Obesity, salt intake, and renal perfusion in healthy humans

Renal perfusion rises as obesity develops during short-term overfeeding in animal studies. In humans, the assessment is complicated by the need to normalize renal perfusion for body size. We made use of the fact that radioactive xenon washout measures renal perfusion per unit of tissue mass to address this issue by comparing 45 moderately obese and 147 lean healthy potential kidney donors. All were disease free. The rationale for involving kidney donors reflects the fact that the xenon method for measuring renal perfusion demands injection of the xenon directly into the renal artery, which can be accomplished during the arteriogram that is a necessary part of potential kidney donor evaluation. In 21 obese subjects !body mass index [BMI], 29.1+/-0.9) in balance on a 10-mmol sodium intake, renal perfusion (352+/-16 mL . 100 g(-1) . min(-1)) was significantly higher than predicted from findings in the 95 lean control subjects (313+/-3 mL . 100 g(-1) . min(-1); P=0.035) after adjustment for age. With a high sodium intake (200 mmol), however, renal perfusion was not significantly different in 24 obese subjects (BMI, 28.8+/-0.7; 323 +/-13 mL . 100 g(-1) min(-1)) in comparison to 52 lean controls (341+/-10 mL . 100 g(-1) . min(-1)) after adjustment for age. Systolic and diastolic blood pressures were similar in obese and age- and gender-matched lean control subjects. Renal vasodilation was seen in association with sustained obesity in humans. While the mechanisms of obesity-related vasodilation are unclear, the dependence on sodium intake in this study is consistent with a role for the renin-angiotensin system. The findings are not in accordance with a reduction in renal perfusion reported in healthy obese humans in whom measured renal perfusion was indexed for body size.