Clinical analgesic nephropathy.
Analgesic nephropathy is recognized worldwide, but the differences in incidence in various countries, or regions, remain unexplained. Analgesic compounds may cause both functional and structural renal damage. This damage may be related to depletion of glutathione and renal vasoconstriction (probably mediated through prostaglandin depletion) and to the fact that the concentrations of glutathione and prostaglandins and their metabolites in the kidneys are manyfold their concentrations in plasma. Most patients with analgesic nephropathy are middle-aged women with histories of peptic ulcer, anemia, psychiatric disorders, headaches, and arthralgias. Investigations often show pyuria, some bacteriuria, and impaired concentrating ability, as well as other abnormalities of tubular function; caliceal abnormalities on intravenous pyelography are also frequent. It is important to discover these patients; evidence exists that with cessation of drug ingestion, renal function may stabilize and, in some cases, may improve.
D000700:Analgesics / Q000009:adverse effects*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D007008:Hypokalemia / Q000139:chemically induced; D007674:Kidney Diseases / Q000139:chemically induced* / Q000473:pathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000139:chemically induced; D012459:Salicylates / Q000009:adverse effects; D019966:Substance-Related Disorders / Q000453:epidemiology
D000700:Analgesics; D012459:Salicylates; D005978:Glutathione