Glasser R J, Michael A F
Lab Invest. 1976 Jun;34(6):616-22.
Urinary kallikrein excretion was studied in two types of experimentally induced renal disease: anti-glomerular basement membrane nephritis (20 rats) and aminonucleoside nephrosis (five rats) with appropriate controls (23 rats) for a period of 6 to 9 weeks following disease induction. In both models there was a prompt significant decrease (p less than 0.01 - 0.001) in urinary kallikrein excretion associated with proteinuria but unrelated to urinary sodium and potassium excretion and urinary volumes. In antiglomerular basement membrane nephritis the fall in kallikrein excretion occurred within the first 24 hours concurrent with the onset of proteinuria. In aminonucleoside nephrosis the decrease antedated the onset of proteinuria by 48 hours beginning within the first 24 hours following injection of the aminonucleoside. Kallikrein inhibitors were not demonstrable in the urines of diseased animals from either model. The mechanism of the decrease in kallikrein excretion in immune and nonimmune glomerular disease associated with proteinuria is unknown.
抗肾小球基底膜肾炎（20只大鼠）和氨基核苷肾病（5只大鼠），并设置了适当的对照组（23只大鼠），在疾病诱发后的6至9周内进行观察。在两种模型中，尿激肽释放酶排泄均迅速显著下降（p小于0.01 - 0.001），这与蛋白尿有关，但与尿钠、钾排泄及尿量无关。在抗肾小球基底膜肾炎中，激肽释放酶排泄的下降在最初24小时内与蛋白尿的出现同时发生。在氨基核苷肾病中，下降在注射氨基核苷后的最初24小时内开始，比蛋白尿的出现提前48小时。在两种模型患病动物的尿液中均未检测到激肽释放酶抑制剂。与蛋白尿相关的免疫性和非免疫性肾小球疾病中激肽释放酶排泄减少的机制尚不清楚。
