Obesity-induced glomerular hyperfiltration: its involvement in the pathogenesis of tubular sodium reabsorption
Obesity-induced glomerular hyperfiltration: its involvement in the pathogenesis of tubular sodium reabsorption
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DOI：
10.1093/ndt/gfn379
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发表时间：
2008-12-01
影响因子：
6.1
通讯作者：
Gafter, Uzi
中科院分区：
文献类型：
--
作者：
Chagnac, Avry;Herman, Michal;Gafter, Uzi
背景肥胖与高血压和肾小球高滤过有关。肥胖相关性高血压的一个主要机制是肾盐潴留。肾小球滤过分数（FF）的增加预计会增加肾小球后压，并增加近端肾小管钠重吸收。本研究的目的是验证肥胖相关的超滤是否会导致肾小球后膜压升高和近端钠重吸收增加。12名肥胖受试者（BMI > 36）和19名瘦受试者参与了该研究。测定肾小球滤过率（GFR）、肾血浆流量（RPF）和锂排泄分数（FE Li）。肥胖组GFR、RPF和FF分别比对照组高61%、28%和29%（GFR P < 0.00001，RPF P < 0.005，FF P < 0.00005）。肥胖组中有一半的FF增加，GFR增加，而另一半的FF正常，GFR正常或增加。高FF的肥胖组肾小球后压比消瘦组高13%（P < 0.03），FE Li比消瘦组低33%（P < 0.005）。肥胖组FF正常者肾小球后压和FE Li均正常。这些结果表明，肾小球高滤过可能导致增加近端肾小管钠重吸收的肥胖。
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.