Dyazide-induced reversible acute renal failure associated with intracellular crystal deposition.
Acute interstitial nephritis due to Dyazide therapy, ie, a combination of hydrochlorothiazide (25 mg) and triamterene (50 mg), has been recently reported in the literature. This had been characterized by nonoliguric renal failure after a long latent period (weeks) following exposure to the drug. Pathologic data have indicated a drug-induced hypersensitivity reaction. We report here one case of oliguric acute renal failure after a massive Dyazide intoxication. Based on the results of the renal biopsy and clinical course, we propose that the oliguria was secondary to a direct toxic effect on the tubules, and intrarenal obstruction was secondary to triamterene crystals and crystal-laden cells. In addition, pathologic findings also suggested a moderate hypersensitivity reaction. After hemodialysis and short-term steroid therapy, the patient achieved complete recovery of renal function within 12 days. Recent knowledge of triamterene-induced nephrolithiasis helps to explain the pathogenesis of acute renal failure in this patient, and is briefly reviewed here.
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000473:pathology; D000328:Adult; D001706:Biopsy; D003460:Crystallization; D004338:Drug Combinations / Q000506:poisoning; D005260:Female; D006801:Humans; D006852:Hydrochlorothiazide / Q000506:poisoning*; D007668:Kidney / Q000473:pathology*; D013406:Suicide, Attempted; D014223:Triamterene / Q000378:metabolism / Q000506:poisoning*
D004338:Drug Combinations; D006852:Hydrochlorothiazide; C020743:hydrochlorothiazide-triamterene; D014223:Triamterene