Acute and chronic toxic nephropathies.
Toxic nephropathies manifest morphologically as glomerulonephritides, vasculitides, tubular necrosis, and acute or chronic tubulointerstitial disease. The most common toxicity is acute interstitial nephritis owing to hypersensitivity. However, focal segmental glomerulosclerosis and necrotizing angiitis secondary to heroin abuse, membranous glomerulopathy owing to gold, penicillamine and captopril, thrombotic microangiopathy associated with mitomycin and tubular necrosis owing to cyclosporine A, cisplatin, aminoglycosides, and cephalosporins are also reviewed. The mechanisms of toxicity are poorly understood in most cases, but hypotheses related to cyclosporine A, cisplatin, gold, aminoglycosides, cephalosporins, intravenous narcotics, sulfonamides, and methotrexate are summarized.
Sanders
M M
MM
Department of Pathology, University of Arkansas, Medical Sciences, Little Rock 72205.
Marshall
A P
AP
D000208:Acute Disease; D000700:Analgesics / Q000009:adverse effects; D002511:Cephalosporins / Q000009:adverse effects; D002908:Chronic Disease; D002945:Cisplatin / Q000009:adverse effects; D015433:Glomerulonephritis, Membranous / Q000139:chemically induced / Q000473:pathology; D006801:Humans; D013287:Illicit Drugs / Q000506:poisoning; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology; D009294:Narcotics / Q000009:adverse effects*
D000700:Analgesics; D002511:Cephalosporins; D013287:Illicit Drugs; D009294:Narcotics; D002945:Cisplatin