L-Arginine-Induced Vasodilation of the Renal Vasculature Is Preserved in Uremic Type 1 Diabetic Patients after Kidney and Pancreas but not after Kidney-Alone Transplantation

Abstract

OBJECTIVE - In uremic type 1 diabetic patients, kidney and pancreas transplantation (KP) and kidney-alone transplantation (KD) provide full restoration of normal renal function; however, only KP, i.e., curing diabetes, is expected to prevent endothelial damages. Our aim was to study L-arginine-induced vasodilation of the renal vasculature in uremic type 1 diabetic patients after KP or KD using magnetic resonance (MR). RESEARCH DESIGN AND METHODS - MR quantitative flow measurements were performed in 15 KP patients (mean age 39.0 ± 1.7 years, 10 men and 5 women), in 11 KD patients (mean age 47.3 ± 1.9 years, 7 men and 4 women), and in 8 nondiabetic kidney transplant patients (mean age 44.0 ± 4.8 years, 7 men and 1 woman), who were used as control subjects, to measure renal blood flow and velocity and renal vascular resistance before and immediately after infusion of L-arginine. RESULTS - Renal blood flow and velocity were not different at baseline in KP, KD, and control subjects. In contrast, during L-arginine administration renal blood flow increased significantly in KP subjects (basal 8.4 ± 0.6 vs. post 9.6 ± 0.8 ml/s, Δ 14.3 ± 44%, P < 0.05) and in control subjects (basal 9.3 ± 0.8 vs. post 9.1 ± 0.8 ml/s, Δ 17.3 ± 6.2%, P < 0.01), while it remained unchanged in KD subjects (basal 10.0 ± 0.8 vs. post 11.6 ± 0.9 ml/s, Δ -1.36 ± 6.9%, NS). Parallel results have been achieved for renal blood velocity (KP subjects: 20.1 ± 4.9%, P < 0. 01; control subjects: 23.0 ± 7.99%, P < 0.01; and KD subjects: -0.3 ± 6.5%; NS). A reduction in renal vascular resistance in response to L-arginine was evident in KP and control subjects but not in KD patients. CONCLUSIONS - L-Arginine vasodilatory response was successfully assessed with MR quantitative flow measurements. KP patients and control subjects, but not those with KD, showed a preserved L-arginine-induced vasodilation of the renal vasculature.