Obesity-induced glomerular hyperfiltration: its involvement in the pathogenesis of tubular sodium reabsorption

Background. Obesity is associated with hypertension and glomerular hyperfiltration. A major mechanism responsible for the obesity-associated hypertension is renal salt retention. An increased glomerular filtration fraction (FF) is expected to raise postglomerular oncotic pressure and to increase proximal tubular sodium reabsorption. The aim of the present study was to verify whether obesity-associated hyperfiltration leads to increased postglomerularoncoticpressureandincreasedproximalsodium reabsorption. Methods. Twelve obese subjects (BMI >36) and 19 lean subjectsparticipatedinthestudy.Theyunderwentmeasurement of glomerular filtration rate (GFR), renal plasma flow (RPF) and fractional excretion of lithium (FE Li). Results. GFR, RPF and FF were 61%, 28% and 29% higher, respectively, in the obese than in the control group (P <0.00001 for GFR,P <0.005 for RPF andP <0.00005 for FF). Half of the obese group had increased FF with increasedGFR,whiletheotherhalfhadnormalFFwithhighnormal or increased GFR. Postglomerular oncotic pressure was 13% higher (P <0.03) and FE Li was 33% lower (P <0.005) in the obese group with high FF than in the leangroup.PostglomerularoncoticpressureandFELiwere normal in the obese group with normal FF. Conclusions. These results suggest that glomerular hyperfiltration may lead to increased proximal tubular sodium reabsorption in the obese.