Postinfectious glomerulonephritis occurs after infection, usually with a nephritogenic strain of group A beta-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.
Most cases are caused by nephritogenic strains of group A
beta-hemolytic streptococci, most notably type 12 [which causes pharyngitis
Tonsillopharyngitis Tonsillopharyngitis is acute infection of the pharynx, palatine tonsils, or both. Symptoms may include sore throat, odynophagia, cervical lymphadenopathy, and fever. Diagnosis is clinical, supplemented... read more
Less common pathogens are nonstreptococcal bacteria, viruses, parasites, rickettsiae, and fungi [see table
Causes of Glomerulonephritis
Causes of Glomerulonephritis
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
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 [sometimes nephrotic-range], oliguria, edema, hypertension, and renal insufficiency. Fever is unusual and suggests persistent infection.
Renal failure that causes fluid overload with heart failure and severe hypertension requiring dialysis affects 1 to 2% of patients.
Uncommonly, nephrotic syndrome may persist after resolution of severe disease.
Clinical manifestations of nonstreptococcal PIGN may mimic other disorders [eg, polyarteritis nodosa, renal emboli, antimicrobial drug–induced acute interstitial nephritis].
Clinical evidence of recent infection
Urinalysis typically showing dysmorphic red blood cells [RBCs], RBC casts, proteinuria, white blood cells [WBCs], and renal tubular cells
Often hypocomplementemia
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 typical clinical findings, some tests can be omitted. Sometimes other tests are done. Biopsy confirms the diagnosis but is rarely necessary.
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. The streptozyme test, which additionally measures antihyaluronidase, antideoxyribonuclease, and other titers detects 95% of recent streptococcal pharyngitis and 80% of skin infections.
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,