Effect of obesity-induced hyperfiltration on renal peritubular capillary oncotic pressure

Studies in animals and humans have shown that salt retention may be involved in the pathogenesis of obesity-induced hypertension. One of the factors which may theoretically promote renal salt reabsorption is an elevated peritubular capillary oncotic pressure. Obesity is associated with elevated filtration fraction (FF) and high glomerular filtration rate (GFR). An increased FF is predicted to elevate the renal peritubular capillary oncotic pressure ( PT), thus promoting salt reabsorption. We have previously reported the effects of weight loss on GFR and RPF in subjects with severe obesity (Chagnac et al, J Am Soc Nephrol, 2003). The aim of the present study is to estimate the effect of weight loss on the PT of obese subjects. Eight subjects with severe obesity (BMI 38 to 61) underwent renal function tests before and after weight loss. GFR and renal plasma flow (RPF) were measured as inulin and amino-hippurate clearance respectively. FF was calculated as GFR/RPF. The afferent arteriolar oncotic pressure ( A) was estimated from the plasma protein concentration. PT was calculated as PT A /(1-FF). Following weight loss, BMI decreased from 48 2.4 to 32.1 1.5 (P 0.001). Systolic blood pressure decreased from 143 6 to 133 6 mm Hg (P 0.005). GFR decreased from 145 14 to 110 7 ml/min (P 0.01). RPF decreased from 732 35 to 628 37 ml/min (P 0.02). FF was 0.18 0.01 before and 0.16 0.01 after weight loss (P 0.07). A was 25.8 1.1 mm Hg before and 24.5 1.0 mm Hg after weight loss (P NS). PT decreased from 31.5 1.4 to 29.2 1.3 mm Hg following weight loss (P 0.05). This study shows that PT decreases following weight loss. This finding suggests that obesity-induced hyperfiltration results in an increased PT. The increased PT may play a role in the pathogenesis of obesity-associated hypertension.