Dopamine and Renall Blood Flow in Radiocontrast-Induced Nephropathy in Humans

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Abstract
Previous studies suggest a role for renal vasoconstriction in the pathogenesis of radiocontrast-induced nephropathy (RCIN). A renal vasodilator such as dopamine may be protective. However, the effect of dopamine on renal blood flow (RBF) in patients with chronic renal failure (CRF) is controversial. Patients with CRF of diabetic (DM) or nondiabetic (NDM) origin were hydrated with 0.45% NaCl intravenously at 100 mL/h for 12 h and then randomized to either 0.45% NaCl IV at 100 mL/h (Group 1) or dopamine IV at 2 μg/kg/min in 0.45% NaCl at 100 mL/h for 2 h during and after cardiac catheterization. Mean arterial pressure (MAP), cardiac output (CO), and RBF were measured at baseline (t = 0), after 5 min of vehicle (Group 1) or dopamine (Group 2) but before ionic radiocontrast (t = 5 min), after ventriculogram (t = 15 min), and after coronary angiography (t = 65 min). Serum creatinine (SCr) was measured at baseline and 24 and 48 h after cardiac catheterization. RCIN was defined as a 25% increase of SCr above baseline 48 h after cardiac catheterization. Baseline characteristics demonstrated the groups to be equivalent in age, SCr, creatinine clearance, CO, MAP, RBF, and radiocontrast dose administered. The incidence of RCIN was not different between Group 1 and Group2 (Group 1, 6 of 15 patients; Group 2, 5 of 15 patients). Dopamine infusion was associated with a significant increase in RBF at 5 min (Group 1, 110 ± 13%; Group 2, 193 ± 40% at t = 5, p <. 05). RBF remained elevated throughout the catheterization in Group 2. Within Group 2, RBF tended to rise only in those patients who subsequently developed RCIN (RCIN, 92 ± 40 mL/min; No RCIN, 203± 24 mL/min, p <. 05 at baseline); at t = 65: RCIN 530 ± 242%; No RCIN, 184 ± 38%, p <. 05. All the patients in the dopamine group who developed RCIN had diabetes mellitus. The patients with DM had lower baseline RBF than the patients with NDM, despite equivalent baseline renal function. The dopamine-stimulated increase in RBF was seen exclusively in the patients with DM. In conclusion, dopamine does not prevent RCIN in patients with CRF despite a significant renal vasodilatory effect. The renal vasodiliatory effect of low-dose dopamine in patients with CRF is heterogeneous, occurring only in patients with DM. Patients who subsequently developed RCIN had lower baseline RBF and the greatest rise in RBF with dopamine. Patients with DM and CRF have lower RBF and higher filtration fraction than NDM patients with equivalent SCr and creatinine clearance. These phenomena are functional (rather than fixed), as evidenced by the renal vasodilatory response to low-dose dopamine.