Effect of quinidine on kidney biochemistry and function in male Sprague-Dawley rats.

Accumulation of the organic anion p-amino hippurate (PAH) and the organic cation tetraethyl ammonium (TEA) was decreased in renal cortical slices incubated with medium containing quinidine. Renal cortical slice oxygen consumption was also decreased. Quinidine reduced respiratory control index (RCI) and ADP/O ratio in isolated kidney cortex mitochondria. The in vitro data suggest that quinidine can alter renal transport and mitochondrial functions. Intraperitoneal administration of quinidine at 75 mg/kg twice a day for four days inhibited PAH and TEA transport in renal cortical slices. Renal cortical slice oxygen consumption was significantly decreased. Mitochondria showed a significant reduction in ADP/O ratio but no effect on RCI. Serum biochemical measurements indicated significantly elevated blood urea nitrogen. The data suggest that quinidine produces adverse renal effects in vitro and at high doses it produces nephrotoxic effects in vivo.