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ACUTE GLOMERULONEPHRITIS (GN)

Often called the "nephritic syndrome." Characterized by development, over days, of azotemia, hypertension, edema, hematuria, proteinuria, and sometimes oliguria. Salt and water retention are due to reduced glomerular filtration rate (GFR) and may result in circulatory congestion. Red blood cell (RBC) casts on urinalysis confirm diagnosis (Dx). Proteinuria is usually <3 g/d. Most forms of acute GN are mediated by humoral immune mechanisms. Clinical course depends on underlying lesion (Table 152-1).

TABLE 152-1CAUSES OF ACUTE GLOMERULONEPHRITIS

Acute Poststreptococcal GN

This is the prototype and most common cause in childhood. Nephritis develops 1–3 weeks after pharyngeal or cutaneous infection with "nephritogenic" strains of group A β-hemolytic streptococci. Dx depends on a positive pharyngeal or skin culture (if available), positive titers for antistreptococcal antigens (ASO, anti-DNAse, or antihyaluronidase), and hypocomplementemia. Renal biopsy reveals diffuse proliferative GN. Treatment consists of correction of fluid and electrolyte imbalance. In most cases the disease is self-limited, although the prognosis is less favorable and urinary abnormalities are more likely to persist in adults.

Postinfectious GN

May follow other bacterial, viral, and parasitic infections. Examples are bacterial endocarditis, sepsis, hepatitis B, and pneumococcal pneumonia. Features are milder than with poststreptococcal GN. Control of primary infection usually produces resolution of GN.

RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS

Defined as a subacute reduction in GFR of >50%, with evidence of a proliferative GN; causes overlap with those of acute GN (Table 152-2). Broadly classified into three major subtypes on the basis of renal biopsy findings and pathophysiology: (1) immune complex–associated, e.g., in systemic lupus erythematosus (SLE); (2) "pauci-immune," associated with antineutrophil cytoplasmic antibodies (ANCA); and (3) associated with anti–glomerular basement (anti-GBM) antibodies, e.g., in Goodpasture's syndrome. All three forms will typically have a proliferative, crescentic GN by light microscopy but differ in the results of the immunofluorescence and electron microscopy components of the renal biopsy.

TABLE 152-2CAUSES OF RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS

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