Arterial stiffness: an independent determinant of adaptive glomerular hyperfiltration after kidney donation.

After kidney donation, the remaining kidney tends to hyperfiltrate, thus limiting the initial loss of renal function. The potential determinants of this adaptive glomerular hyperfiltration (GHF) and specifically the influence of arterial function are poorly known. In 45 normotensive healthy kidney donors [51 ± 10 yr (mean ± SD), 39 females], glomerular filtration rate (GFR) was measured as the clearance of continuously infused (99m)Tc-DTPA and timed urine collections at baseline, i.e., before donation, and 1 yr after donation. GHF was computed as postdonation GFR minus half of baseline GFR. Arterial function was assessed as baseline carotid-femoral pulse wave velocity (PWV) and carotid augmentation index (AIx). After kidney donation, no significant change in blood pressure (BP) was observed, but two subjects developed hypertension. GFR decreased from 107 ± 19 to 73 ± 15 ml·min(-1)·1.73 m(-2), and mean GHF was 20 ± 10 ml·min(-1)·1.73 m(-2). In univariate analysis, GHF was inversely correlated to age (r(2) = 0.24, P = 0.01), baseline PWV (r(2) = 0.23, P = 0.001), and Aix (r(2) = 0.11, P = 0.031). Nevertheless, GHF was not correlated to baseline peripheral or central BP. In multivariate analysis, baseline PWV, but not AIx, remained inversely correlated to GHF, independently of age, baseline mean BP, and GFR (model r(2) = 0.34, P < 0.001). In healthy subjects selected for renal donation, increased arterial stiffness is associated with decreased postdonation compensatory hyperfiltration.