Nephrotoxicity from angiographic contrast material. A prospective study.

Abstract

Three hundred and seventy-eight hospitalized patients undergoing nonrenal angiography were evaluated for subsequent changes in renal function. Acute renal failure was defined as a rise in the serum creatinine level of 1.0 mg/dl or more. Several factors that appeared to play no significant role in causing acute renal failure included: the volume of contrast material injected, the anatomic site of injection and the presence of a prior history of cardiovascular disease or diabetes mellitus. The single risk factor identified was the presence of preexistent azotemia (blood urea nitrogen of 30 mg/dl and serum creatinine of 1.5 mg/dl). Whereas nonazotemic patients had a 2 percent incidence of definite acute renal failure, patients with chronic azotemia (mean blood urea nitrogen/creatinine = 47/2.3 mg/dl) had a 33 percent incidence. Three patients required short-term dialysis, and two required potassium-exchange resin therapy. No patient required permanent dialysis, and no patient died of acute renal failure. The persistence of a positive nephrogram 24 hours after angiography was a sensitive detector of a rise in the serum creatinine level although more expensive than the creatinine determination. While urine sediment analysis confirmed the diagnosis in many cases, it was relatively insensitive. Monitoring of urine volume proved to be of little value. We recommend a screening serum creatinine determination 24 to 48 hours after infusion of angiographic contrast material in azotemic patients.