Renal function in analgesic nephropathy.
Comprehensive one-day renal function tests in 20 patients with a history of analgesic abuse showed varying degrees of chronic renal failure in all. There was no evidence of a selective defect in proximal tubular function, while a defective concentrating mechanism, usually considered necessary for the diagnosis of analgesic-induced renal damage, could be demonstrated in only 16 patients. A urinary acidification defect associated with a concentrating defect was found in nine cases and was thought to reflect specific collecting duct dysfunction. Urinary ammonium excretion was reduced in 13 subjects, owing to a reduced number of functioning nephrons or inadequate acidification, or both. Low citrate excretion was frequently encountered, and this, as well as defective urinary acidification, may play some part in predisposing patients with analgesic nephropathy to intrarenal calcification and progressive renal failure.
D000136:Acid-Base Equilibrium; D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000175:diagnosis; D000328:Adult; D000368:Aged; D000700:Analgesics / Q000009:adverse effects*; D002951:Citrates / Q000652:urine; D003404:Creatinine / Q000652:urine; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007671:Kidney Concentrating Ability; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D019966:Substance-Related Disorders; D014667:Vasopressins
D000700:Analgesics; D002951:Citrates; D014667:Vasopressins; D003404:Creatinine