria, tenesmus, colicky abdominal pain, lumbar pain, and proteinuria. Renal vein thrombosis Grossly bloody hematuria usually occurs in renal vein thrombosis In abrupt venous obstruction, the patient experiences severe flank and lumbar pain as well as epigastric and CVA tenderness Other features include a fever, pallor, proteinuria, peripheral edema and, when the obstruction is bilateral, oliguria or anuria and other uremic signs. The kidneys are easily palpable. Gradual venous obstruction causes signs of nephrotic syndrome, proteinuria and, occasionally, peripheral edema. Schistosomiasis Schistosomiasis usually causes intermittent hematuria at the end of urination It may be accompanied by dysuria, colicky renal and bladder pain, and palpable lower abdominal masses. Sickle cell anemia Sickle cell anemia is a hereditary disorder in which gross hematuria may result from congestion of the renal papillae Associated signs and symptoms may include pallor, dehydration, chronic fatigue, polyarthralgia, leg ulcers, dyspnea, chest pain, impaired growth and development, hepatomegaly and, possibly, jaundice Auscultation reveals tachycardia and systolic and diastolic murmurs.
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Systemic lupus erythematosus (SLE) Gross hematuria and proteinuria may occur when SLE involves the kidneys Cardinal associated features include nondeforming joint pain and stiffness, a butterfly rash, photosensitivity, Raynauds phenomenon, seizures or psychoses, a recurrent fever, lymphadenopathy, oral or nasopharyngeal ulcers, anorexia, and weight loss. Urethral trauma Initial hematuria may occur, possibly with blood at the urinary meatus, local pain, and penile or vulvar ecchymoses. Vasculitis Hematuria is usually microscopic in vasculitis Associated signs and symptoms include malaise, myalgia, polyarthralgia, a fever, increased blood pressure, pallor and, occasionally, anuria Other features, such as urticaria and purpura, may reflect the etiology of vasculitis. Other causes Diagnostic tests Renal biopsy is the diagnostic test most commonly associated with hematuria This sign may also result from biopsy or manipulative instrumentation of the urinary tract such as in cystoscopy. Drugs Drugs that commonly cause hematuria are anticoagulants, aspirin (toxicity), analgesics, cyclophosphamide, metyrosine, phenylbutazone, oxyphenbutazone, penicillin, rifampin, and thiabendazole. Herb alert When taken with an anticoagulant, herbal remedies, such as garlic and ginkgo biloba, can cause adverse reactions, including excessive bleeding and hematuria. Treatments Any therapy that involves manipulative instrumentation of the urinary tract, such as transurethral prostatectomy, may cause microscopic or macroscopic hematuria Following a kidney transplant, a patient may experience hematuria with or without clots, which may require indwelling urinary catheter irrigation.
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Acute poststreptococcal glomerulonephritis: Causes and incidence (Professional Guide to Diseases (Eighth Edition)) APSGN results from the entrapment and collection of antigen-antibody (produced as an immunologic mechanism in response to streptococcus) in the glomerular capillary membranes, inducing inflammatory damage and impeding glomerular function. Sometimes, the immune complement further damages the glomerular membrane. The damaged and inflamed glomerulus loses the ability to be selectively permeable, and allows red blood cells (RBCs) and proteins to filter through as the glomerular filtration rate (GFR) falls. Uremic poisoning may result. APSGN is most common in males ages 3 to 7, but it can occur at any age. Incidence is rising in the United States and Europe, with epidemics occurring in developing countries in Africa, the West Indies, and the Middle East. Up to 95% of children and up to 70% of adults with APSGN recover fully; the rest may progress to chronic renal failure within months. Chronic glomerulonephritis: Causes and incidence (Professional Guide to Diseases (Eighth Edition)) Common causes of chronic glomerulonephritis include primary renal disorders, such as membranoproliferative glomerulonephritis, membranous glomerulopathy, focal glomerulosclerosis, rapidly progressive glomerulonephritis and, less often, poststreptococcal glomerulonephritis. Systemic disorders that may cause chronic glomerulonephritis include lupus erythematosus, Goodpastures syndrome, or hemolytic-uremic syndrome. Chronic glomerulonephritis is twice as common in males as it is in females. Hematuria: Principal Causes of Hematuria (The Diagnostic Approach to Symptoms and Signs in Pediatrics) 1. Hematuria without proteinuria 1. Glomerular disorders 1. Acute postinfectious glomerulonephritis 2. Immunoglobulin A nephropathy 3. Henoch-Schnlein nephritis 4. Alport syndrome 5. Membranoproliferative glomerulonephritis 6. Systemic lupus erythematosus
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7. Familial benign hematuria (thin basementmembrane nephropathy) 8. Nonfamilial benign hematuria 2. Nonglomerular disorders 1. Urinarytract infection 2. Trauma 3. Exercise 4. Hydronephrosis 5. Renal vein thrombosis 6. Hemoglobinopathies 7. Idiopathic hypercalciuria 8. Urolithiasis 9. Polycystic kidney disease 10. Renal tuberculosis 11. Vascular malformations 12. Foreign body in the urethra or bladder 13. Neoplasm 14. Bleeding disorders 15. Drugs 2. Hematuria with proteinuria 1. Glomerulardisorders 1. Acutepostinfectious glomerulonephritis 2. Immunoglobulin A nephropathy 3. Henoch-Schnlein nephritis 4. Alport syndrome 5. Membranoproliferative glomerulonephritis 6. Systemic lupus erythematosus 7. Membranous nephropathy 8. Glomerulonephritis of chronic infection 9. Idiopathic rapidly progressive glomerulonephritis 10. Hemolytic-uremic syndrome 11. Polyarteritis nodosa 12. Antiglomerular basement membrane disease(Goodpasture disease) 13. Focal segmental glomerulosclerosis 14. Wegener granulomatosis Treatments for Primary Glomerulonephritis Acute poststreptococcal glomerulonephritis: Treatment (Professional Guide to Diseases (Eighth Edition)) The goals of treatment are relief of symptoms and prevention of complications. Vigorous supportive care includes bed rest, fluid and dietary sodium restrictions, and correction of electrolyte imbalances (possibly with dialysis, although this is rarely necessary). Therapy may
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include diuretics to reduce extracellular fluid overload and an antihypertensive. The use of antibiotics is recommended for 7 to 10 days if staphylococcal infection is documented. Otherwise, antibiotic use is controversial. Chronic glomerulonephritis: Treatment (Professional Guide to Diseases (Eighth Edition)) Treatment is essentially nonspecific and symptomatic, with its goals to control hypertension with antihypertensives and a sodium-restricted diet, to correct fluid and electrolyte imbalances through restrictions and replacement, to reduce edema with diuretics such as furosemide, and to prevent heart failure. Treatment may also include antibiotics (for symptomatic urinary tract infections [UTIs]), dialysis, or transplantation. Hematuria: Patient counseling (Professional Guide to Signs & Symptoms (Fifth Edition)) Teach the patient how to collect serial urine specimens using the threeglass technique. This technique helps determine whether hematuria marks the beginning, end, or entire course of urination. Hematuria: Patient counseling (Signs & Symptoms: A 2-in-1 Reference for Nurses) Teach the patient how to collect serial urine specimens using the threeglass technique. This technique helps determine whether hematuria marks the beginning, end, or entire course of urination. Encourage the patient to drink plenty of fluids, unless contraindicated. Hematuria: Nursing considerations (Nursing: Interpreting Signs and Symptoms) Check vital signs frequently. Monitor intake and output, including the amount and pattern of hematuria. If the patient has an indwelling urinary catheter in place, ensure its patency and irrigate it if necessary to remove clots and tissue that may impede urine drainage. Administer prescribed analgesics, and enforce bed rest as indicated. Prepare the patient for diagnostic tests, such as blood and urine studies, cystoscopy, and renal X-rays or biopsy.
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Monitor hemoglobin level and hematocrit; administer blood products as ordered. Patient teaching Show the patient how to collect urine specimens. Emphasize the need to increase fluid intake. Explain the underlying cause of hematuria and its treatment. Hematuria: Nursing considerations (Nursing: Interpreting Signs and Symptoms) Check vital signs frequently. Monitor intake and output, including the amount and pattern of hematuria. If the patient has an indwelling urinary catheter in place, ensure its patency and irrigate it if necessary to remove clots and tissue that may impede urine drainage. Administer prescribed analgesics, and enforce bed rest as indicated. Prepare the patient for diagnostic tests, such as blood and urine studies, cystoscopy, and renal X-rays or biopsy. Monitor hemoglobin level and hematocrit; administer blood products as ordered.
Patient teaching Show the patient how to collect urine specimens. Emphasize the need to increase fluid intake. Explain the underlying cause of hematuria and its treatment. The kidneys are a vital part of the body. Their main job is to remove waste products from the blood, which are passed out of the body in urine. There are about a million tiny filters in each kidney called glomeruli. If these filtering units get inflamed (swollen) for some reason this is called glomerulonephritis. It means the kidneys are unable to work properly. Salt and excess fluid can build up, leading to complications such as high blood pressure and in some cases, kidney failure. There are several types of glomerulonephritis; some are more serious and long-term than others. Glomerulonephritis may be short-lived
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(acute) and need minimal treatment. It may be present for many years without causing trouble, or it can develop into a long-term (chronic) condition. Glomerulonephritis often follows an infection such as an infection of the throat (pharyngitis). There are other conditions that cause glomerulonephritis and swelling in the kidneys such as infection, tumour growth, or disease within the kidney from long-term use of NSAIDs (non-steroidal anti-inflammatory drugs) such as aspirin. Glomerulonephritis is more common in men than women. It often affects children and young people. Kidneys Kidneys are a pair of bean-shaped organs located at the back of the abdomen, which remove waste and extra fluid from the blood and pass them out of the body as urine. Blood Blood supplies oxygen to the body and removes carbon dioxide. It is pumped around the body by the heart. High blood pressure Hypertension is when the pressure of the blood in your bloodstream is regularly above 140/90 mmHG. Acute Acute means occuring suddenly or over a short period of time. Chronic Chronic usually means a condition that continues for a long time or keeps coming back. Swelling Inflammation is the body's response to infection, irritation or injury, which causes redness, swelling, pain and sometimes a feeling of heat in the affected area. Anti-inflammatory Anti-inflammatory medicines reduce swelling and inflammation. Symptoms of glomerulonephritis There are several types of glomerulonephritis. If it has been caused by an infection, the early symptoms may include a sore throat. Inflammation in the kidneys may not be obvious at first. Symptoms of
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kidney damage can come on suddenly or appear up to three weeks after infection. As a result of damage to the kidneys, glomerulonephritis can cause:

swollen ankles, a puffy face, problems breathing, pale skin, headaches, visual problems, fever, loss of appetite, and vomiting.
In addition, there may be small amounts of blood in the urine and it may be cloudy. The normal urine output for an adult is between 0.8 and 2.5 litres per day. This can vary according to a number of factors such as how much you exercise and how hot or cold you are. In severe cases of glomerulonephritis, some people find that they do not urinate at all for two to three days. Once they are able to urinate again, there may still be blood and protein in the urine. Some people get pain in the kidneys (in the upper back, behind the ribs). Kidney pain may be due to a kidney infection or kidney stones and not glomerulonephritis, so it is important to see your GP for correct diagnosis.
Causes of glomerulonephritis Glomerulonephritis is usually caused by changes in the body's immune system. This is a complicated process involving antigens and antibodies. Antigens are foreign substances in the body such as proteins and toxins. Antibodies circulate in the blood and their job is to get rid of antigens. If these antigens and antibodies gather in the kidneys for any reason it can cause an inflammatory reaction (swelling). This reaction may just affect the kidney or may cause problems in other parts of the body. Anyone who already has a chronic autoimmune condition, such as lupus, is at risk of developing glomerulonephritis. An autoimmune condition means that the body attacks its own cells accidentally. Commonly, acute glomerulonephritis is linked to streptococci bacteria (beta haemolytic). This is referred to as acute post streptococcal glomerulonephritis (ASGN) and can follow a throat or skin infection. Glomerulonephritis is also recognised as a serious complication of some other infections including AIDS, HIV, Hepatitis B, Hepatitis C, tuberculosis and syphilis. For this reason, injecting drug users are particularly at risk of developing glomerulonephritis. Glomerulonephritis is a complication of many other diseases, including:

cancer and leukaemia, Hodgkin's disease, diabetes, Goodpastures syndrome (an autoimmune disorder that affects the lungs and kidneys), liver disease, and sickle cell disease
It is also recognised as a side effect of long-term use of certain drugs. Such drugs include, non-steroidal anti-inflammatory drugs (e.g. ibuprofen), gold injections (used in the treatment of rheumatoid arthritis), lithium (used in the treatment of depression) and penicillamine (used in the treatment of arthritis). Your GP should monitor your kidney function with renal tests if you are taking medicines that affect the function of the kidney. Diagnosing glomerulonephritis Often there are no symptoms at all. Sometimes glomerulonephritis is only diagnosed following a routine medical check-up, or during tests related to having high blood pressure, feeling tired or being pregnant. If you already have kidney disease, your doctor may want to test you for glomerulonephritis.
If you have glomerulonephritis, a urine test will show up blood and protein in the urine. A range of tests will be carried out to assess how well your kidneys are working (renal function tests). These will include blood samples to find out levels of sodium, chloride, potassium and urea. Tests may show that you are producing less urine than usual overall. If glomerulonephritis is suspected, the doctor may take a throat swab sample (scraping some cells from the back of your throat) to confirm the diagnosis. Some varieties of glomerulonephritis are more serious than others. Your doctor may remove and examine a small sample of kidney tissue (a biopsy) to see how serious the glomerulonephritis is. This is usually done using local anaesthetic and a small needle. The test carries a small risk of bleeding. Treating glomerulonephritis Treating the original infection Streptococci bacteria are usually destroyed with antibiotics such as penicillin. Other infections may require other types of antibiotics or antiviral drugs. Treating glomerulonephritis If you have glomerulonephritis the doctor treating you will focus on treating the cause as well as the condition. You may be advised to drink less fluid (restrict your fluid intake) and to avoid certain drinks such as alcohol and drinks with a lot of sodium chloride (salt) or potassium in them. Your diet should be controlled carefully. Your GP or dietician will give you advice on eating protein and controlling your intake of potassium and salt. Your blood chemistry will be regularly reviewed to ensure that levels of potassium, sodium and chloride are at the right level and that the amount of fluid in your diet is correct. Your treatment may include corticosteroids and a drug called cyclophosphamide. Other drugs used will relate to the underlying cause of the condition and the body's response to glomerulonephritis. Treating high blood pressure High blood pressure damages the kidney further and causes other health problems. Your blood pressure will be monitored by the doctor treating you, and you may need to take medicines such as ACE (angiotensin-converting enzyme) inhibitors. This type of medicine relaxes the blood vessels and reduces the workload of the heart. Treating chronic kidney disease or kidney failure
In cases of chronic kidney disease or kidney failure, kidney dialysis (using a machine to do the kidneys job of removing waste products from the body) or a kidney transplant will be needed. Complications of glomerulonephritis Possible complications vary according to glomerulonephritis but can include the following. High blood pressure This is a common complication of glomerulonephritis, because the kidneys help control the blood pressure in the body. Many people with glomerulonephritis are prescribed drugs to lower blood pressure. It is important to take these to protect the kidneys against further damage and also to reduce the risks of heart disease and stroke. If blood pressure is untreated it can lead to heart failure and fluid in the lungs (pulmonary oedema). Disease in other internal organs In most patients, glomerulonephritis affects only the kidneys. However, in some cases, the immune system that damages the kidneys can also affect other parts of the body, for example giving a blotchy red rash on the skin or pain in the joints. Discuss any symptoms you may have with your doctor to see if they could be related to glomerulonephritis. If you develop a blotchy red skin rash you should see your GP immediately. Kidney disease or kidney failure This is rare, but glomerulonephritis can cause so much damage to the kidneys that they fail completely. Preventing glomerulonephritis Glomerulonephritis is not generally preventable. Early detection (especially for people who have conditions linked to the disease), diagnosis and treatment are important to avoid other complications. Streptococcal throat infections should be treated as early as possible with antibiotics, to avoid kidney damage occurring. Glomerulonephritis the type of
What is glomerulonephritis? Glomerulonephritis is a type of kidney disease that involves the glomeruli. The glomeruli are very small, important structures in the kidneys that supply blood flow to the small units in the kidneys that filter urine, called the nephrons. During glomerulonephritis, the glomeruli become inflamed and impair the kidney's ability to filter urine. What causes glomerulonephritis? Glomerulonephritis is caused by several different disease states, including the following:

systemic immune disease such as systemic lupus erythematosus (SLE, or lupus) other systemic diseases may include: polyarteritis nodosa group - an inflammatory disease of the arteries. Wegener vasculitis - A progressive disease that leads to widespread inflammation of all of the organs in the body. Henoch-Schvnlein purpura - A disease usually seen in children that is associated with purpura (small or large purple lesions on the skin and internally on the organs) and involves multiple organ systems. Glomerulonephritis can also result from a gene on the X chromosome passed on from carrier mothers who have no features, or minimal features of the problem, to their sons, who are affected with the disorder in 50 percent of the cases. In children, a common cause of glomerulonephritis is from a streptococcal infection, such as strep throat or upper respiratory infection. Glomerulonephritis usually occurs more than one week after an infection. This is often referred to as acute poststreptococcal glomerulonephritis, or APSGN.
What are the symptoms of glomerulonephritis? The following are the most common symptoms of glomerulonephritis. However, each child may experience symptoms differently. Symptoms may include:

dark brown-colored urine (from blood and protein) sore throat diminished urine output fatigue lethargy increased breathing effort headache high blood pressure seizures (may occur as a result of high blood pressure) rash, especially over the buttocks and legs weight loss joint pain
pale skin color fluid accumulation in the tissues (edema)
The symptoms of glomerulonephritis may resemble other conditions and medical problems. Always consult your child's physician for a diagnosis. How is glomerulonephritis diagnosed? In addition to a thorough physical examination and complete medical history, your child's physician may recommend the following diagnostic tests:

throat culture urine tests blood tests electrocardiogram (ECG or EKG) - a test that records the electrical activity of the heart, shows abnormal rhythms (arrhythmias or dysrhythmias), and detects heart muscle damage. renal ultrasound (Also called sonography.) - a non-invasive test in which a transducer is passed over the kidney producing sound waves which bounce off of the kidney, transmitting a picture of the organ on a video screen. The test is used to determine the size and shape of the kidney, and to detect a mass, kidney stone, cyst, or other obstruction or abnormalities. chest x-ray- a diagnostic test which uses invisible electromagnetic energy beams to produce images of internal tissues, bones, and organs onto film. renal biopsy- a procedure where a small sample of tissue is taken from the kidney through a needle. The tissue is sent for special testing to determine the specific disease.
Treatment for glomerulonephritis: Specific treatment for glomerulonephritis will be determined by your child's physician based on:

your child's age, overall health, and medical history the extent of the disease your child's tolerance for specific medications, procedures, or therapies expectations for the course of the disease your opinion or preference
If glomerulonephritis is caused by a streptococcal infection, then treatment will be focused on curing the infection and treating the symptoms associated with the infection. Unfortunately, glomerulonephritis caused by a different reason cannot be cured. Therefore, treatments focus on slowing the progression of the disease preventing complications. Treatment for glomerulonephritis may include:
fluid restriction decreased protein diet decreased salt and potassium diet medication, such as: diuretics blood pressure medications phosphate binders - medications to decrease the amount of the mineral phosphorus in the blood. immunosuppressive agents dialysis - dialysis may be required for short term or long term therapy. Dialysis is a medical treatment to remove wastes and additional fluid from the blood after the kidneys have stopped functioning.
If glomerulonephritis does not resolve, long term kidney failure may need to be addressed. Glomerulonephritis The Facts Glomerulonephritis is a progressive kidney disease that involves the glomeruli, the individual filtering units of the kidney that produce urine. When the glomeruli become inflamed, the kidneys can't filter urine properly. This results in a build-up of excess fluid and toxins in the body. Glomerulonephritis can lead to chronic renal (kidney) failure. There are two main types of glomerulonephritis: primary and secondary. Primary glomerulonephritis affects the kidneys directly, while in secondary glomerulonephritis, the kidneys are damaged as a result of another illness. Glomerulonephritis seems to happen twice as often in males as in females. Causes Most people with glomerulonephritis have no known cause or risk factors. The most common known causes are bacterial (most often streptococcal) and viral infections. Doctors have found that many children with glomerulonephritis had been diagnosed with a streptococcal infection, such as strep throat, not long before developing signs of kidney damage. People with hepatitis or an infection of the liver can also develop glomerulonephritis. People with autoimmune disorders, such as lupus, also seem to be at risk of developing glomerulonephritis. The immune system, instead of attacking bacteria or viruses, attacks the body and the kidneys so that they can't function properly.
Symptoms and Complications The kidneys play three major roles in regulating the body. They:

filter urine to remove wastes from the body, keeping toxins from building up in the bloodstream regulate the minerals or electrolytes (sodium, calcium, and potassium, for example) and the levels of fluid in the body produce hormones that control other body functions, such as blood pressure, bone maintenance, and the production of red blood cells
Because of the large role the kidneys play in maintaining the body's health, the symptoms of glomerulonephritis and kidney failure are quite varied. Symptoms of glomerulonephritis include:

blood in the urine excessive foaming of the urine increased urination
Chronic renal (kidney) failure may develop. Symptoms are a direct result of the kidneys' inability to eliminate waste and excess fluid from the body, and when kidney failure is severe or near end stage, they include:

confusion decreased urination high blood pressure fatigue headache loss of appetite itchy skin thirst muscle twitching or cramping nausea and vomiting a yellowish-brown tint to the skin puffy eyes, hands, and feet (called edema) nosebleeds shortness of breath weight loss
The symptoms can become more severe if the inflammation isn't treated and kidney damage gets worse. Seizures and coma are possible in the later stages. Glomerulonephritis is serious. If left untreated, glomerulonephritis can lead to chronic renal failure, end-stage renal disease, high blood pressure, congestive heart failure, pulmonary edema, and an increased risk of other infections, especially urinary tract and kidney infections.
Making the Diagnosis Kidney damage is slow and progressive, so it's not usually obvious at first. Unfortunately, a lot of damage can be done before any symptoms become noticeable, and sometimes it's only picked up during routine blood or urine testing. If glomerulonephritis is suspected, your doctor will review your medical history. The history is followed by a physical exam and any of the following tests might be ordered:

blood tests urine tests kidney or abdominal ultrasounds kidney or abdominal CT or CAT (computed tomography) scans an IVP (intravenous pyelogram) - an X-ray examination of the kidneys, ureters, and bladder chest X-rays (if heart failure is suspected) a kidney biopsy
The blood tests show any build-up of body wastes in the bloodstream (such as urea), while urine tests reveal elements that shouldn't be present, such as protein or red blood cells. Ultrasounds and scans show kidney size (kidneys become enlarged in glomerulonephritis) and anything unusual, such as tumors or blockages. Finally, a kidney biopsy might be performed to confirm the diagnosis. A biopsy is done by inserting a fine needle into the kidney using an ultrasound as a guide and taking a tiny tissue sample that is then checked for damage or disease using a microscope. Treatment and Prevention Treatment of glomerulonephritis varies greatly from person to person, depending on whether it's acute or chronic and on how much damage has been done to the kidneys. For acute glomerulonephritis, the first goal is to reduce the symptoms and try to prevent more kidney damage. If high blood pressure (hypertension) has developed, it will be treated with anti-hypertensive medications (i.e., medications to lower blood pressure). If the condition is due to a bacterial infection, antibiotics will be prescribed. It's very important to take antibiotics exactly as instructed for the full course of treatment, even if the symptoms of infection disappear after a few days of treatment. This is to make sure that the infection is truly gone. Viral infections can't be treated by antibiotics and must run their course. Your doctor might also prescribe a diuretic. Diuretics increase the body's urine output, causing one to urinate larger amounts more frequently; these medications are often referred to as "water pills." It's usually best
to take diuretics in the morning or early afternoon to avoid having to get up often during the night to urinate. Vitamin or mineral supplements may be recommended, depending on the results of the blood tests, to help keep the levels of electrolytes (e.g., sodium, calcium, and potassium) balanced. People with kidney problems might be advised to change to a diet that cuts down on the waste build-up in the bloodstream. A special diet might also help control nausea and vomiting. These diets aren't usually needed if the kidney damage is mild. The prognosis of glomerulonephritis depends on whether it's an acute, first-time episode or whether it's chronic. The cause of the inflammation is another important factor. If the inflammation is treated early, and the cause is treatable, and the kidney damage is minor, the prognosis is good. In severe cases of glomerulonephritis, however, kidney damage can get worse, leading to chronic renal failure and other associated problems such as hypertension and heart failure. In severe cases, dialysis may be needed. Dialysis isn't a cure, and people who are on dialysis must follow special diets, restrict fluids, and take medications as prescribed by their doctors. The type of dialysis performed - peritoneal dialysis or hemodialysis - is chosen by the health care team according to individual needs. Dialysis removes excess fluids and waste using a membrane, instead of a kidney, as a filter.
What is glomerulonephritis? Glomerulonephritis is a type of kidney disease that involves the glomeruli. The glomeruli are very small, important structures in the kidneys that supply blood flow to the small units in the kidneys that filter urine, called the nephrons. During glomerulonephritis, the glomeruli become inflamed and impair the kidney's ability to filter urine. What causes glomerulonephritis? Glomerulonephritis is caused by several different disease states, including the following:
systemic immune disease such as systemic lupus erythematosus (SLE, or lupus) other systemic diseases may include:
polyarteritis nodosa group - an inflammatory disease of the arteries. Wegener vasculitis - A progressive disease that leads to widespread inflammation of all of the organs in the body. Henoch-Sch?nlein purpura - A disease usually seen in children that is associated with purpura (small or large purple lesions on the skin and internally on the organs) and involves multiple organ systems.
Glomerulonephritis can also result from a gene on the X chromosome passed on from carrier mothers who have no features, or minimal features of the problem, to their sons, who are affected with the disorder in 50 percent of the cases. In children, a common cause of glomerulonephritis is from a streptococcal infection, such as strep throat or upper respiratory infection. Glomerulonephritis usually occurs more than one week after an infection. This is often referred to as acute poststreptococcal glomerulonephritis, or APSGN. What are the symptoms of glomerulonephritis?
The following are the most common symptoms of glomerulonephritis. However, each child may experience symptoms differently. Symptoms may include:

dark brown-colored urine (from blood and protein) sore throat diminished urine output fatigue lethargy increased breathing effort headache high blood pressure seizures (may occur as a result of high blood pressure) rash, especially over the buttocks and legs weight loss
If need be, your health care team will assess you for a kidney transplant. As frightening as this may be, kidney transplants are relatively common now and have a good success rate. Someone who has had a successful transplant can go on to live a normal, healthy life. Glomerulonephritis can't really be anticipated, but doctors may be able to prevent some of the problems associated with the kidney damage if it's caught early enough. People with known risk factors for kidney failure, such as lupus, should be aware of what signs and symptoms to watch for. Infection should be taken seriously and treated. If antibiotics are prescribed, they should be taken as directed and for the full length of treatment. Glomerulonephritis (GN) Glomerulonephritis includes a range of immune-mediated disorders that cause inflammation within the glomerulus and other compartments of the kidney.1 Glomerulonephritis results from a variety of immune and inflammatory mechanisms. It is often described as primary, when there is no associated disease elsewhere, or secondary, when glomerular involvement is part of a systemic disease, e.g. systemic lupus erythematosus (SLE), polyarteritis nodosa. Primary glomerulonephritis may be classified according to the clinical syndrome produced, the histopathological appearance or the underlying aetiology. There is no direct correlation between the clinical syndrome produced and the pathological description. Glomerulonephritides may be:

Minimal change Diffuse: affects all glomeruli Focal: affects only some of the glomeruli Segmental: only parts of an affected glomeruli are affected
Many cases of glomerulonephritis result in a mild, asymptomatic illness that remains undiagnosed.1 Histological patterns The commonly used pathological classification depends on light microscopy, but immunofluorescence and electron microscopy provide additional information and may give clues as to the aetiology. Minimal change disease
Light microscopy is virtually normal, but electron microscopy shows widespread fusion of the epithelial cell foot processes on the outside of the glomerular basement membrane. Immunofluorescence is usually negative. Most often presents in children aged between two and four years. Accounts for 90% of cases of nephrotic syndrome in children, and about 20% of cases in adults.
Clinical features: nephrotic syndrome with selective proteinuria; normal renal function, normal blood pressure, normal complement levels; increased risk of infections, especially urinary tract infections and pneumococcal peritonitis (therefore give prophylactic penicillin if oedematous). Associated with atopy in children, especially those who are HLADR7 positive. May also be related to underlying Hodgkin's disease in adults. Usually responds to a course of high-dose prednisolone, but relapse is frequent. Relapsing disease may go into remission following treatment with prednisolone and cyclophosphamide or ciclosporin. One third of patients have one episode, one third develop occasional relapses and one third have frequent relapses which stop before adulthood. Minimal change disease does not progress to end-stage chronic renal failure. Focal segmental glomerulosclerosis
Some of the glomeruli show segmental scarring, together with foot process fusion as in minimal change disease. Common cause of nephrotic syndrome in older children and younger adults; it may be associated with haematuria, hypertension and impaired renal function. About 50% of patients may respond to a course of high-dose prednisolone, although treatment for up to 4 months is often required in adults. If this is unsuccessful, some patients may respond to the addition of cyclophosphamide, and ciclosporin can be used to reduce proteinuria. Progresses to end-stage renal failure over several years in up to 50% of patients, but progression may be halted by treatment with corticosteroids. A variant known as 'collapsing glomerulopathy' is associated with HIV infection. Membranous nephropathy
Widespread thickening of the glomerular basement membrane occurs. Immunofluorescence reveals granular deposits of immunoglobulin and complement. Although most cases are idiopathic, it may also be secondary to SLE, hepatitis B, malignancy, or the use of gold or penicillamine. More common in men.
Most common cause of nephrotic syndrome in adults. May present with proteinuria or nephritic syndrome, hypertension. Haematuria is rare. The idiopathic form may respond to a treatment regimen involving alternate months of corticosteroids with chlorambucil or cyclophosphamide, or to ciclosporin. It progresses to end-stage renal failure in 30-50% of patients. The remainder with idiopathic membranous nephropathy have a complete or partial spontaneous remission of nephrotic syndrome with stable renal function. Mesangiocapillary glomerulonephritis (MCGN)
Also known as membranoproliferative glomerulonephritis. Proliferation of mesangial cells, an increase in mesangial matrix and thickening of the glomerular basement membrane. Can be subdivided according to the appearance on electron microscopy. Uncommon. May present with nephrotic syndrome or nephritic syndrome in children and young adults. Associated with low levels of C3. Secondary forms of the disease are associated with hepatitis C with or without cryoglobulins, other chronic infections and SLE. Nephrotic patients are often treated with corticosteroids but there is no treatment of proven benefit. Approximately 50% of patients will develop end-stage renal failure within ten years. Mesangial proliferative nephritis
Mesangial cell proliferation combined with matrix expansion occurs. It is most often seen in the context of IgA deposition, when it is known as IgA nephropathy. Other immunoglobulins and complement components may also be present. IgA nephropathy (Berger's disease) often presents with macroscopic haematuria, which may be precipitated within a few days by an upper respiratory tract infection. It is also detected as asymptomatic haematuria and/or proteinuria, and can present with nephrotic syndrome. More common in males. Association with HLA B35 and D4, Coeliac disease, alcoholic liver disease and HIV. Some studies suggest that a course of high-dose prednisolone can reduce proteinuria and delay renal impairment. In patients with deteriorating renal function, immunosuppressive drugs are also often used.
Although progression is slow, 20-30% of patients (unusual in children but more common in adults) may eventually develop endstage renal failure. The renal lesion of Henoch-Schonlein purpura is similar to that of IgA nephropathy, and this may be a variant of the same disease. 20% develop impaired renal failure and 5% develop end-stage renal failure. Diffuse proliferative glomerulonephritis
Widespread hypercellularity occurs, caused by both infiltrating inflammatory cells and proliferation of endothelial and mesangial cells. There is generally deposition of immunoglobulins and complement around the capillary loops. Generally presents with an acute nephritic syndrome two or more weeks after an infection. Classically caused by streptococcal infection. Rare in developed countries, but post-streptococcal glomerulonephritis remains common in the developing world. Many other bacterial and viral causes have now been described and is also associated with SLE. Almost all children will recover without treatment (other than antibiotics for the infection), but a small proportion of adults may develop renal impairment. Focal segmental proliferative glomerulonephritis
Usually occurs secondary to systemic disease, e.g. SLE, Alport's syndrome. There is often associated segmental necrosis of the capillary loops, which is followed by crescent formation. The term crescentic glomerulonephritis is used when there is an accumulation of cells outside the capillary loops, but within Bowman's capsule. Crescentic glomerulonephritis
May occur as part of the evolution of certain forms of primary glomerulonephritis (e.g. IgA nephropathy or mesangiocapillary glomerulonephritis), but is more often seen in conditions such as Goodpasture's syndrome and systemic vasculitis. Idiopathic crescentic glomerulonephritis is now regarded as a form of anti-neutrophil cytoplasm antibody (ANCA)-positive vasculitis limited to the kidney. It presents with the clinical syndrome of rapidly progressive glomerulonephritis. Without treatment, the disease progresses to end-stage renal failure within a few months Prednisolone and cyclophosphamide
are generally effective in patients before severe renal damage occurs. Plasma exchange is recommended in patients with advanced renal disease. Goodpasture's syndrome: Due to autoantibodies directed against the alpha 3 chain of type IV collagen, which is a major structural component of the glomerular basement membrane. 50% of patients also have pulmonary haemorrhage. The syndrome presents with rapidly progressive glomerulonephritis, usually leading to renal failure within 6 months if untreated. Treatment with prednisolone, cyclophosphamide and plasma exchange is generally effective as long as it is started before renal disease is advanced. It is very rare for patients to relapse, and the long-term outcome is good following successful treatment.
Presentation There is a spectrum of disease, from asymptomatic urinary abnormalities to the nephritic and nephrotic syndromes.2

Asymptomatic haematuria and/or proteinuria. Nephrotic syndrome: heavy proteinuria, hypoalbuminaemia and fluid retention. Nephritic syndrome: haematuria (sometimes macroscopic), proteinuria, a fall in glomerular filtration rate, salt and water retention, and hypertension. Rapidly progressive glomerulonephritis: rapid loss of renal function, such that the patient will be in end-stage renal failure within weeks or months. Chronic glomerulonephritis involves a much slower deterioration in renal function, usually over several years, accompanied by haematuria, proteinuria and hypertension.
Investigations The investigations consist of an assessment of the severity of glomerular injury, together with a search for the cause:

Urine dipstick and microscopy: haematuria and/or proteinuria will be found and, in some forms, red-cell casts. Urine protein quantification: measured in 24-hour urine sample or by protein:creatinine ratio. Glomerular filtration rate: is provided by most biochemistry laboratories as the estimated glomerular filtration rate (eGFR) but can be calculated by 24-hour creatinine clearance or from the serum creatinine by the Cockcroft and Gault formula:
Male: GFR = (140 - age) x (weight) / (serum creatinine x 72) Female: GFR = (140 - age) x (weight) x 0.85 / (serum creatinine x 72) Full blood count, ESR, CRP. Biochemistry: renal function, electrolytes, liver function; serum albumin low in nephrotic syndrome; high potassium, low bicarbonate and high phosphate in renal failure. Glucose: to exclude diabetes. Serum immunoglobulins, serum and urine protein electrophoresis: to exclude myeloma. Serum complement: low in systemic lupus erythematosus and cryoglobulinaemia and some forms of primary glomerulonephritis. Autoantibodies: ANA, anti-double stranded DNA, Antineutrophil cytoplasm antibody (ANCA), anti-glomerular basement membrane antibodies. HBsAg; anti-HCV; anti-streptolysin O titre (ASOT). Radiology: renal ultrasound, chest x-ray. Renal biopsy: except in the mildest cases, or in nephrotic syndrome in children.
Management Management will depend on type, severity and complications of glomerulonephritis. General measures

Monitoring of haematuria and proteinuria. Treatment of oedema with diuretics and potassium supplementation. Blood pressure management: establishing target blood pressures and treatment of hypertension with angiotensin-converting enzyme inhibitor or angiotensin II receptor antagonists. Diet: advice on protein content will depend on presence and degree of nephrotic syndrome or renal failure. Lipid-lowering therapy. Specific management measures
Dependent on the type and degree of histological changes but include: Immunosuppressive therapies including corticosteroids, alkylating agents (e.g. cyclophosphamide, chlorambucil), other cytotoxics (e.g., azathioprine, mizoribine), levamisole, and ciclosporin A. Antithrombotics, such as dipyridamole, warfarin, and aspirin therapy. Intravenous immunoglobulin. Dialysis.
Complications
Hypertension may accelerate the decline in renal function so tight blood pressure control is an essential part of the management of all forms of glomerulonephritis. Nephrotic syndrome: e.g. thrombotic episodes, pneumococcal infection. End-stage renal failure. Depends on the type of glomerulonephritis but treatments for glomerulonephritis remain non-specific, often leading to sideeffects, and only partly successful. Glomerulonephritis is a common cause of end-stage chronic renal failure. Treatment of Primary Glomerulonephritis
Prognosis
Renal medicine is largely a disappointing discipline for the practicing physician. Although dialysis and transplantation can nowadays successfully substitute for renal function when kidneys have failed, there are almost no effective treatments for chronic glomerular diseases. Large-scale clinical trials have investigated ways to protect what is left of renal mass after injury or to retard inexorable progression toward renal failure, but there are no well-designed studies with sufficient statistical power concerning the specific treatment of glomerulonephritis. This may be due partly to insufficient knowledge of the mechanism (or mechanisms) of the glomerular injury and partly to the relative rarity of these syndromes. Modern nephrology was born when orderly classification of glomerular diseases was achieved. This classification is based on the pathologic description of the injured glomerulus, and it distinguishes primary forms (not associated with extrarenal manifestations) from secondary forms, which are associated with systemic diseases. The book of Ponticelli and Glassock is an excellent overview of all the efforts to treat primary glomerular diseases. The opening chapter examines all the aspects of symptomatic or supportive therapy the measures to correct or attenuate the biochemical imbalance and pathophysiologic disturbances that follow renal damage. In the second chapter, 52 of the book's 260 pages are devoted to an exhaustive and up-to-date review of the clinical pharmacology of drugs that have been used to treat glomerular diseases (or are at an investigational stage). This chapter contains abundant information regarding the side effects of the various drugs, which offers the practicing physician the opportunity to balance the advantages and risks of these treatments. The subsequent chapters summarize the
natural history of primary glomerular diseases and the effects of various treatments. All the chapters are replete with references to small, uncontrolled studies and to larger, controlled clinical trials, although the latter could rarely be considered statistically powerful enough to allow definitive conclusions. The authors make generous use of tables and figures to summarize the results of these studies. Concise algorithms illustrate the authors' suggested plan for a patient affected by a given glomerular disease. As a matter of fact, practical recommendations are what nephrologists look for in a book like this, and the authors fulfill this need. However, I am not sure that all their recommendations can be taken for granted. Most of them are based on small, uncontrolled clinical trials, and it is difficult to pack together sparse observations in one conclusive statement on the efficacy of a proposed therapy. In fact, small studies generally have positive results, but when therapeutic hypotheses are tested on a large scale they often fail to show a definitive benefit. Curiously, there is a contradiction in the book regarding the use of metaanalysis in nephrology. Ponticelli and Passerini criticize the application of this method to studies on membranous nephropathy, noting that pooling the results of studies with different designs, populations, and forms of therapy is an intrinsic limit of the meta-analysis. Yet in another chapter, Glassock states that meta-analysis of trials in IgA nephropathy supports the beneficial effect of steroid therapy on reduction of proteinuria. One has the general impression that this book is a collection of conscientiously documented chapters but lacks internal consistency and a unifying overview of the mechanisms of damage, and therefore of the therapeutic approach. It is probably time to look at the glomerular diseases with a different perspective. It appears that minimal lesions respond well to steroids; active inflammatory lesions, such as those in crescenteric forms, are often sensitive to immunosuppressive drugs; and when sclerosis is the prevailing pathologic feature, there is very little hope of avoiding progression and renal failure, whatever the treatment. While we are waiting for such an approach to be consecrated in print, this book should be considered a good, up-to-date source of information and references on the treatment of glomerular diseases and should be consulted critically by all those facing these problems in the daily practice of nephrology. Background: Few epidemiological studies have investigated the longterm outcome of primary glomerulonephritis (GN) and its determinants in the decade since angiotensin-converting enzyme inhibitors entered widespread use. Aim: To study several traditional and less traditional risk factors for kidney disease progression in a cohort of patients with primary GN.
Design: Retrospective cohort study. Methods: We included 536 patients with primary GN first diagnosed between 1994 and 2001: 283 IgA nephropathy (IgA), 129 membranous nephropathy (MN), and 124 focal and segmental glomerulosclerosis (FSGS). Adjusted hazard ratios (HR) or dialysis or preemptive transplantation for end-stage renal disease (ESRD) according to various characteristics were estimated with Cox proportional-hazard models. Results: At diagnosis, mean patient age was 43 17 years, 74% were men, and the mean estimated glomerular filtration rate (eGFR) was 69 31 mL/mn/1.73m2. After a mean follow-up of 7-years, 104 patients had started ESRD treatment and 14 had died before reaching ESRD. The 7year renal survival rate was 69% for FSGS, 88% for MN, and 82% for IgAN (p < 0.01). In patients with FSGS, younger age was associated with a higher risk of ESRD. Baseline proteinuria, diabetes, and haemoglobin (Hb) concentration were strongly associated with shorter time to ESRD independent of baseline eGFR, but gender, hypertension and smoking were not. Adjusted HRs for ESRD were 2.6 [95% confidence interval, 1.25.8] for diabetes and 2.4 [1.34.5] for the lowest and 1.9 [1.03.6] for the intermediate Hb tertiles versus the highest. Discussion: In patients with primary GN, renal survival is clearly lower for FSGS than for IgAN and MN. Independent predictors for progression were baseline diabetes and anaemia, as well as proteinuria, for all GN types, and younger age, for FSGS. Glomerulonephritis (nephritic syndrome) is a disorder of glomeruli (clusters of microscopic blood vessels in the kidneys with small pores through which blood is filtered). It is characterized by body tissue swelling (edema), high blood pressure, and the presence of red blood cells in the urine. Glomerulonephritis can be caused by various disorders, such as infections, an inherited genetic disorder, or autoimmune disorders. People may have tissue swelling, headaches, visual disturbances, and seizures. Diagnosis is based on tests of blood and urine and sometimes imaging tests, a biopsy of the kidneys, or both. People need to restrict salt and protein intake and take diuretics or antibiotics until kidney function improves. Glomerulonephritis can develop over a short time period (acute glomerulonephritis) or develop and progress slowly (chronic glomerulonephritis). In 1% of children and 10% of adults who have acute glomerulonephritis, it evolves into rapidly progressive
glomerulonephritis, in which most of the glomeruli are destroyed, resulting in kidney failure Causes Glomerulonephritis can be primary, affecting only the kidneys, or secondary, caused by a vast array of disorders that affect other parts of the body. Acute Glomerulonephritis: Acute glomerulonephritis most often occurs as a complication of throat or skin infection by streptococcus, a type of bacteria. Acute glomerulonephritis that occurs after a streptococcal infection (post-streptococcal glomerulonephritis) typically develops in children between the ages of 2 and 10 following recovery from the infection. Infections with other types of bacteria, such as staphylococcus and pneumococcus, viral infections, such as chickenpox, and parasitic infections, such as malaria, can also result in acute glomerulonephritis. Acute glomerulonephritis that results from any of these infections is called postinfectious glomerulonephritis. Noninfectious causes of acute glomerulonephritis include membranoproliferative glomerulonephritis, immunoglobulin A (IgA) nephropathy, thin basement membrane disease, Henoch-Schnlein purpura, systemic lupus erythematosus (lupus), cryoglobulinemia, Goodpasture's syndrome, and Wegener's granulomatosis. Acute glomerulonephritis that develops into rapidly progressive glomerulonephritis most often results from conditions that involve an abnormal immune reaction. Chronic Glomerulonephritis: Often, chronic glomerulonephritis seems to result from one of the same conditions that cause acute glomerulonephritis, such as IgA nephropathy or membranoproliferative glomerulonephritis. Sometimes, acute glomerulonephritis does not resolve and instead becomes chronic. Occasionally, chronic glomerulonephritis is caused by hereditary nephritis, an inherited genetic disorder. In many people, the cause of chronic glomerulonephritis cannot be identified. Symptoms About half of the people with acute glomerulonephritis have no symptoms. If symptoms do occur, the first to appear are tissue swelling (edema) due to fluid retention, low urine volume, and production of urine that is dark because it contains blood. Edema may first appear as puffiness of the face and eyelids but later is prominent in the legs. Blood pressure increases as kidney function becomes impaired. In turn, high blood pressure and swelling of the brain may produce headaches, visual disturbances, and more serious disturbances of brain function (for
example, seizures or coma). In older people, nonspecific symptoms, such as nausea and a general feeling of illness (malaise), are more common. When rapidly progressive glomerulonephritis develops, weakness, fatigue, and fever are the most frequent early symptoms. Loss of appetite, nausea, vomiting, abdominal pain, and joint pain are also common. About 50% of people have a flu-like illness in the month before kidney failure develops. These people have edema and usually produce very little urine. High blood pressure is uncommon and rarely severe when it does occur. Because chronic glomerulonephritis usually causes only very mild or subtle symptoms, it goes undetected for a long time in most people. Edema may occur. High blood pressure is common. The disease may progress to kidney failure, which can cause itchiness, fatigue, decreased appetite, nausea, vomiting, and difficulty breathing. Diagnosis Doctors investigate the possibility of acute glomerulonephritis in people whose laboratory test results indicate kidney dysfunction or blood in the urine and in people who develop symptoms of the disorder, particularly those who have had strep throat or other infections. Laboratory tests show variable amounts of protein and blood cells in the urine and often kidney dysfunction, as shown by a high concentration of urea and creatinine (waste products) in the blood. In people with rapidly progressive glomerulonephritis, casts (clumps of red blood cells or white blood cells) are almost always visible in a urine sample that is examined under a microscope. Blood tests detect anemia and often an abnormally high number of white blood cells. When doctors suspect glomerulonephritis, a biopsy of the kidney is usually done to confirm the diagnosis, help determine the cause, and determine the amount of scarring and potential for reversibility. Kidney biopsy is done by inserting a needle in one of the kidneys under ultrasound or computed tomography (CT) guidance to obtain a small amount of kidney tissue. Although kidney biopsy is an invasive procedure and occasionally can become complicated, it is usually safe. Additional tests are sometimes helpful for identifying the cause. For example, a throat culture may provide evidence of streptococcal infection. Blood levels of antibodies against streptococci may be higher than normal or progressively increase over several weeks. Acute glomerulonephritis that follows an infection other than strep throat is usually easier to diagnose, because its symptoms often begin while the
infection is still obvious. Cultures and blood tests that help identify the organisms that cause these other types of infections are sometimes needed to confirm the diagnosis. Chronic glomerulonephritis develops gradually, and therefore, a doctor may not be able to tell exactly when it began. It may be discovered when a urine test, done as part of a medical examination, reveals the presence of protein and blood cells in a person who is feeling well, has normal kidney function, and has no symptoms. Doctors usually do an imaging test of the kidneys, such as an ultrasound, CT scan, or magnetic resonance imaging (MRI) scan. A kidney biopsy is the most reliable way to distinguish chronic glomerulonephritis from other kidney diseases. A biopsy, however, is rarely done in advanced stages. In these cases, the kidneys are shrunken and scarred, and the chance of obtaining specific information about the cause is small. Doctors suspect that the kidneys are shrunken and scarred if kidney function has been poor for a long time and the kidneys appear abnormally small on an imaging test. Prognosis Acute poststreptococcal glomerulonephritis resolves completely in most cases, especially in children. About 0.1% of children and 25% of adults develop chronic kidney failure. The prognosis for people with rapidly progressive glomerulonephritis depends on the severity of glomerular scarring and whether the underlying disease, such as infection, can be cured. In about 75% of the people who are treated early (within weeks to a few months), kidney function is preserved and dialysis is not needed. However, because the early symptoms can be subtle and vague, many people who have rapidly progressive glomerulonephritis are not aware of the underlying disease and do not seek medical care until kidney failure develops. If treatment occurs late, the person is more likely to develop chronic kidney failure. The prognosis also depends on the cause, the person's age, and any other diseases the person might have. When the cause is unknown or the person is older, the prognosis is worse. In some children and adults who do not recover completely from acute glomerulonephritis, other types of kidney disorders develop, such as asymptomatic proteinuria and hematuria syndrome or nephrotic syndrome. Other people with acute glomerulonephritis, especially older adults, often develop chronic glomerulonephritis. Diseases of the Kidney and the Urinary Tract Nephritis, nephrotic syndrome and nephrosis can be signs of infections, systemic
conditions, autoimmune and chronic or degenerative diseases affecting the kidney. They can also be secondary to prolonged medication, exposure to poisons or traumatic injury. The causes are varied.They can be hereditary or acquired and may be secondary to other Leading causes of death manifesting as end-stage renal disease(ESRD There are problems in obtaining routine countrywide data reflecting the prevalence of kidney diseases. However, the mortality trends for diseases of the kidney and urinary tract are generally increasing at a slow phase. Studies indicate that around 9,500 Filipinos develop fatal diseases of the kidneys annually. Nephritis, nephrotic syndrome and nephrosis accounted for 7,963 deaths registered in 2000. This translates to a death rate of 10.4 per 100,000 population, the tenth highest among the causes of death in the country. In addition, kidney infections and calculi at any portion of the urinary tract had mortality rates of 0.8 and 0.5 per 100,000 population, respectively, during that year. A significant proportion of ESRD is secondary to the top causes of chronic illness in the country. Studies by two leading hospitals in Metro Manila indicate that the most common underlying diseases for ESRD are chronic glomerulonephritis, chronic pyelonephritis, diabetes mellitus and hypertensive nephrosclerosis. In short, deaths from renal causes are the consequences of prolonged or uncontrolled assault of infectious or metabolic agents on the kidneys and are regarded as degenerative. ESRD is expected to increase proportionately with the incidence of degenerative or lifestyle-related diseases. Unless these underlying diseases are controlled, prevalence of ESRD will remain high. Since the cost of treatment is prohibitive, deaths from ESRD will also be staggering. (National Objectives for Health Philippines 20052010), Department of Health (DOH). Primary or idiopathic Nephrotic Syndrome is a collective term that describe the clinical picture of nephritic syndrome occurring in the absence of systemic disease, with an annual incidence of approximately 1-2 new cases per 100,000 population under the age of 16 years. Percutaneous renal biopsy of these children revealed that Mesangial proliferative glomerulonephritis was found to be the most predominant histopathology at prevalent histopathologic type of primary nephritic syndrome The clinical features of this histopathologic finding conformed to that of the established features of nephritic syndrome. Frequent relapse was
the most prevalent outcome. Treatment response has no significant association with the results of the immunofluorescence studies. Moreover, there was note of common occurrence of URTI preceding relapse. Therefore, attempts to prevent and limit exposure to subject of respiratory tract infection may be beneficial together with pneumococcal vaccination. (Primary nephrotic syndrome-mesangial proliferative glomerunephritis in children: Clinicopathology and treatment outcome Violeta Valderama, M.D., Isabel Vilvar, M.D., Jimmylito Solomon, M.D., Maria Angeles Marbella, M.D., Ofelia de Leon, M.D., Solita Tadoy, M.D., Zenaida Antonio, M.D., Myrna Rosel, M.D.) The list of possible underlying conditions mentioned in various sources for Glomerulonephritis includes:
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Streptococcal infection - for post-streptococcal glomerulonephritis Strep throat Streptococcal skin infection Bacterial infection Viral infection Parasitic infection SLE Certain cancers Certain blood disorders
Abdominal pain Haematuria-Blood in the urine is called "hematuria" and can indicate quite severe problems. Bleeding can arise within the urinary system in areas such as the kidneys, bladder, prostate or other parts of the urinary tract. Blood in urine may appear as reddening or darkened urine or other urine color changes such as smoky, orangish or pinkish hues. Streaks of blood may also appear in the urine. Bleeding must be distinguished from other causes of urine discoloration or urine color changes. The appearance of blood in the urine or any urine color changes needs prompt professional medical investigation. (www.wrongdiagnosis.com)
The Facts Glomerulonephritis is a progressive kidney disease that involves the glomeruli, the individual filtering units of the kidney that produce urine. When the glomeruli become inflamed, the kidneys can't filter urine properly. This results in a build-up of excess fluid and toxins in the body. Glomerulonephritis can lead to chronic renal (kidney) failure. There are two main types of glomerulonephritis: primary and secondary. Primary glomerulonephritis affects the kidneys directly, while in secondary glomerulonephritis, the kidneys are damaged as a result of another illness. Glomerulonephritis seems to happen twice as often in males as in females. Causes Most people with glomerulonephritis have no known cause or risk factors. The most common known causes are bacterial (most often streptococcal) and viral infections. Doctors have found that many children with glomerulonephritis had been diagnosed with a streptococcal infection, such as strep throat, not long before developing signs of kidney damage. People with hepatitis or an infection of the liver can also develop glomerulonephritis. People with autoimmune disorders, such as lupus, also seem to be at risk of developing glomerulonephritis. The immune system, instead of attacking bacteria or viruses, attacks the body and the kidneys so that they can't function properly. (http://health.abqjournal.com) The results of treatment of glomerulonephritis (GN) in childhood with oral corticosteroids, immunosuppressive drugs, anticoagulants and the newer regimens of pulsed, high-dose intravenous methylprednisolone and plasma exchange are reviewed and compared with the natural history of the untreated condition. Poststreptococcal GN and the nephritis of Schnlein-Henoch purpura need no specific treatment unless extensive glomerular crescents are present. The progression of mesangiocapillary GN can probably be slowed or even reversed with long-term, alternate-day steroid therapy. As in adults, recovery of renal function in GN due to antibody to glomerular basement membrane can be achieved in some patients using plasma exchange, but only those in whom some renal function is still present when treatment is started. In rapidly progressive (extracapillary) GN with crescents, traditional therapy with oral steroids, immunosuppressive drugs and
anticoagulants reduces renal mortality from 85%90% to about 50%, while pulsed methylprednisolone and plasma exchange improve the outcome further, mortality falling to about 25%. It is recommended that children with crescentic GN and deteriorating function be treated initially with pulsed methylprednisolone, followed by plasma exchange in those who fail to respond or who deteriorate following temporary response to pulse therapy. Treatment must be given early in the course of the illness if good results are to be obtained. (The treatment of glomerulonephritis in children, Journal of Pediatric Nephrology, George B. Haycock, January 12, 1998) How is glomerulonephritis diagnosed? In addition to a thorough physical examination and complete medical history, your child's physician may recommend the following diagnostic tests:

throat culture urine tests blood tests electrocardiogram (ECG or EKG) - a test that records the electrical activity of the heart, shows abnormal rhythms (arrhythmias or dysrhythmias), and detects heart muscle damage. renal ultrasound (Also called sonography.) - a non-invasive test in which a transducer is passed over the kidney producing sound waves which bounce off of the kidney, transmitting a picture of the organ on a video screen. The test is used to determine the size and shape of the kidney, and to detect a mass, kidney stone, cyst, or other obstruction or abnormalities. chest x-ray - a diagnostic test which uses invisible electromagnetic energy beams to produce images of internal tissues, bones, and organs onto film. renal biopsy - a procedure where a small sample of tissue is taken from the kidney through a needle. The tissue is sent for special testing to determine the specific disease.
If glomerulonephritis is caused by a streptococcal infection, then treatment will be focused on curing the infection and treating the symptoms associated with the infection. Unfortunately, glomerulonephritis caused by a different reason cannot be cured. Therefore, treatments focus on slowing the progression of the disease preventing complications. How is glomerulonephritis diagnosed? In addition to a thorough physical examination and complete medical history, your child's physician may recommend the following diagnostic tests:

throat culture urine tests blood tests electrocardiogram (ECG or EKG) - a test that records the electrical activity of the heart, shows abnormal rhythms (arrhythmias or dysrhythmias), and detects heart muscle damage. renal ultrasound (Also called sonography.) - a non-invasive test in which a transducer is passed over the kidney producing sound waves which bounce off of the kidney, transmitting a picture of the organ on a video screen. The test is used to determine the size and shape of the kidney, and to detect a mass, kidney stone, cyst, or other obstruction or abnormalities. chest x-ray - a diagnostic test which uses invisible electromagnetic energy beams to produce images of internal tissues, bones, and organs onto film. renal biopsy - a procedure where a small sample of tissue is taken from the kidney through a needle. The tissue is sent for special testing to determine the specific disease.
If glomerulonephritis is caused by a streptococcal infection, then treatment will be focused on curing the infection and treating the symptoms associated with the infection. Unfortunately, glomerulonephritis caused by a different reason cannot be cured. Therefore, treatments focus on slowing the progression of the disease preventing complications. Treatment for glomerulonephritis may include:

fluid restriction decreased protein diet decreased salt and potassium diet medication, such as: o diuretics o blood pressure medications o phosphate binders - medications to decrease the amount of the mineral phosphorus in the blood. o immunosuppressive agents dialysis Dialysis may be required for short-term or long-term therapy. Dialysis is a medical treatment to remove wastes and additional fluid from the blood after the kidneys have stopped functioning.
If glomerulonephritis does not resolve, long-term kidney failure may need to be addressed. (http://www.childrensnyp.org)
Glomerulonephritis Each of your kidneys contains approximately 1 million filters (glomeruli). Each glomerulus is attached to the opening of a small fluid-collecting tube (tubule). Together, the glomerulus and tubule create a nephron.
When to seek medical advice Talk to your doctor if you have a condition that's associated with glomerulonephritis or if you're experiencing any of the signs or symptoms of glomerulonephritis. Screening and diagnosis Specific signs and symptoms may suggest glomerulonephritis, but the condition often comes to light when a routine urinalysis is abnormal. The urinalysis may show red blood cells, an indicator of possible damage to the glomeruli; white blood cells, a common indicator of infection; or increased protein, which may indicate nephron damage. Other indicators, such as increased blood levels of creatinine or urea, also are red flags. Or, your hard-to-control high blood pressure may cause your doctor to suspect glomerulonephritis. If your doctor suspects glomerulonephritis, you may undergo one or more of the following diagnostic procedures, in addition to urine testing:
Blood tests. These can provide information about kidney damage and impairment of the filtering mechanisms by measuring levels of waste products, such as creatinine and blood urea nitrogen. Imaging tests. If your doctor detects evidence of damage, he or she may recommend diagnostic studies that allow visualization of your kidneys, such as a kidney X-ray, an ultrasound examination or a computerized tomography (CT) scan. Kidney biopsy. This procedure involves using a special needle to extract small pieces of kidney tissue for microscopic examination to help determine the cause of the inflammation. A kidney biopsy is almost always necessary to confirm a diagnosis of glomerulonephritis.
Complications Complications of glomerulonephritis may include:
Acute kidney failure. Loss of function in the filtering part of the nephron may cause waste products to accumulate rapidly. This condition may require emergency dialysis, an artificial means of
removing extra fluids and waste from your blood, typically by an artificial kidney machine (dialyzer). Chronic kidney failure. In this extremely serious complication, the kidneys gradually lose function. Kidney function at less than 10 percent of normal capacity indicates end-stage kidney disease, which usually requires dialysis or a kidney transplant to sustain life. High blood pressure. Damage to your kidneys and the resultant buildup of wastes in the bloodstream can raise your blood pressure. Nephrotic syndrome. This is a group of signs and symptoms that may accompany glomerulonephritis and other conditions that affect the filtering ability of the glomeruli. Nephrotic syndrome is characterized by high protein levels in the urine, resulting in low protein levels in the blood, high serum cholesterol, and swelling of the eyelids, feet and abdomen.
Treatment Treatment and outcome of glomerulonephritis depend on whether you have an acute or chronic form of the disease, on the underlying cause, and on the type and severity of your signs and symptoms. Some cases of acute glomerulonephritis, especially those that follow a strep infection, often improve on their own and require no specific treatment. To control your high blood pressure and slow the decline in kidney function, your doctor may prescribe one of several medications, including:

Diuretics Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor agonists Calcium channel blockers Beta blockers
Your doctor also may prescribe drugs to treat the underlying cause of glomerulonephritis:

Strep or other bacterial infection. Your doctor likely will prescribe an appropriate antibiotic. Lupus or vasculitis. Doctors often prescribe corticosteroids and immune-suppressing drugs.
IgA nephropathy. Fish oil supplements have been successful in some people with IgA nephropathy and are under study. Goodpasture's syndrome. Plasmapheresis is sometimes used to treat people with Goodpasture's syndrome. Plasmapheresis is a mechanical process that removes antibodies from your blood by taking the plasma out of your blood and replacing it with fluid or donated plasma.
Therapies for associated kidney failure For acute glomerulonephritis and acute kidney failure, temporary dialysis can help remove excess fluid and control high blood pressure. The only long-term therapies for end-stage kidney failure are kidney dialysis and kidney transplantation. When a transplant isn't possible, often because of poor general health, dialysis becomes the only option. Prevention There's no way to prevent most forms of glomerulonephritis. However, you can seek prompt treatment of a strep infection causing a sore throat or impetigo. To prevent infections, such as HIV and hepatitis, that can lead to some forms of glomerulonephritis, follow safe sex guidelines and avoid intravenous drug use. Controlling your blood sugar may prevent diabetic nephropathy, and controlling your blood pressure makes damage to your kidneys caused by hypertension less likely. Self-care Your doctor may recommend changes in your diet, including restricting salt intake to prevent or minimize fluid retention, swelling and hypertension. Cutting back on protein and potassium consumption may slow the buildup of wastes in your blood. If you have diabetes, maintaining a healthy weight and controlling your blood sugar levels and blood pressure may help slow kidney damage. Coping skills Living with chronic glomerulonephritis and chronic kidney failure can tax your emotional resources. Talk with your doctor to be sure you know your treatment options. Also, you might benefit from joining a support
group. Such a group can provide both sympathetic listening and useful information. (http://www.revolutionhealth.com)
III. METHOD/PROCEDURES Since the cases that were handled by the group at the National Kidney and Transplant Institute are limited, and the involvement of larger groups of participants is not possible, a study of only one (1) case has been conducted. This involves extensive observations of a
few individuals. Data collection has included watching behavior, interviews and record searching. The Dean has assigned the group with a particular case that will be studied. The group was then given a chance to study the patients chart and interview the client and/or the family.
IV. DEVELOPMENTAL MILESTONE Glomerular filtration and absorption values are reached between 1 to 2 years of age. The kidneys ability to concentrate urine increases at 3 months of age with urea synthesis and excretion reaching adult levels by this time; by age 2, urine is concentrated at the adult level.
Excretion of water and hydrogen ions is reduced during infancy and excretion of sodium is also reduced during the 1st month of life with an inefficient reabsorption of sodium.
The volume of urinary output varies with age : Infant : 5 to 10 ml/hr 10 yr old: 10 to 25 ml/hr
The number of voidings/day vary but decrease with age as urine becomes more concentrated.
Voluntary control of the urethral sphincter is achieved between 18 to 24 months of age with night control of bladder usually achieved by 3 years of age; by 4 years of age, bladder capacity reaches 250 ml which allows the child to remain dry at night.
The amount of total body water varies with age, growth and sex and decreases as the child grows and develops Birth: 3 yr old: 12 yr old: 75 to 80% of weight 63% of weight 58% of weight
Extracellular fluid levels decrease within the 1st year. Intracellular fluid volume increases with the growth of muscles and organs.
The infant and the young child have greater intake and output relative to size than older children, and water loss or decreased intake are more likely to cause dehydration as this age group is more vulnerable to fluid and electrolyte alterations.
The increased amount of extracellular fluid results in a high water turnover (50% of the extracellular fluid is exchanged daily) and higher tendency to develop dehydration.
Water loss through respirations, increased metabolism is greater in children; the greater surface area increases water loss through the skin.
Acid-base balance is maintained by a buffer system that is less mature in children.
The newborn is at risk of developing severe metabolic acidosis because hydrogen ion excretion is reduced, immature kidneys cannot conserve water efficiently, high metabolic levels produce increased acid, and plasma bicarbonate levels are low.
Sodium excretion is reduced in the immediate newborn period, and the kidneys are less able to adapt to deficiencies and excesses of sodium.
Infants have a diminished capacity to reabsorb glucose and, during the 1st few days of life, to produce ammonium ions.
Three Years Prior to Admission: Toddler JKM was weeks overdue, his mother underwent labor but the doctor decided to submit the mother under caesarian section. Baby
JKM was born at the East Avenue Medical Center and reported to have ingested meconium.
3 Days Prior to Admission: The client complained of abdominal pain, and exhibited generalized weakness. The parents also noticed edema on the clients periorbital area. 2 Days Prior to Admission: The client was brought to East Avenue Medical Center, and was referred to the National Kidney and Transplant Institute for further tests.
V. BRIEF COURSE IN THE WARD
Toddler JKM was admitted to NKTI last November 20, 2008. The details of his case are as follows:
Name: Age: Sex:
Toddler JKM 3 years old Male
Chief Complaint: Abdominal pain, edema, generalized weakness Diagnosis: Diet: IVF: Medications: Primary Glomerulonephritis low salt diet None Furosemide Dobutamine Pen G Paracetamol Dopamine 5 micro drops/minute Lanoxin Milrinone IV Laboratory: Vital Signs: 2D Echo Blood pressure: Oxygen Saturation: Pulse Rate: Respiratory Rate:
VI. ANATOMY
The human kidney anatomy is well equipped to perform all its crucial functions. The following kidney diagram represents the structure of a kidney... sliced vertically.
KIDNEY DIAGRAM
KIDNEY ANATOMY The kidneys are dark-red, bean-shaped organs. One side of the kidney bulges outward (convex) and the other side is indented (concave). There is a cavity attached to the indented side of the kidney, called the Renal Pelvis... which extends into the ureter.
Each Kidney is enclosed in a transparent membrane called the renal capsule... which helps to protect them against infections and trauma. The kidney is divided into two main areas... a light outer area called the renal cortex, and a darker inner area called the renal medulla. Within the medulla there are 8 or more cone-shaped sections known as renal pyramids. The areas between the pyramids are called renal columns. Kidney Anatomy and Excretion The most basic structures of the kidneys, are nephrons. Inside each kidney there are about one million of these microscopic structures. They are responsible for filtering the blood... removing waste products. The renal artery delivers blood to the kidneys each day. Over 180 liters (50 gallons) of blood pass through the kidneys every day. When this blood enters the kidneys it is filtered and returned to the heart via the renal vein. The process of separating wastes from the body fluids and eliminating them, is known as excretion. The body has four organ systems which are responsible for excretion. The urinary system is one of the organ systems responsible for excretion. It excretes a broad variety of metabolic wastes, toxins, drugs, hormones, salts, hydrogen irons, and water. The kidneys are the main organs of the urinary system. Kidney Anatomy and Blood Vessels The kidney is full of blood vessels. Blood vessels are integral to efficient kidney function. Every function of the kidney involves blood, therefore, it requires a lot of blood vessels to facilitate these functions. Together, the two kidneys contain about 160 km of blood vessels. KIDNEY LOCATION The normal kidney location is towards the back of the abdominal cavity, just above the waist. If you put your hands on your hips, your kidneys are located just about where your thumbs are. One kidney is normally located just below the liver, on the right side of the abdomen and the other is just below the spleen on the left side. In rare cases, however, one or both kidneys may be located much lower in the abdomen. This is not necessarily a problem except probably in the
case of pregnancy. As the fetus begins to develop in the womb this could sometimes place pressure on the kidney which is located in the lower abdomen.
NORMAL KIDNEY SIZE The normal kidney size of an adult human is about 10 to 13 cm (4 to 5 inches) long and about 5 to 7.5 cm (2 to 3 inches) wide. It is approximately the size of a conventional computer mouse. A kidney weighs approximately 150 grams. Kidneys weigh about 0.5 percent of total body weight. The human kidney anatomy, though relatively simple, enables it to perform extremely complex but essential functions. If any area of the kidney is damaged or becomes diseased, this could significantly affect its ability to perform these functions.
VII. PATHOPHYSIOLOGY Primary Glomerulonephritis Is a kidney inflammation due to autoimmune causes and not associated with any other disease. Primary glomerulonephritis is one of the main causes of end-stage renal failure in people under 45. Approximately 0.02% of the US population suffer from primary glomerulonephritis. Glomerulonephritis is a progressive kidney disease that
involves the glomeruli, the individual filtering units of the kidney that produce urine. When the glomeruli become inflamed, the kidneys can't filter urine properly. This results in a build-up of excess fluid and toxins in the body. Glomerulonephritis can lead to chronic renal (kidney) failure. There are two main types of glomerulonephritis: primary and secondary. Primary glomerulonephritis affects the kidneys directly, while in secondary glomerulonephritis, the kidneys are damaged as a
result of another illness. Glomerulonephritis seems to happen twice as often in males as in females.
Nearly all forms of acute glomerulonephritis have a tendency to progress to chronic glomerulonephritis. The condition is characterized by irreversible and progressive glomerular and tubulointerstitial fibrosis, ultimately leading to a reduction in the glomerular filtration rate (GFR) and retention of uremic toxins. If disease progression is not halted with therapy, the net result is chronic kidney disease (CKD), end-stage renal disease (ESRD), and cardiovascular disease. The diagnosis of CKD can be made without knowledge of the specific cause. The National Kidney Foundation defines CKD as (1) evidence of kidney damage based on abnormal urinalysis results (eg, proteinuria, hematuria) or structural abnormalities observed on ultrasound images or (2) a GFR of less than 60 mL/min for 3 or more months. Based on this definition, the National Kidney Foundation developed guidelines that classify the progression of renal disease into 5 stages, from kidney disease with a preserved GFR to end-stage kidney failure. This classification includes treatment strategies for each progressive level, as follows:
Stage 1: This stage is characterized by kidney damage with a normal GFR (>90 mL/min). The action plan is diagnosis and treatment, treatment of comorbid conditions, slowing of the progressing of kidney disease, and reduction of cardiovascular disease risks. Stage 2: This stage is characterized by kidney damage with a mild decrease in the GFR (60-90 mL/min). The action plan is estimation of the progression of kidney disease. Stage 3: This stage is characterized by a moderately decreased GFR (30-59 mL/min). The action plan is evaluation and treatment of complications. Stage 4: This stage is characterized by a severe decrease in the GFR (15-29 mL/min). The action plan is preparation for renal replacement therapy.
Stage 5: This stage is characterized by kidney failure. The action plan is kidney replacement if the patient is uremic.
At the later stages of glomerular injury, biopsy results cannot help distinguish the primary disease. Histology and clues to the etiology are often derived from other systemic diseases, if present. Considerable cause-specific variability is observed in the rate at which acute glomerulonephritis progresses to chronic glomerulonephritis. Pathophysiology Reduction in nephron mass from the initial injury reduces the GFR. This reduction leads to hypertrophy and hyperfiltration of the remaining nephrons and to the initiation of intraglomerular hypertension. These changes occur in order to increase the GFR of the remaining nephrons, thus minimizing the functional consequences of nephron loss. The changes, however, are ultimately detrimental because they lead to glomerulosclerosis and further nephron loss. In early renal disease (stages 1-3), a substantial decline in the GFR may lead to only slight increases in serum creatinine levels. Azotemia (ie, a rise in BUN and serum creatinine levels) is apparent when the GFR decreases to less than 60-70 mL/min. In addition to a rise in BUN and creatinine levels, the substantial reduction in the GFR results in decreased production of (1) erythropoietin, thus resulting in anemia; (2) decreased production of vitamin D, resulting in hypocalcemia, secondary hyperparathyroidism, hyperphosphatemia, and renal osteodystrophy; (3) reduction in acid, potassium, salt, and water excretion, resulting in acidosis, hyperkalemia, hypertension, and edema; and (4) platelet dysfunction, leading to increased bleeding tendencies. Accumulation of toxic waste products (uremic toxins) affects virtually all organ systems. Azotemia occurring with the signs and symptoms listed above is known as uremia. Uremia occurs at a GFR of approximately 10 mL/min. Some of these toxins (eg, BUN, creatinine, phenols, guanidines) have been identified, but none has been found to be responsible for all the symptoms.
Frequency United States Chronic glomerulonephritis is the third leading cause of ESRD and accounts for 10% of patients on dialysis in the United States. International Chronic glomerulonephritis accounted for up to 40% of patients on dialysis in Japan and some Asian countries. However, more recent data suggest that, in Japan, for instance, the rate of chronic glomerulonephritis in patients on dialysis is 28%. The cause of this declining rate is not known. Concurrent with the decline in chronic glomerulonephritis in these countries is an increase in diabetic nephropathy in up to 40% of patients on dialysis. Mortality/Morbidity ESRD and death are common outcomes unless renal replacement therapy is instituted. Clinical History The history should focus on cause-specific symptoms to determine the causes of CKD (if unknown) and on symptoms related to uremia to determine if renal replacement therapy is needed.
Cause-specific history: Obtain a cause-specific history so that further workup and management of the disease (if systemic) can be planned. Uremia-specific history
o
The following symptoms suggest uremia: Weakness and fatigue Loss of energy, appetite, and weight Pruritus Early morning nausea and vomiting Change in taste sensation
o o o o o o o o o
Reversal in sleep pattern (ie, sleepiness in daytime, wakefulness at night) Peripheral neuropathy Seizures Tremors
The presence of edema and hypertension suggests volume retention. Dyspnea or chest pain that varies with position suggests fluid overload and pericarditis, respectively. Leg cramps may suggest hypocalcemia or other electrolyte abnormalities. Weakness, lethargy, and fatigue may be due to anemia.
Physical Cause-specific physical examination findings are discussed in articles on the specific causes. See Causes for links to such articles.
Uremia-specific findings
o o o o o o o o o o
Hypertension Jugular venous distension (if severe volume overload is present) Pulmonary rales (if pulmonary edema is present) Pericardial friction rub in pericarditis Tenderness in the epigastric region or blood in the stool (possible indicators for uremic gastritis or enteropathy) Decreased sensation and asterixis (indicators for advanced uremia)
Causes The progression from acute glomerulonephritis to chronic glomerulonephritis is variable. Whereas complete recovery of renal function is the rule for patients with poststreptococcal glomerulonephritis, several other glomerulonephritides, such as immunoglobulin A (IgA) nephropathy, often have a relatively benign course and many do not progress to ESRD.
Rapidly progressive glomerulonephritis or crescentic glomerulonephritis: Approximately 90% of patients progress to ESRD within weeks or months. Focal segmental glomerulosclerosis: Approximately 80% of patients progress to ESRD in 10 years. Patients with the collapsing variant, which is termed malignant focal segmental glomerulosclerosis, have a more rapid progression. This form may be idiopathic or related to HIV infection. Membranous nephropathy: Approximately 20-30% of patients with membranous nephropathy progress to chronic renal failure (CRF) and ESRD in 10 years. Membranoproliferative glomerulonephritis: Approximately 40% of patients with membranoproliferative glomerulonephritis progress to CRF and ESRD in 10 years. IgA nephropathy: Approximately 10% of patients with IgA nephropathy progress to CRF and ESRD in 10 years. Poststreptococcal glomerulonephritis: Approximately 1-2% of patients with poststreptococcal glomerulonephritis progress to CRF and ESRD. Older children who present with crescentic glomerulonephritis are at greatest risk. Lupus nephritis: Overall, approximately 20% of patients with lupus nephritis progress to CRF and ESRD in 10 years; however, patients with certain histologic variants (eg, class IV) may have a more rapid decline.
GLOMERULONEPHRITIS Post-streptococcal infection (group A, beta-hemolytic) Release of material from the organism into the circulation (antigen) Formation of antibody Immune-complex reaction in the glomerular capillary Inflammatory response Proliferation of endothelial cells lining glomerulus and cells between endothelium and epithelium of capillary membrane Swelling of capillary membrane and infiltration with leukocytes Increased permeability of base membrane Occlusion of the capillaries of glomeruli Vasospasm of afferent arterioles Decreased ability to form filtrate from glomeruli plasma flow Retention of water and sodium Reduced circulatory volume (hypervolemia) Circulatory congestion Edema (peripheral and periorbital) Hypertension Decreased urinary output (hematuria, proteinuria) Urine dark in color
Anorexia Irritability lethargy Acute glomerulonephritis
VIII. DRUG ANALYSIS 1. Furosemide Infusions Usage: Congestive heart failure and Acute renal failure that is unresponsive to bolus treatments. Complications: Digitalis toxicity, hypokalemia, ventricular ectopy, ototoxicity, electrolye imbalance, esp potassium and magnesium. Adverse Reactions: Hypotension, vertigo, tinnitus, hearing loss, rash, weakness, muscle spasm, photosensitivity, ventricular ectopy. Equipment Maintenance: Furosemide infusions must be run through an infusion pump. Standing orders: 1. Verify concentration, infusion rate and VS parameters 2. Assess serum potassium levels. 3. Monitor and document VS at least every 15 minutes. 4. Notify Base Command if B/P drops below 15% of initial baseline. 5. Monitor EKG. 6. Common dosage: 250 mg of Lasix in 250 cc of NS yielding 1 mg/cc. 7. Maintenance dose: .1-.4 mg/kg/hr not to exceed 4 mg/min. 8. Do not give IV bolus medications through the Lasix infusion.
Nursing Interventions - Watch potassium levels. Watch for hearing loss. Give with caution in patients receiving neurotoxic drugs (see Edecrin) When giving IV push - give 10 mg/min. 2. Dobutamine Usage: When parenteral therapy is necessary for inotropic support for short term treatment.with cardiac decompensation due to depressed contractility. In patients with atrial fib and rapid ventricular response, a digitalis preparation should be used prior to Dobutamine. Complications: Increase HR, BP, may develop rapid ventricular response in atrial fib. Ectopics - may precipitate or exacerbate. Rarely causes VT. Hypersensitivity - rash, fever, eosinophilia, bronchospasm. Adverse Reactions: In patients who have shown previous manifestations of hypersensitivity to Dobutamine. May be ineffective if received beta blockers; may have increased peripheral vascular resistance. Equipment Use: IV should be infused via infusion pump. Standing Orders: 1. Verify infusion rate, infusion dosage, patients weight. 2. Monitor BP and heart rate continuously. If heart rate increases more than 15% of baseline or hypotension occurs, notify base station physician. 3. Refer to compatibility chart before infusing any medication through the Dobutamine line. No IV push drugs can be given through a Dobutamine infusion. 4. If any redness, swelling, tenderness, warmth appears at IV site, discontinue IV Nursing Interventions Monitor the clients vital signs. Report signs of increasing blood pressure and increasing pulse rate. 3. Penicillin G potassium for Injection Usage: To reduce development of drug-resistant bacteria and maintain the effectiveness of other antibacterial drugs.
Complications: Hemolytic anemia, leucopenia, thrombocytopenia, nephropathy, and neuropathy are rarely observed adverse reactions and are usually associated with high intravenous dosage. Patients given continuous intravenous therapy with penicillin G potassium in high dosage (10 million to 100 million units daily) may suffer severe or even fatal potassium poisoning, particularly if renal insufficiency is present. Hyperreflexia, convulsions, and come may be indicative of this syndrome. Serious and occasionally fatal hypersensitivity (anaphylactoid) reactions have been reported in patients on penicillin theraphy. These reactions are more likely to occur in individuals with a history of penicillin hypersensitivity and/or a history of sensitivity to multiple allergens. There have been reports of individuals with a history of penicillin hypersensitivity who have experienced severe reactions when treated with cephalosporins. Before initiating therapy with any penicillin, careful inquiry should be made concerning previous hypersensitivity reactions to penicillin, cephalosporins, or other allergens. If an allergic reaction occurs, the drug should be discontinued and the appropriate therapy instituted. Serious anaphylactoid reactions require immediate emergency treatment with epinephrine, oxygen, intravenous steroids, and airway management including intubation, should also be administered as indicated. Cardiac arrhythmias and cardiac arrest may also occur. Nursing Interventions Check the client for allergic reaction to the penicillin product especially after the 1st and 2nd doses. This may be a mild reaction, such as a rash, or a severe reaction, such as respiratory distress or anaphylaxis. 4. Digoxin Usage: Digoxin is one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium. Complications: Digoxin may cause anorexia, nausea, vomiting, and diarrhea. Rarely, the use of digoxin has been associated with abdominal pain, intestinal ischemia, and hemorrhagic necrosis of the intestines. Digoxin can produce visual disturbances (blurred or yellow vision), headache, weakness, dizziness, apathy, confusion, and mental disturbances (such
as anxiety, depression, delirium and hallucination). Gyncomastia has been occasionally observed following the prolonged use of digoxin. Thrombocytopenia and maculopapular rash, and other skin reactions have been rarely observed. Nursing Interventions Check the apical pulse rate before administering digoxin. Do not administer if pulse rate is <60 bpm. Check the signs of peripheral and pulmonary edema, which indicate congestive heart failure. 5. Milrinone Usage: Milrinone is indicated for the short-term intravenous treatment of patients with acute decompensated heart failure. Patients receiving PRIMACOR should be observed closely with appropriate electrocardiographic equipment. The facility for immediate treatment of potential cardiac events, which may include life threatening ventricular arrhythmias, must be available. The majority of experience with intravenous Milrinone has been in patients receiving Digoxin and diuretics. There is no experience in controlled trials with infusions of Milrinone for periods exceeding 48 hours. Loading Dose: Milrinone should be administered slowly with a loading dose of 50mcg/kg. Complications: Cardiovascular Effects: In patients receiving PRIMACOR in Phase II and III clinical trials, ventricular arrhythmias were reported in 12.1%: Ventricular ectopic activity, 8.5%; nonsustained ventricular tachycardia, 2.8%; sustained ventricular tachycardia, 1% and ventricular fibrillation, 0.2% (2 patients experienced more than one type of arrhythmias). Holter recordings demonstrated that in some patients injection of PRIMACOR increased ventricular ectopy, including nonsustained ventricular tachycardia. Life-threatening arrhythmias were infrequent and when present have been associated with certain underlying factors such as preexisting arrhythmias, metabolic abnormalities (e.g. hypokalemia), abnormal digoxin levels and catheter insertion. PRIMACOR was not shown to be arrhythmogenic in an electrophysiology study. Supraventricular arrhythmias were reported in 3.8% of the patients receiving PRIMACOR. The incidence of both
supraventricular and ventricular arrhythmias has not been related to the dose or plasma milrinone concentration. Other cardiovascular adverse reactions include hypotension, 2.9% and angina/chest pain, 1.2%. In the post marketing experience, there have been rare cases of "torsades de pointes" reported. CNS Effects: Headaches, usually mild to moderate in severity, have been reported in 2.9% of patients receiving Milrinone. Other Effects: Other adverse reactions reported, but not definitely related to the administration of Milrinone include hypokalemia, 0.6%; tremor, 0.4%; and thrombocytopenia, 0.4%. Isolated spontaneous reports of bronchospasm and anaphylactic shock. Liver function test abnormalities and skin reactions such as rash. Nursing Interventions Check the apical pulse rate before administering digoxin. Do not administer if pulse rate is <60 bpm. Check the signs of peripheral and pulmonary edema, which indicate congestive heart failure.
IX. NURSING DIAGNOSES High risk for decreased cardiac output related to cardiac decompensation.
Nursing Intervention Rationale Place on cardiopulmonary Medications such as Penicillin G, monitor Dopamine, Lanoxin, and Milrinone may result to cardiac arrythmia, ventricular arrythmia, heart block respectively. High back rest or position client Medications such as Dopamine, for comfort ease of respiration and Lanoxin may result to dyspnea, nausea and vomiting, positioning the client in high back rest will facilitate ease of respiration and prevent possible aspiration when vomiting occurs. Administer humidified oxygen To prevent dryness of the mucosa and facilitate ease of respiration. Complete bed rest, no bathroom Restriction of activities will privileges. Restrict activity to decrease cardiac demands. decrease cardiac demands Limit oral and fluid intake Fluid intake should be proportional to kidneys ability to filter. Prepare patient and family for This will prepare the family possible repeat dialysis emotionally, financially, and spiritually for possible treatments associated with the clients illness. Fluid Volume Filtration Excess Related To Diminished Glomerular
Nursing Intervention Restrict fluid intake.
Provide a no-added salt Restrict K only if oliguric. Restrict protein.
Rationale To equal urinary and insensible loss when signs of hypertension, renal, or cardiac failure are present. diet. To prevent water retention.
If azotemia, elevated BUN, oliguria are present. Administer antihypertensives and To control blood pressure and fluid in severe cases, furosemide as volume especially when other prescribed. diuretics have not been useful.
Keep patient on bedrest.
To enhance diuresis.
Pain Related to Inflammatory Response Nursing Intervention Explain cause of pain. Encourage bedrest, assist with repositioning. Provide warm or cool packs as desired. Do not administer pain medications unnecessarily. Rationale To alleviate pain.
As the inflammation diminishes, so will the pain. Medications can be nephrotoxic and pose an unnecessary risk.
Knowledge Deficit Related to Hospitalization Nursing Intervention Provide information about course of disease and all treatments, procedures. Explain home care measures: I/O, BP measurement. Explain need for follow-up care. Rationale For the patient to understand the disease process and required follow-up care. For the patient to understand the disease process and required follow-up care. Although most patients recover completely (70%) there may be persistent hematuria and aboveaverage BUN for some weeks. A small percentage may progress to chronic GN or acute renal failure.
Activity Intolerance related to generalized weakness Nursing Intervention Assess wekness, fatigue, ability to move about in bed and participate in play activities. Rationale Provides information about energy reserves during the acute phase of the disease and acceptance of bed rest status. Schedule care and provide rest Provides adequate rest and periods following any activity in a reduces stimuli and fatigue.
quiet environment. Maintain bed rest during the Conserves energy and decreases acute stage, disturb only when production of waste materials necessary. which increases work of the kidneys. Provide for quiet play, reading, Provides diversion, stimulation and TV, games as symptoms subside. requires minimal energy expenditures. Explain reason for activity Promotes understanding of the restriction to parents and child. need to conserve energy and rest to promote recovery. Inform parents and child to rest Prevents fatigue and conserves followng ambulation or any energy during recovery. activity. Instruct parents and child to rest Prevents fatigue and promotes when feeling tired. recovery. X. DISCHARGE PLANNING Date Plan outcome and Target Date Nursing Interventions ( ) Assess needs of client/family beginning on the day of admission and continue assessment during hospitalization ( ) Anticipated needs/services. ( ) Involve the patient/family in the discharge process. ( ) Discuss with physician the discharge plan and obtain orders if needed ( ) Contact Date Achiev ed
( ) The patient/familys discharge planning will begin on day of admission including preparation for education and/or equipment. ( ) On the day of discharge, client/family will receive verbal and written instructions concerning: -Medications
-Diet -Activity -Treatments -Follow up appointments -Signs and symptoms to observe (when to contact the doctor) -Others
appropriate personnel with orders ( ) Provide written and verbal instructions at the client/familys level of understanding. ( ) Verbally explain instructions to patient/family prior to discharge and provide patient/family with a written copy. ( ) Ascertain that patient has follow-up care arranged at discharge. ( ) Provide verbal and written information on what signs and symptoms to observe and when to contact the physician. ( ) Assess if any community resources should be utilized, and contact appropriate personnel. ( ) Document all discharge teaching on Discharge Instruction Sheet and Nursing Notes.
XI. CARING-HEALING INQUIRY FOR HOLISTIC NURSING PRACTICE The research model, caring-healing inquiry for holistic nursing practice, integrates the values of the health system, principles that guide nursing governance, and caring theory and research in nursing. The guiding values for the model are compassion, hospitality, and stewardship; guiding principles include excellence, collaboration, and leadership. Caring-healing practices and a caring-healing environment contribute to the goal of human wholeness and quality care. The focus of inquiry may be on the person, family, or community; on the nurse, health team, or health system; or the relationships between them. Within this model, multiple modalities of caring-healing practice and multiple methods of inquiry are encouraged, thus honoring the art and science of nursing. The components of the model are illustrated in Figure 1.
To illustrate how the caring-healing inquiry model is effective in framing EVIDENCE-BASED PRACTICE improvements, an example from a painperformance-improvement initiative is described. The pain-performanceimprovement initiative is guided by the value of compassion. The project incorporates the principles of excellence through practice improvement and collaboration through interdisciplinary team effort. The performance-improvement activities include staff development
regarding pain management and revision of policies and procedures relating to pain management. Both of these activities contribute to a caring-healing environment. More frequent and intentional assessment of the pain experience for patients reflects caring-healing practices that have been instituted. Outcomes of the project show improved patient satisfaction with pain control demonstrating improved quality care. As the research program develops, research and EVIDENCE-BASED PRACTICE projects are increasingly framed from the caring model perspective. A task force of nurses representing advanced practice nurses, directors, managers, and staff nurses meets regularly to study caring theory and its potential to frame practice and improve professional practice. The use of caring instruments to measure outcomes of caring is being explored.
XII. CONCLUSIONS AND RECOMMENDATIONS CONCLUSIONS
Acute glomerulonephritis (AGN) is an alteration in renal function caused by a glomerular injury, which is displayed by the classic symptoms of gross hematuria, mild proteinuria, edema(usually
periorbital), hypertension, and oliguria. AGN is also classified as either: a primary disease, associated with Group A, beta-hemolytic streptococcal infection; or a secondary disease associated with various systemic diseases(i.e. systemic lupus erythematosus, sickle cell disease,
Henochs chorea purpura). The most common type of AGN is the primary disease, described as an immune-complex disease (or an antigenantibody complex formed during the streptococcal infection which becomes entrapped in the glomerular membrane, causing inflammation 8 to 14 days after the onset of this infection). AGN is primarily observed in the early school-age child, with a peak of onset of 6 to 7 years. The onset of the classic symptoms of AGN is usually abrupt, selflimiting(unpredictable), and prolonged hematuria and proteinuria may occur. AGN results in decreased glomerular filtration rate causing retention of water and sodium (edema); expanded plasma and interstitial fluid volumes that lead to circulatory congestion and edema (hypervolemia); hypertension (cause is unexplained; plasma rennin activity is low during the acute phase, hypervolemia is suspected to be the cause). The implications for nurses of the information gleaned from this study are numerous. AGN may ultimately be treated differently. It is
important for the nurse to be knowledgeable about this disease process and its treatment(s) in order to provide appropriate education to families. Knowledge about support groups for patients with AGN is also important information for the nurse to have so that referrals can be made. Because it is a severe disease, patients and their family members often feel that there is no one with whom to talk who understands their situation. Nurses can assist patients in finding AGN networking systems so that patients and their families can find additional emotional and educational support. Nephrology nurses are often the first people that patients and families meet following a diagnosis that can be frightening. A nurse who gives knowledgeable answers to questions about the disease and who is empathetic to fears for the health of a child or loved one is important. The nephrology nurse can best serve her patients by keeping abreast of the new medications, medical therapies, research, and support communities for patients with AGN and their families.
RECOMMENDATIONS Since acute glomerulonephritis is most common in children between the ages 5 and 10 years, the age group most susceptible to streptococcal infections where boys appear to develop the disease more often than girls, all children who have had a strep throat, tonsilitis, otitis media, or impetigo caused by streptococcal infection, should have urinalysis 2 weeks after the infection to evaluate for glomerulonephritis. Without frightening them unduly, tell parents that this is an extremely important follow-up test. These parents and children may need to talk about their feelings more openly and provide frequent reports of subtle positive changes in a childs condition. It is the nurses responsibility to be certain that parents know the date and place of a return visit for follow-up care. Because this is a perplexing disease, the nurses have to be sure that the parents have a telephone number to call if they have questions about their childs care or
condition. Parents need to weigh children daily to detect fluid accumulation(use the same scale with the child in the same clothing at the same time of day) and to measure intake and output accurately. They need clear instructions about heir responsibilities, including keeping the child free of infection, perhaps by limiting exposure to friends, and giving prednisone, or oral diuretics and a potassium supplement. Review medication instructions with parents and have them repeat the instructions. Help them begin to view the child as well again so they do not continue to shelter him unnecessarily but allow for normal growth and development. Areas that would most benefit from nursing research could include: determining parents or childrens ability to accurately selfassess for proteinuria after streptococcal infections, identifying the specific needs of children, designing ways to make diets more appealing to children, or designing ways that organ donation can be presented to make it more appealing to potential donors.
XII. APPENDICES Appendix A Glomerular Diseases by Age and Presentation Age Nephritic Nephrotic Mixed Nephritic and (yr) Syndrome Syndrome Nephrotic Syndrome < 15 Mild PIGN Minimal change Lupus nephritis disease IgA Membranoproliferative nephropathy Focal and GN segmental Thin basement glomerulosclerosis membrane
disease Hereditary nephritis HenochSchnlein purpura
Lupus (membranous nephropathy)
Lupus nephritis 15 IgA Focal and 40 nephropathy segmental glomerulosclerosis Thin basement membrane Minimal change disease disease
Membranoproliferative GN Fibrillary and immunotactoid GN*
IgA nephropathy Lupus nephritisMembranous nephropathy Hereditary nephritis Diabetic nephropathy Mesangial proliferative Preeclampsia GN Late PIGN RPGN IgA nephropathy PIGN > 40 IgA Focal and IgA nephropathy nephropathy segmental glomerulosclerosis Fibrillary and RPGN immunotactoid GN* Membranous Vasculitides nephropathy PIGN Diabetic nephropathy Minimal change disease IgA nephropathy Amyloidosis
(primary) Light chain deposition disease Benign nephrosclerosis Late PIGN

*More commonly manifests as nephrotic syndrome. PIGN = postinfectious glomerulonephritis; GN = glomerulonephritis, RPGN = rapidly progressive glomerulonephritis Adapted from Rose BD. Pathophysiology of Renal Disease (2nd edition). New York: McGraw-Hill, 1987, p. 167.
Appendix B
Causes of Nephrotic Syndrome Causes Primary causes Idiopathic Fibrillary and immunotactoid GN, focal segmental glomerulosclerosis, IgA nephropathy*, membranoproliferative GN, membranous nephropathy, minimal change disease, rapidly progressive GN* Examples
Secondary causes Metabolic Immunologic Idiopathic Amyloidosis, diabetes mellitus Cryoglobulinemia, erythema multiforme, Henoch-Schnlein purpura, polyarteritis nodosa, serum sickness, Sjgren's syndrome, SLE Castleman disease, sarcoidosis Neoplastic Carcinoma (bronchus, breast, colon, stomach, kidney), leukemia, lymphomas, melanoma, multiple myeloma Gold, heroin, interferon, lithium NSAIDs, mercury, pamidronate, penicillamine Infectious Bacterial (infective endocarditis, leprosy, postinfectious GN, syphilis, vascular prosthetic nephritis) Viral (Epstein-Barr virus, hepatitis B and C,
Drug-related
herpes zoster virus, HIV) Protozoal (filariasis, schistosomiasis) Allergic helminthic, malaria,
Antitoxins, insect stings, poison ivy or oak, snake venoms Alport's syndrome*, congenital nephrotic syndrome (Finnish type), corticosteroidresistant nephrotic syndrome, Denys-Drash syndrome, Fabry's disease, familial FSGS Adaptation to reduced nephrons, obesity, oligomeganephronia Chronic allograft nephropathy, hypertension, preeclampsia morbid
Genetic syndromes
Physiologic
Miscellaneous
malignant
*More commonly manifests as nephritic syndrome. GN = glomerulonephritis; FSGS = focal segmental glomerulonephritis.

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Case Study/Term Paper

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New therapeutic strategies glomerulonephritis

diabetes hypertension family member with kidney disease

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A couple of signs or symptoms of protenuria include:

foamy urine hands, feet, abdomen, face swelling

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Race No racial predilection is recognized. Sex

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Acute nephritic syndrome

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DIFFERENTIALS Other Problems to be Considered

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15 endocarditis cryoglobulinemia nephropathy polyarteritis nephritis

Evidence of preceding streptococcal infection

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Case Study/Term Paper

Submitted by Hoser Saavedra

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Surgical Care Surgical care is not indicated. Consultations

Nutritionist or dietitian Nephrologist

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