Nitroprusside-induced acute azotemia

A patient with congestive heart failure and pneumonia was begun on a nitroprusside infusion for cardiac afterload reduction. Urine output declined sharply and azotemia ensued despite little change in arterial pressure. Further evaluation supported a prerenal mechanism with dramatic recovery related to tapering and discontinuation of the nitroprusside. The mechanism of renal deterioration is possibly related to a 'steal' syndrome due to preferential dilation of vascular beds other than the renal.