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晚期失代偿性肝硬化患者常发生“少尿性肾衰”。其诱因除少尿引起外,并与高氮素血症,稀释性低Na~+血症及低比重尿Na~+排泄等有关,肾组织学检查几乎无特征性变化。目前将此种病变称之“肝肾综合征”但作者认为该名称并不确切。本病发病机理是肾皮质血流减少引起功能性肾功能不全。作者对149例肝硬化患者(代偿性67例,失代偿性82例)进行研究。结果:(1)尿液检查:凡蛋白尿在(±以上为阳性。66例代偿性患者中10例阳性(15.2%),81例失代偿性患者中17例阳性(21.0%),后者阳性率略高于前者,但无明显差异,血尿在(±)以上为阳性,66例代偿性患者中7例(10.6%),81例失代偿性患者中12例(14.8%)阳性。后者略高于前者。尿沉淀检查,除扁平上皮,透明管型外,红、白细胞,移行上皮,肾小管上皮细胞及颗粒管型等出现程度在(±)以上为阳性,66例代偿性患者中有7例(10.6%),81例
Patients with advanced decompensated cirrhosis often “oliguric renal failure.” In addition to its incentives caused by oliguria, and with hypernatremia, low dilution of Na ~ + blood and urinary excretion of urinary excretion of low specific gravity, renal histological examination almost no characteristic changes. The current lesion is called “hepatorenal syndrome” but the author does not think the name is exact. The pathogenesis of this disease is a decrease in renal cortical blood flow caused by functional renal insufficiency. The authors studied 149 cirrhotic patients (compensated 67 cases, decompensated 82 cases). Results: (1) Urine examination: Proteinuria was positive (±) in 10 cases (15.2%) and 81 cases (81%) in 66 cases of compensated patients, 17 cases were positive (21.0%), The latter positive rate was slightly higher than the former, but no significant difference, hematuria positive (±) above, 66 cases of compensatory patients in 7 cases (10.6%), 81 cases of decompensated patients in 12 cases (14.8% ) .The latter was slightly higher than the former.Purple sedimentation examination, in addition to flat epithelium, transparent tube, red, white blood cells, transitional epithelium, tubular epithelial cells and granularity appear more than (±) positive, 66 Seven cases (10.6%) and 81 cases were compensated patients