1.6: Arterial Stiffness is An Independent Determinant of Compensatory Hyperfiltration After Kidney Donation

After kidney donation, the remaining kidney tends to hyperfiltrate thus limiting the initial loss of renal function. However, the potential determinants of this compensative hyperfiltration (CHF) and the possible influence of arterial function are not known. In 26 normotensive healthy kidney donors (51 +/− 9 yrs [mean+/−SD], 22 females), glomerular filtration rate (GFR) was measured by the clearance of continuously infused Tc99m-DTPA and timed urine collections at baseline -i.e. before donation- and 1 year after donation. CHF was computed as post-donation GFR minus half of baseline GFR. Arterial function was assessed at baseline through carotido-femoral pulse wave velocity (PWV) and carotid augmentation index (AIx). After kidney donation, there were no significant changes in blood pressure (BP), but 2 subjects became hypertensive. GFR decreased from 104+/−17 to 71+/−11 mL/min/1.73m 2 and mean CHF was 19+/−9 mL/min/1.73m 2 . In univariate analysis, CHF was inversely correlated to baseline age (r 2 =0.15, p=0.049) and PWV (r 2 =0.23, p=0.012), but not mean BP or AIx. In multivariate analysis, CHF remained inversely correlated to PWV (p=0.020), independently of baseline age, mean BP and GFR (model r 2= 0.45, p=0.002). In conclusion, in healthy subjects, increased arterial stiffness seems to be associated with a limited magnitude of post-donation hyperfiltration. This could reflect an influence of arterial function on renal reserve, providing further insights into the relationship between macrocirculation and renal microcirculation.