Acute Glomerulonephritis (AGN)

 Synonyms

and related keywords:

acute glomerulonephritis, acute glomerular nephritis, acute hemorrhagic glomerulonephritis, acute nephritis, acute poststreptococcal glomerulonephritis, nephritic syndrome, acute nephritic syndrome, nephritis syndrome, acute nephritis syndrome, kidney disease, renal disease

 Acute

glomerulonephritis (AGN) is active inflammation in the glomeruli. Each kidney is composed of about 1 million microscopic filtering "screens" known as glomeruli that selectively remove uremic waste products. The inflammatory process usually begins with an infection or injury (e.g., burn, trauma), then the protective immune system fights off the infection, scar tissue forms, and the process is complete

 There

are many diseases that cause an active inflammation within the glomeruli. Some of these diseases are systemic (i.e., other parts of the body are involved at the same time) and some occur solely in the glomeruli. When there is active inflammation within the kidney, scar tissue may replace normal, functional kidney tissue and cause irreversible renal impairment.

 The

severity and extent of glomerular damage focal (confined) or diffuse (widespread) determines how the disease is manifested. Glomerular damage can appear as subacute renal failure, (CRF); progressive chronic renal failure (CRF); or simply a urinary abnormality such as hematuria (blood in the urine)or proteinuria (excess protein in the urine).

Pathophysiology
 Cellular

proliferation, infiltration of glomerulus by leukocytes glomerular trapping of circulating immune complexes thickening of glomerular filtration membrane scarring and loss of filtering surface renal failure

Postinfectious GN has no predilection for any racial or ethnic group. A higher incidence (related to poor hygiene) may be observed in some socioeconomic groups.  Sex: Acute GN predominantly affects males (ie, 2:1 male-to-female ratio). male-to Age: Postinfectious GN can occur at any age but usually develops in children. Outbreaks of PSGN are common in children aged 6-10 years. 6 Race:

 History:

Taking a proper history is important and helpful.

onset of disease: Ask the patient about onset and duration of illness.  Identify a possible etiologic agent (eg, streptococcal throat infection [pharyngitis], skin infection [pyoderma]): Recent fever, sore throat, joint pains, hepatitis, travel, valve replacement, and/or intravenous drug use may be causative factors. Rheumatic fever rarely coexists with acute PSGN.
 Determine

 Identify

systemic disease (eg, arthralgia, diabetes).  Assess the consequences of the disease process (eg, uremic symptoms): Inquire about loss of appetite, generalized itching, tiredness, listlessness, nausea, easy bruising, nose bleeds, facial swelling, leg edema, and shortness of breath.

y Identify clinical features: Inquire about edema, decreased volume and frequency of urination, systemic hypertension, uremic symptoms, costovertebral tenderness (ie, enlarged kidneys [rare]), and gross hematuria. Gross hematuria is the most common abnormality observed in patients with acute PSGN and often manifests as smoky-, coffee-, or colasmoky- coffeecolacolored urine.

Physical:
 Signs of fluid overload  Periorbital and/or pedal edema  Edema and hypertension due to

overload - In 75% of patients  Crackles (ie, if pulmonary edema)  Elevated jugular venous pressure  Ascites and pleural effusion (possible)  Rash (ie, vasculitis, Henoch-Schnlein Henochpurpura)  Pallor  Renal angle (ie, costovertebral) fullness or tenderness, joint swelling, or tenderness

fluid

Causes:
 The

causal factors that underlie this syndrome can be broadly divided into infectious and noninfectious groups.

Infectious


Streptococcal: Poststreptococcal GN usually develops 1-3 1weeks following acute infection with specific nephritogenic strains of group A beta-hemolytic betastreptococcus. The incidence of GN is approximately 5-10% in 5persons with pharyngitis and 25% in those with skin infections.

Nonstreptococcal postinfectious glomerulonephritis  Bacterial - Infective endocarditis, shunt nephritis, sepsis, pneumococcal pneumonia, typhoid, secondary syphilis, meningococcemia, and infection with methicillin-resistant methicillinStaphylococcus aureus (MRSA)  Viral - Hepatitis B, infectious mononucleosis, mumps, measles, varicella, vaccinia, echovirus, parvovirus, and coxsackievirus  Parasitic - Malaria, toxoplasmosis

Noninfectious
 Multisystem

systemic diseases - Systemic lupus erythematosus, vasculitis, HenochHenochSchnlein purpura, Goodpasture syndrome, Wegener granulomatosis  Primary glomerular diseases Membranoproliferative GN (MPGN), Berger disease (ie, immunoglobulin A [IgA] nephropathy), "pure" mesangial proliferative GN  Miscellaneous - Guillain-Barr syndrome, Guillainradiation of Wilms tumor, diphtheriadiphtheriapertussispertussis-tetanus vaccine, serum sickness

Lab Studies:

Urinalysis and sediment examination



Hematuria, proteinuria, red cell casts, white cells, renal epithelial cells

 Blood,

urea, and nitrogen (BUN); serum creatinine; and serum electrolytes (especially serum potassium level)  Complete blood cell count  Erythrocyte sedimentation rate

Imaging Studies:
 Abdominal

ultrasound Assesses renal size Assesses echogenicity of renal cortex Excludes obstruction

Procedures:
 Generally,

a renal biopsy is not necessary for diagnosis of acute PSGN; however, in most cases, it is important because histology guides both prognosis and therapy.

Medical Care
:

Treatment of acute PSGN is mainly supportive because there is no specific therapy for renal disease. Treat the underlying infections when acute GN is associated with chronic infections.

 Antimicrobial

therapy  Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts.  Antimicrobial therapy does not appear to prevent the development of GN, except if given within the first 36 hours.

Loop diuretic therapy

Loop diuretics may be required in patients who are edematous and hypertensive in order to remove excess fluid and to correct hypertension.  Relieves edema and controls volume, thereby helping to control volume-related elevation in BP. volume

Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present.  Glucocorticoids and cytotoxic agents are of no value, except in severe cases of PSGN.

Consultations: Consultations: Nephrologist

Diet:
 Sodium

and fluid restriction - For treatment of signs and symptoms of fluid retention (eg, edema, pulmonary edema)  Protein restriction for azotemic patients - If no evidence of malnutrition

Activity:
 Recommend

bed rest until signs of glomerular inflammation and circulatory congestion subside. Prolonged inactivity does not benefit in the patient recovery process.

FOLLOWFOLLOW-UP

Further Inpatient Care: Patients may require hospitalization for control of edema and hypertension. Further Outpatient Care: Monitor renal function, BP, edema, serum albumin, and urine protein excretion rate. In/Out Patient Meds: Patient may require medication to control BP. Transfer: The expertise available in the ICU may be needed for management of patients with hypertensive encephalopathy or pulmonary edema.

Deterrence/Prevention:
 Early

antibiotic therapy of streptococcal infection (ie, within 36 h of onset) may prevent development of PSGN.  Antibiotic treatment of close contacts of the index case may help prevent development of PSGN.

Complications:
 Renal

failure (rare)  Pulmonary edema  Generalized anasarca and hypoalbuminemia (secondary to severe proteinuria)  Hypertension  Hypertensive encephalopathy

Patient Education:


Counsel patients about the need for the following measures:

   

Salt restriction during the acute phase to control edema and volume-related hypertension volumeBP monitoring at periodic intervals Ongoing long-term monitoring of patients with longpersistent urinary abnormalities and elevated BP Consideration of protein restriction and angiotensin converting enzyme inhibitors (in patients who show evidence of persistent abnormalities or in those who develop late evidence of progressive disease) Early antibiotic treatment of close contacts