Sanders E, Davies M, Coles G A
Ren Physiol. 1980;3(1-6):355-9.
Lysosomal proteinase activity was assayed in urines from 157 patients with renal disease. 16 were found to be excreting acid and neutral proteinases. 15 of these 16 had a severe proliferative glomerulonephritis with polymorphonuclear leucocyte (PMN) infiltration of the glomeruli. These same 16 patients excreted excess quantities of glomerular basement membrane (GBM) antigen. Only urines with neutral proteinase activity were capable of degrading GBM in vitro. Clinical recovery was accompanied by disappearance of both proteinases and excess GBM fragments from the urine. Detailed studies on one patient showed that the neutral proteinase activity was, at least in part, due to PMN lysosomal elastase. Calculation shows that in these patients enough PMN neutral proteinase was present in the glomeruli to cause significant GBM damage.
对157例肾病患者的尿液进行了溶酶体蛋白酶活性检测。发现16例患者排泄酸性和中性蛋白酶。这16例患者中有15例患有严重的增殖性肾小球肾炎,肾小球有多形核白细胞(PMN)浸润。同样这16例患者排泄过量的肾小球基底膜(GBM)抗原。只有具有中性蛋白酶活性的尿液在体外能够降解GBM。临床康复伴随着尿液中蛋白酶和过量GBM片段的消失。对一名患者的详细研究表明,中性蛋白酶活性至少部分归因于PMN溶酶体弹性蛋白酶。计算表明,在这些患者的肾小球中存在足够的PMN中性蛋白酶,足以造成显著的GBM损伤。