Radiocontrast-induced nephropathy in humans: Role of renal vasoconstriction

Abstract

Radiocontrast-induced nephropathy (RCIN) is a common cause of acute renal failure in hospitalized patients. Renal vasoconstriction figures prominently in the proposed pathogenesis of RCIN based on animal experiments. Prior human studies examining renal hemodynamic changes after contrast medium (CM) injection are inconclusive. No previous study of animals or humans has established a relationship between CM-associated renal hemodynamic changes and the subsequent development of RCIN. In the present study, we examined the renal hemodynamic effects of CM in patients at high risk of RCIN. In addition, we related those effects to the subsequent development of RCIN. Using renal vein thermodilution catheters, we measured renal blood flow (RBF) in 12 patients with chronic renal failure [serum creatinine (S(Cr)) ≥159 μmol/liter] during ionic CM injection for cardiac catheterization. We made measurements at the start of the procedure (t = 0), before the ventriculogram (t = 5), after the ventriculogram (t = 15), and after the coronary angiogram (t = 65). We measured S(Cr) at t = 0 and again 24 and 48 hours later. Mean RBF for the group tended to increase after the ventriculogram, and increased significantly by t = 65 (P < 0.005 vs. t = 0). When examined by individual patient, RBF fell below baseline in three patients (30%) at t = 15, but rose above baseline again by t = 65. Only one patient (8.3%) had a fall in RBF below baseline at t = 65. RCIN (defined as an increase in S(Cr) ≥25% above baseline) developed in six patients (50%) within 48 hours. Of those only two (33%) had shown a fall in RBF at t = 15, and none at t = 65. Of the four patients in the group as a whole whose RBF had fallen at any time, only two (50%) developed RCIN. We conclude that intracardiac injection of ionic CM is not associated with a fall in total RBF in most patients with chronic renal failure. Furthermore, there appears to be no relationship between the development of RCIN and any change in total RBF. Global renal vasoconstriction does not appear to play a pathogenic role in RCIN in humans with chronic renal failure.