CHAPTER I INTRODUCTION 1.1.

Background Glomerulonephritis is the major cause of end stage renal failure and high rates of morbidity in children. Glomerulonephritis terminology used here is to show that the first and major abnormalities occurred in the glomerulus. Glomerulonephritis is an inflammatory disease of bilateral kidneys. Inflammation begins in gromelurus and manifests as proteinuria and or hematuria. Although the primary lesion in gromelurus, but the entire nephron in the end will be damaged, resulting in kidney failure.1 Indonesia in 2009, reported 260 patients treated in teaching hospitals in 12 months. Most patients treated in Surabaya (26.5%), followed in succession in Jakarta (24.7%), Bandung (17.6%), and Palembang (8.2%). Patients of men and women versus 2: 1 and most in children aged between 68 years (40.6%).3 Symptoms of glomerulonephritis can occur in a sudden (acute) or chronic (chronic) are often not known because it does not cause symptoms. Symptoms may include nausea, anemia, or hypertension. Common symptoms like swollen eyelids, oliguria, and usually accompanied by hypertension. The disease is usually (about 80%) healed spontaneously, 10% become chronic, and 10% resulted fatal.2 1.2. Problems In this paper, I will discuss about acute glomerulonephritis (AGN). In overview, acute glomerulonephritis is an immunological reaction in the kidney to specific bacterial or viral which often occurs is due to streptococcal bacterial infection. Most (75%) of acute post-streptococcal glomerulonephritis arise after upper respiratory tract infections, caused by the bacteria Streptococcus group A beta hemolitikus.3

1.3. Limitation of Problems -

What is the definition of Acute Glomerulonephritis? How about the etiology of Acute Glomerulonephritis? How about the pathophysiology of Acute Glomerulonephritis? What are the symptoms of Acute Glomerulonephritis? How can we diagnose it? What do we can see in laboratory overview? What kind of therapy we can give to the patient?

1.4. Frame of Writing I. Introduction

1.1 Background 1.2 Problems 1.3 Limitation of Problems 1.4 Frame of Writing II.

Kidney Reviews 2.1 Anatomy 2.2 Function

III.

Acute Glomerulonephritis
3.1 Definiton 3.2 Etiology 3.3 Pathophysiology 3.4 Prevalence

3.5 Clinical Symptoms 3.6 Laboratory Overview

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3.7 Overview Patology 3.8 Diagnose 3.9 Theraphy

IV. V. VI.

Acute Glomerulonephritis and Urinary System Conclusion References CHAPTER II KIDNEY REVIEWS

2.1. Anatomy Kidney is the bilateral organ that located in the abdominal area, between vertebra retroperitoneal lumbal 1 and 4. In neonates is sometimes palpable. The kidneys consist of cortex and medulla. Each kidney consists of pyramid-shaped lobes 8-12. Basic pyramid is located in the cortex and the peak is called the papilla empties into the calyx minor. In the cortex region propagated glomeruli, proximal and distal tubules contortus. The length and weight of kidney average 6 cm and 24 grams in baby, to 12 cm or more than 150 grams. In the fetal kidney surface uneven, lobes, then disappears with increasing ages. Kidney contains 1 million nephrons (glomeruli and tubules associated with it). In humans, nephron formation is completed in 35 weeks fetus. No new nephrons formed after birth. Further development is hypertrophy and hyperplasia of existing structures along with maturation fungsional. Nephron consists of the glomerulus and Bowman's capsule, proximal tubule, Anse Henle and distal tubules. Glomeruli with Bowman's capsule premises also called maplphigi body.4
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2.2. Function Primary function of kidney is to maintain extracellular fluid volume and composition within normal limits. Composition and extracellular fluid volume is controlled by glomerular filtration, reabsorption and secretion tubulus. The main function of kidney is divided into:
1. The function of excretion

To maintain plasma osmolality by altering water excretion, maintain a plasma pH of about 7.4 to remove excess H + and HCO3 reshape, maintaining levels of each plasma electrolytes in normal range, excrete the end products of nitrogen and protein metabolism, especially urea, uric acid and creatin.
2. Non-excretion function

Produce renin is important to regulate blood pressure, produce erythropoietin is an important factor in stimulating red blood cell products by the bone marrow, metabolize vitamin D into its active form, degradation of insulin and produce prostaglandins The basic function is to cleanse or purify nephron blood plasma and the substance is not required when the body's blood through the kidneys. The most important substance to be cleaned is the end result of metabolism such as urea, creatine, uric acid and others. In addition, sodium ions, potassium, chloride and hydrogen tend to accumulate in the body.

Glomerulus normal capillary

No plasma proteins larger than albumin in the filtrate gromerulus declare the effectiveness of the glomerular capillary wall as a barrier filtration. Endothelial cells, epithelial basement membrane and glomerular capillary wall have strong negative ion content. The charge of this anion is result than 2 negative charges: proteoglycans (heparan-sulfate) and acid-containing glycoproteins sialat. Proteins in blood relatively low isoelectric and carry a negative charge is pure. Therefore, they are rejected by the capillary wall of gromerulus which negative, and limiting the filtration.5

CHAPTER III ACUTE GLOMERULONEPHRITIS (AGN) 3.1. Definitions Acute glomerulonephritis (GNA) is an immunological reaction in the kidney to specific bacterial or viral which often occurs is due to streptococcal bacterial infection. Glomerulonephritis is a term used to describe various kinds of kidney disease who experience glomerular proliferation and inflammation caused by an immunological mechanism. While the acute term (acute glomerulonephritis) reflects the correlation clinics in addition to showing a picture of etiology, pathogenesis, disease and prognosis.

Acute glomerulonephritis also called post sterptokokus (GNAPS) is a non-suppurative inflammatory process that the glomeruli, as a result of bacterial infection of group A streptococcal beta hemolitikus, type nefritogenik elsewhere. 3.2. Etiology Most (75%) of acute post-streptococcal glomerulonephritis arise after upper respiratory tract infections, caused by the bacteria Streptococcus group A beta hemolitikus type 1, 3, 4, 12, 18, 25, 49. Medium Type 2, 49, 55, 56, 57 and 60 cause skin infections 8-14 days after streptococcal infection, clinical symptoms arise. Hemolitikus beta streptococcal bacterial infection has a risk of acute post-streptococcal glomerulonephritis ranged 10-15%. Climatic factors, nutritional status, general condition and allergy also influence after infection with the germ GNA Streptococcuss. There are several causes of acute glomerulonephritis, but the most commonly found because of streptococcal infection, other causes include: 1. Bacterial : streptococcal group C, meningococcocus, Sterptoccocus Viridans, gonococcus, Leptospira, Mycoplasma pneumoniae, Staphylococcus albus, Salmonella typhi etc. 2. Virus 3. Parasites : hepatitis B, varicella, vaccinia, echovirus, parvovirus, influenza, etc. : malaria and Toxoplasma

Streptococcal Streptococcus is round-shaped gram-positive bacteria that typically form pairs or chains during growth. Streptococcus is a heterogeneous group of bacteria. More than 90% of streptococcus infections in human caused by hemolytic Streptococcus group A. This collection was given the species name S. pyogenes.5 3.3. Pathophysiology
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Actually not streptococcus causes the damage of the kidneys. Allegedly there is an antibody directed against an especially antigen which is the element of streptococcus specific plasma membrane. Antigen-antibody complex formed in the blood and circulates into the glomerulus where the complex is mechanically trapped in the membrane basale then result the lesions and inflammation that attract polymorphonuclear leukocytes (PMN) and platelets to the lesion. Phagocytosis and enzyme release of lysosomes also damage the glomerular basement membrane endothel. In response to lesions that occur, proliferation of endothelial cells followed mesangium cells and subsequent epithelial cells. The increased capillary leak gromerulus causing protein and red blood cells can get out into the urine that is being formed by the kidneys, resulting in proteinuria and hematuria. Presumably the antigen-antibody complex is seen as subepithelial nodules in the electron microscope and as a granular form on immunofluorescence microscopic; the glomeruli looked swollen light examination and accompanied the invasion PMN.6 3.4. Prevalence AGNPS can occur in all age groups, but the commonest in the age group 5-15 years and rarely occurs in infants. Other references mentioned most often found in children aged 6-10 years. This disease can occur in men and women, but men are two times more often than women. Comparison between men and women is 2:1. Allegedly there is a risk factor associated with age and gender. Tribe or race is not related to the prevalence of this disease, but the possibility of increased prevalence in people with low socioeconomic, so the neighborhood does not health.3 3.5. Clinical Symptoms Clinical features show the variability. Sometimes mild symptoms but not infrequently a child comes with severe symptoms. Damage to the capillary of gromelurus resulted in haematuria and albuminuria, as has been stated previously. Urine may appear reddish or like coffee sometimes
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accompanied by mild edema around the eyes or restricted throughout the body. Generally there is severe edema in oliguria and if there is heart failure. Edema that occurs associated with decreased glomerular filtration rate (GFR), resulting in excretion of water, sodium, nitrogen substances may be reduced, resulting in edema and azotemia. Increased aldosterone may also play a role in water and sodium retention. Morning edema often occurs on the face especially periorbita edema, although edema is most evident under section member body when midmorning. The degree of edema usually depends on the weight of glomerulus inflammation, whether accompanied with congestive heart trouble.7 Hypertension is present in 60-70% of children with the GNA on the first day, then at the end of the first week to be normal again. If there is damage to kidney tissue, the blood pressure will remain high for several weeks and become permanent if the condition becomes chronic illness. Not some high body temperature, but can be very high on the first day. Sometime symptoms of fever persist is existed, even though no symptoms of other infections that preceded it. Gastrointestinal symptoms such as vomiting, no appetite, constipation and diarrhea are not uncommon GNA. Hypertension always occurred despite an increase in blood pressure may be only moderate. Hypertension occurs due to expansion of extracellular fluid volume. 3.6. Laboratory Overview Urinalysis showed proteinuria (+1 to +4), macroscopic hematuria was found almost in 50% of patients, abnormalities of urine sediment with erythrocytes disformik, leukosituria and granular, erythrocyte albumin (++), (+), leukocyte cylinders (+) and others. Sometimes the levels of serum urea and creatin increased with signs of kidney failure such as hypercalemia, acidosis, and hypocalcaemia, hiperphospatemia. Sometimes it appears the massive proteinuria with nephrotic syndrome symptoms. C3 is very noticeable decline in patients with acute glomerulonephritis pascastreptokokus with levels between 20-40 mg / dl (normal 50-140 mg/dl). The decline is not related C3 with severity of illness and healing.8 Streptococcus infection should be sought by the throat and skin cultures. Cultures may be negative if it had been given antimicrobial. Several serological tests against antigens sterptokokus can be used to prove the existence of infection, among others antisterptozim, Asto,
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antihialuronidase, and anti-Dnase B screening antisterptozim quite useful by being able to measure antibodies against several antigens sterptokokus. Titer of anti sterptolisin O may increase in 75-80% of patients with GNAPS with pharyngitis, although some do not produce sterptolisin. 3.7. Overview pathology Macroscopic kidney looked a little enlarged, pale and there is bleeding spots on the cortex. Microscopic look almost all glomeruli affected, so that could be called glomerulonephritis difuse. Proliferation of glomerular endothelial cell seems harsh resulting in capillary lumen and Bowman closed the hoop space. In addition there is also a capsule epithelial cell infiltration, infiltration polimorfonucleus cells and monocytes. On electron microscope examination will appear irregularly thickened basal membrane. There are lumps humps in subepitelium which may be formed by gamma-globulin, complement and antigen of Streptococcus. Histopathology of glomerulonefritis by 20 magnification of light microscope. Caption: Images taken using a light microscope (hematosylin and eosin with a magnification 25 ). Figure shows that make glomerular urinary space enlargement and hypercelluler. Hypercelluler happened by proliferation of endogenous cells and PMN leukocyte infiltration. Histopathology of glomerulonephritis by light microscopy 40 magnification

Histopathology microscope.

of

glomerulonephritis

by

electron

Caption: Images taken using an electron microscope. Figure shows proliferation of endothel cells and mesangial cells also infiltrating leucocytes which joined with deposit electrons in subephitelia.9

3.8. Diagnosis Diagnosis of acute glomerulonephritis pascastreptococcus need to be suspected in patients with clinical symptom such as a real hematuria arising suddenly, swollen and acute renal failure after streptococcal infection. Distinctive mark on urinalysis glomerulonephritis, evidence of streptococcal infection in laboratory and low levels of complement C3 supports evidence for a diagnosis. But some other circumstances may resemble acute glomerulonephritis pascastreptokok in early disease like IgA nephropathy and chronic glomerulonephritis. Children with IgA nephropathy, hematuria often show real symptoms suddenly soon after upper respiratory tract infections such as acute glomerulonephritis pascastreptokok, but macroscopic hematuria in IgA nephropathy, occur simultaneously during faringitas (synpharyngetic hematuria), while in acute glomerulonephritis arise pascastreptokok hematuria 10 days after faringitas , while hypertension and swollen rarely seen in nephropathy-IgA. Other chronic glomerulonephritis also showed a clinical picture of acute macroscopic hematuria, swollen, hypertension and kidney failure. Some who showed symptoms of chronic glomerulonephritis was membranoproliferatif glomerulonephritis, lupus nephritis, and proliferative glomerulonephritis kresentik. Differences with acute glomerulonephritis pascastreptokok difficult to know at the beginning infected. In acute glomerulonephritis pascastreptokok history of the disease rapidly improved (hypertension, swollen and will quickly recover renal failure), proteinuria, nephrotic syndrome and still more rarely seen in acute glomerulonephritis pascastreptokok than in chronic glomerulonephritis. The pattern of serum C3 complement levels during follow-up is a sign
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(marker) that is important to distinguish acute glomerulonephritis chronic glomerulonephritis pascastreptokok with another.9 3.9. Theurapy There are no specific treatments that affect healing in glomerular abnormalities. - Absolute rest for 3-4 weeks. Previously recommended rest for 6-8 weeks to allow the kidneys to heal. But the latest investigation shows that the mobilization of patients after 3-4 weeks of the first occurrence of no adverse effects on disease course of their illness. - Giving penicillin in the acute phase. Antibiotics do not affect the severity of glomerulonephritis, but reduce the spread of streptococcal infections that may still exist. Giving penicillin is recommended only for 10 days, while providing a long prophylaxis after nefritisnya recovers against germs that cause is not recommended because there is a permanent immunity. Theoretically, a child may become infected again with germs nefritogen other, but this possibility is very small. Giving penicillin can be combined with amoksislin 50 mg / kg divided into 3 doses for 10 days. If the group is allergic to penicillin, erythromycin was replaced with 30 mg / kg / day divided into 3 doses.10 -Food. In the acute phase are given low-protein diet (1 g / kg / day) and low salt (1 g / day). Soft food given to the patients for high temperatures and ordinary food when the temperature was normal again. In patients without complications of fluid administration are adjusted to the needs, while if there are complications such as heart failure, edema, hypertension and oliguria, the amount of fluid given should be limited. - Treatment of hypertension. Giving fluids is reduced, giving sedativa to calm patients so that they can simply relax. In hypertension with cerebral symptoms given reserpin and hidralazin. Parenteral magnesium sulfate is not recommended anymore because of toxic effects. - When anuria last long (5-7 days), then urea must be removed from the blood in several ways such as peritoneum dialysis, hemodialysis, rinses the stomach and intestines (this action is less effective, exchange transfusion). If the above procedure cannot be done because of technical difficulties, then the expenditure venous blood can be done and sometimes help as well. 11

CHAPTER IV
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ACUTE GLOMERULONEPHRITIS AND URINARY SYSTEM Acute glomerulonephritis certainly make things worse our urinary system. The most fatal relationship is if someone with acute glomerulonephritis and acute renal insufficiency resulting in kidney failure and even it happened because oliguria to anuria which can last 2-3 days. Occur as a result of reduced glomerular filtration. Although oliguria or anuria the old rare in children.12 CHAPTER V CONCLUSION Glomerunefritis kidney disease is bilateral trade. Acute glomerulonephritis most commonly occurs in children 3 to 7 years, although young adults and teenagers can also be attacked, a comparison of this disease in men and women 2:1. GNA is an immunological reaction in the kidney to specific bacterial or viral. Common symptoms associated with the onset of the disease are fatigue, anorexia and sometimes fever, headache, nausea, vomiting. Overview of the most frequently found were: hematuria, oliguria, edema, and hypertension. The main objective in the management of glomerulonephritis is to minimize damage to the glomerulus, minimizing the metabolism of the kidney, improve kidney function. There are no specific treatments that affect healing glomerular abnormalities. We can give penicilin to heal all residual infections, bed rest during the acute stage, diet if there is edema or symptoms of heart failure and the antihypertensive if necessary, while corticosteroids had no effect on acute post-infection glomerulofritis strepkokus. Prognosis diseases in children both while the prognosis in adults is not so good.

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REFERENCES 1. Price, Sylvia A, 1995 Patofisiologi :konsep klinis proses-proses penyakit, ed 4, EGC, Jakarta. 2. Staf Pengajar Ilmu Kesehatan Anak FKUI, 1985, Glomerulonefritis akut, 835-839, Infomedika, Jakarta. 3. Ilmu Kesehatan Nelson, 2000, vol 3, ed Wahab, A. Samik, Ed 15, Glomerulonefritis akut pasca streptokokus, 1813-14, EGC, Jakarta. 4. http://www/.5mcc.com/ Assets/ SUMMARY/TP0373.html. Accessed April 8th, 2009.
5. http://www.Findarticles.com/cf0/g2601/0005/2601000596/pi/article.jhtm?term=g

lomerunopritis+salt+dialysis. Accessed April 8th, 2009. 6. markum. M.S, Wiguno .P, Siregar.P,1990, Glomerulonefritis, Ilmu Penyakit Dalam II, 274-281, Balai Penerbit FKUI,Jakarta. 7. Donna J. Lager, M.D.http;//www.vh.org/adult/provider/pathologi/GN/GNHP.html.

Accessed April 8th, 2009. 8. http;//www.enh.org/encyclopedia/ency/article/000475.asp. Accessed April 8th, 2009. 9. http://www.kalbefarma.com/files/cdk/files/08_KlarifikasiHistopatologik.pdf/08_Klarifika siHistopatologik.html. Accessed April 8th, 2009. 10. http://www.kalbe.co.id/files/cdk/files/11_HematuriPadaAnak.pdf/11_HematuriPadaAnak .html. Accessed April 8th, 2009. 11. http://pkukmweb.ukm.my/~danial/Streptococcus.html. Accessed April 8th, 2009.

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12. http://medlinux.blogspot.com/2007/09/glomerulonephritis-akut.html. Accessed April 8th, 2009.

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