The glomerular response to injury: Progression or resolution?

Abstract

A 20-year-old white man with a history of cocaine use presented with headache, mucopurulent sinusitis, and hypertension. The patient had had microscopic hematuria 6 months previously. He had no history of intravenous drug use. On physical examination, the blood pressure was 160/100mm Hg. A left facial paralysis (thought to be an idiopathic Bell's palsy) was present. The lungs were clear to auscultation, and the cardiac examination was normal. He had no hepatosplenomegaly and no edema. The serum creatinine was 4.1 mg/dl; BUN, 35 mg/dl; albumin, 2.9 g/dl; glucose, 130 mg/dl; sodium, 138 mEq/liter; potassium, 4.4 mEq/liter; chloride, 97 mEq/liter; and bicarbonate, 27 mEq/liter. Urinalysis revealed a pH of 6.5; specific gravity, 1.020; 4+ protein; 2+ blood; 10—20 erythrocytes/high-power field; and erythrocyte and granular casts. A 24-hour urine collection contained 10 g protein, and the creatinine clearance was 15 mI/mm. Other laboratory studies included C3, 118 mg/dl (normal, 60—150 mg/dl); C4, 44 mg/dl (normal, 12—40 mg/dl); ANA, negative; ANCA, negative; rheumatoid factor, negative; anti-GBM antibodies, negative; and negative hepatitis B virus and hepatitis C virus serologies. A renal biopsy was performed. Light microscopy revealed 10 glomeruli per section, of which one-half demonstrated global glomerulosclerosis. Mesangial cell proliferation, with an increase in both cellularity and matrix, was present in intact glomeruli. Focal cellular crescents were present in 2 glomeruli. Coincident extensive tubular atrophy was associated with interstitial fibrosis and a nonspecific mononuclear cell infiltrate; there was no evidence of vasculitis. Immunofluorescence demonstrated 3+ IgA deposition in the mesangium with no significant