TY - JOUR
T1 - Obesity-induced glomerular hyperfiltration
T2 - Its involvement in the pathogenesis of tubular sodium reabsorption
AU - Chagnac, Avry
AU - Herman, Michal
AU - Zingerman, Boris
AU - Erman, Arie
AU - Rozen-Zvi, Benaya
AU - Hirsh, Judith
AU - Gafter, Uzi
PY - 2008/12
Y1 - 2008/12
N2 - 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.
AB - 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.
KW - Hyperinsulinaemia
KW - Insulin resistance
KW - Metabolic syndrome
KW - Peritubular oncotic pressure
KW - Tubular reabsorption
UR - http://www.scopus.com/inward/record.url?scp=56749183891&partnerID=8YFLogxK
U2 - 10.1093/ndt/gfn379
DO - 10.1093/ndt/gfn379
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AN - SCOPUS:56749183891
SN - 0931-0509
VL - 23
SP - 3946
EP - 3952
JO - Nephrology Dialysis Transplantation
JF - Nephrology Dialysis Transplantation
IS - 12
ER -
