Interstitial inflammation, sodium retention, and the pathogenesis of nephrotic edema: a unifying hypothesis.
Interstitial inflammation, sodium retention, and the pathogenesis of nephrotic edema: a unifying hypothesis.
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DOI：
10.1111/j.1523-1755.2002.kid561.x
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发表时间：
2002-10
影响因子：
19.6
通讯作者：
B. Rodriguez-Iturbe;J. Herrera-Acosta;Richard J. Johnson
中科院分区：
文献类型：
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作者：
B. Rodriguez-Iturbe;J. Herrera-Acosta;Richard J. Johnson
背景肾病综合征水肿的病理生理学是有争议的。一些研究者认为，钠潴留可能是由于原发性肾功能不全导致血容量“过度充盈”。相反，其他作者认为，由于低血压，液体逸出血管室，钠潴留是对“充盈不足”血容量的代偿性生理反应。最符合“未满”假说的患者是患有微小病变型肾病综合征（MCNS）的儿童。方法：根据最近的证据表明炎症浸润可能在原发性肾钠潴留中发挥作用，我们批判性地分析了支持和反对每种致病机制的现有证据。结果肾脏炎性浸润是肾病综合征与原发性钠潴留相关的一个恒定特征，在大多数儿童MCNS病例中不存在。结论我们认为，肾病综合征中原发性钠潴留取决于肾脏炎性浸润的存在和强度，在大多数儿童MCNS病例中明显不存在，在其他与大量蛋白尿相关的疾病中存在。肾小管间质炎性浸润与导致肾小管钠重吸收增加的血管收缩介质增加和降低滤过钠负荷的肾小球血流动力学变化相关。
BACKGROUND The pathophysiology of edema in the nephrotic syndrome is controversial. Some investigators believe that sodium retention may result from a primary renal defect that causes an "overfilled" blood volume. In contrast, other authors believe that fluid escapes the vascular compartment due a low oncotic pressure, and sodium retention is a compensatory physiological response to an "underfilled" blood volume. The patients that best fit the "underfilled" hypothesis are children with minimal-change nephrotic syndrome (MCNS). METHODS We analyzed critically the available evidence for and against each proposed pathogenic mechanism in the light of recent evidence indicating that the inflammatory infiltrate may play a role in primary renal sodium retention. RESULTS Inflammatory infiltrate in the kidney is a constant characteristic in nephrotic syndrome associated with primary sodium retention and it is absent in most cases of MCNS in children CONCLUSIONS We propose that primary sodium retention in the nephrotic syndrome depends on the existence and the intensity of renal inflammatory infiltrate, conspicuously absent in most cases of MCNS in children and present in other conditions associated with massive proteinuria. The tubulointerstitial inflammatory infiltrate is associated with increased vasoconstrictive mediators that result in increased tubular sodium reabsorption and with glomerular hemodynamic changes that reduce filtered sodium load.