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.