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

Avry Chagnac*, Michal Herman, Boris Zingerman, Arie Erman, Benaya Rozen-Zvi, Judith Hirsh, Uzi Gafter

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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 postglomerular oncotic pressure and increased proximal sodium reabsorption. Methods. Twelve obese subjects (BMI >36) and 19 lean subjects participated in the study. They underwent measurement 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 and P < 0.00005 for FF). Half of the obese group had increased FF with increased GFR, while the other half had normal FF with high-normal 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 lean group. Postglomerular oncotic pressure and FE Li were 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.

Original languageEnglish
Pages (from-to)3946-3952
Number of pages7
JournalNephrology Dialysis Transplantation
Issue number12
StatePublished - Dec 2008


  • Hyperinsulinaemia
  • Insulin resistance
  • Metabolic syndrome
  • Peritubular oncotic pressure
  • Tubular reabsorption


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