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进行性肾衰竭中的血液流变学异常:非免疫性肾小球损伤的一个因素?

Abnormal blood rheology in progressive renal failure: a factor in non-immune glomerular injury?

作者信息

Gordge M P, Faint R W, Rylance P B, Neild G H

机构信息

Department of Renal Medicine, St Philip's Hospital, London, UK.

出版信息

Nephrol Dial Transplant. 1988;3(3):257-62.

PMID:3140097
Abstract

Chronic renal insufficiency progresses by a final common pathway of glomerular damage characterised by microvascular injury and glomerulosclerosis. In order to investigate the possible role of blood rheology in this process, rheological indices were compared between healthy controls and a group of patients with progressive renal failure due to renal diseases that were not considered to be immunologically mediated. Plasma viscosity was significantly increased in the renal insufficiency group (P less than 0.005), and correlated with raised plasma concentrations of fibrinogen (r = 0.63; P less than 0.005). Whole-blood viscosity corrected to a standard haematocrit of 0.45 was also raised. A weak but significant correlation was seen between plasma viscosity and 24-h urinary protein excretion (r = 0.50; P less than 0.005). Our data show that in chronic renal insufficiency, rheology is abnormal. Proteinuria correlates with plasma viscosity, which is consistent with the hypothesis that raised plasma viscosity leads to an increase in glomerular capillary pressure and thence glomerular permeability. Correction of rheological abnormalities might help to preserve kidney function and reduce proteinuria in these patients.

摘要

慢性肾功能不全通过以微血管损伤和肾小球硬化为特征的肾小球损伤这一最终共同途径进展。为了研究血液流变学在此过程中的可能作用,对健康对照者和一组因非免疫介导性肾脏疾病导致进行性肾衰竭的患者的流变学指标进行了比较。肾功能不全组的血浆粘度显著升高(P<0.005),且与纤维蛋白原血浆浓度升高相关(r = 0.63;P<0.005)。校正至标准血细胞比容0.45的全血粘度也升高。血浆粘度与24小时尿蛋白排泄之间存在微弱但显著的相关性(r = 0.50;P<0.005)。我们的数据表明,在慢性肾功能不全中,血液流变学异常。蛋白尿与血浆粘度相关,这与血浆粘度升高导致肾小球毛细血管压力增加进而导致肾小球通透性增加的假设一致。纠正流变学异常可能有助于保护这些患者的肾功能并减少蛋白尿。

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