Nephrotoxicity of sodium iopanoate in hydrated and dehydrated dogs.
The nephrotoxic effect of sodium iopanoate, infused intravenously in dosages of 1.5, 3 and 6 g over a 2-hour period in eight dogs (22--27 kg) in both the hydrated and dehydrated stages, were investigated. On biochemical, hemodynamic and morphological studies, the nephrotoxic effect was found to be clearly dose-dependent and greater in the dehydrated stage. Previously suggested mechanisms for acute renal failure, such as a direct tubular toxicity, tubular obstruction and hypotension, could not be supported as main factors in the development of acute renal failure post-cholecystography, although they might well have a contributory effect. The primary cause of renal failure post-cholecystography cannot be determined unequivocally from this investigation. However, the observed findings would appear to be consistent with a toxic effect of iopanoate in the small vessels possibly resulting in ischemic tubular necrosis.
D058186:Acute Kidney Injury / Q000139:chemically induced*; D000792:Angiography; D000818:Animals; D001794:Blood Pressure; D002765:Cholecystography / Q000009:adverse effects; D003404:Creatinine / Q000097:blood; D003681:Dehydration / Q000378:metabolism; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D007455:Iodine / Q000378:metabolism; D007480:Iopanoic Acid / Q000009:adverse effects*; D007668:Kidney / Q000098:blood supply / Q000473:pathology; D008297:Male; D012039:Regional Blood Flow; D014527:Uric Acid / Q000652:urine
D014527:Uric Acid; D007455:Iodine; D003404:Creatinine; D007480:Iopanoic Acid