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Postinfectious glomerulonephritis occurs after infection, usually with a nephritogenic strain of group A β-hemolytic streptococcus. Diagnosis is suggested by history and urinalysis and confirmed by finding a low complement level and sometimes by antibody testing. Prognosis is excellent. Treatment is supportive.
Postinfectious glomerulonephritis (PIGN), a nephritic syndrome (see Overview of Nephritic Syndrome), is the most common cause of a glomerular disorder in children between 5 and 15 yr; it is rare in children < 2 yr and uncommon in adults > 40 yr.
Most cases are caused by nephritogenic strains of group A β-hemolytic streptococci, most notably type 12 (which causes pharyngitis) and type 49 (which causes impetigo); an estimated 5 to 10% of patients with streptococcal pharyngitis and about 25% of those with impetigo develop PIGN. A latency period of 6 to 21 days between infection and GN onset is typical, but latency may extend up to 6 wk.
Less common pathogens are nonstreptococcal bacteria, viruses, parasites, rickettsiae, and fungi (see Causes of Glomerulonephritis). Bacterial endocarditis and ventriculoatrial shunt infections are additional important conditions in which PIGN develops; ventriculoperitoneal shunts are more resistant to infection.
The mechanism is unknown, but microbial antigens are thought to bind to the glomerular basement membrane and activate primarily the alternate complement pathway both directly and via interaction with circulating antibodies, causing glomerular damage, which may be focal or diffuse. Alternatively, circulating immune complexes could precipitate on the glomerular basement membrane.
Symptoms and signs range from asymptomatic hematuria (in about 50%) and mild proteinuria to full-blown nephritis with microscopic or gross hematuria (cola-colored, brown, smoky, or frankly bloody urine), proteinuria, oliguria, edema, hypertension, and renal insufficiency. Severe, late disease is a relatively uncommon cause of nephrotic syndrome. Renal failure that causes fluid overload with heart failure and severe hypertension requiring dialysis affects 1 to 2% of patients and may manifest as a pulmonary-renal syndrome with hematuria and hemoptysis (see Pulmonary-Renal Syndrome). Fever is unusual and suggests persistent infection.
Clinical manifestations of nonstreptococcal PIGN may mimic other disorders (eg, polyarteritis nodosa, renal emboli, antimicrobial drug–induced acute interstitial nephritis).
Streptococcal PIGN is suggested by history of pharyngitis or impetigo plus either typical symptoms of PIGN or incidental findings on urinalysis. Tests done to confirm the diagnosis depend on clinical findings. Antistreptolysin O, antihyaluronidase, and antideoxyribonuclease (anti-DNAase) antibodies are commonly measured. Serum creatinine and complement levels (C3 and total hemolytic complement activity) are also usually measured; however, in patients with classic findings, some tests can be omitted. Sometimes other tests are done. Biopsy confirms the diagnosis but is rarely necessary; demonstration of hypocomplementemia is essentially confirmatory.
Antistreptolysin O level, the most common laboratory evidence of recent streptococcal infection, increases and remains elevated for several months in about 75% of patients with pharyngitis and in about 50% of patients with impetigo, but it is not specific. An increase in antihyaluronidase and antideoxyribonuclease titers is more specific for detecting recent streptococcal skin infection but is not widely available.
Urinalysis typically shows proteinuria (0.5 to 2 g/m2/day); dysmorphic RBCs; WBCs; renal tubular cells; and possibly RBC, WBC, and granular casts. Random (spot) urinary protein/creatinine ratio is usually between 0.2 and 2 (normal, < 0.2) but may occasionally be in the nephrotic range (≥ 3).
Serum creatinine may rise rapidly but usually peaks below a level requiring dialysis.
C3 and total hemolytic complement activity (CH50) levels fall during active disease and return to normal within 6 to 8 wk in 80% of PIGN cases; C1q, C2, and C4 levels are only minimally decreased or remain normal. Cryoglobulinemia may appear and persist for several months, whereas circulating immune complexes are detectable for only a few weeks.
Biopsy specimens show enlarged and hypercellular glomeruli, initially with neutrophilic infiltration and later with mononuclear infiltration. Epithelial cell hyperplasia is a common early, transient feature. Microthrombosis may occur; if damage is severe, hemodynamic changes due to cellular proliferation and edema of the glomerulus cause oliguria, occasionally accompanied by epithelial crescents (formed within Bowman space from epithelial cell hyperplasia). Endothelial and mesangial cells multiply, and the mesangial regions often are greatly expanded by edema and contain neutrophils, dead cells, cellular debris, and subepithelial deposits of electron-dense material. Immunofluorescence microscopy usually shows immune complex deposition with IgG and complement in a granular pattern. On electron microscopy, these deposits are semilunar or hump-shaped and are located in the subepithelial area. The presence of these deposits and of small subendothelial and mesangial deposits initiates a complement-mediated inflammatory reaction that leads to glomerular damage. Although the immune complex is presumed to contain an antigen related to streptococcal organisms, no such antigen has been found.
Normal renal function is retained or regained by 85 to 95% of patients. GFR usually returns to normal over 1 to 3 mo, but proteinuria may persist for 6 to 12 mo and microscopic hematuria for several years. Transient changes in urinary sediment may recur with minor URIs. Renal cellular proliferation disappears within weeks, but residual sclerosis is common. In 10% of adults and 1% of children, PIGN evolves into rapidly progressive GN.
Treatment is supportive and may include restriction of dietary protein, Na, and fluid and, in more severe cases, treatment of edema and hypertension. Dialysis is occasionally necessary. Antimicrobial therapy is preventive only when given within 36 h of infection and before GN becomes established.
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