Complement-independent nephrotoxic nephritis in the guinea pig.
Complement-independent nephrotoxic nephritis in the guinea pig.
复制标题
豚鼠补体非依赖性肾毒性肾炎。
DOI：
10.1038/ki.1977.25
复制
发表时间：
1977
影响因子：
19.6
通讯作者：
N. Jermanovich
中科院分区：
文献类型：
--
作者：
W. Couser;M. Stilmant;N. Jermanovich
用抗豚鼠肾小球基底膜（GBM）羊抗血清（NTS）注射豚鼠，研究蛋白尿的免疫学机制。绵羊γ 1和γ 2 IgG的线性沉积导致白蛋白排泄迅速但短暂（36 h）增加，从对照值0.026 +/- 0.013 mg/h增加至6 h时的最大值26+/-12.1 mg/rh，除肾小球多阴离子和上皮细胞足突融合染色减少外，未检测到组织学或电子显微镜变化。GBM对阴离子铁蛋白的渗透性在蛋白尿期间没有增加。抗GBM抗体沉积物在体内或体外均不固定GP C3或C4。NTS诱导的蛋白尿在正常豚鼠中是相同的，C3至C9消耗大于95%，C4遗传缺陷，循环多形核白细胞（PMN）消耗。先前服用抗组胺药、类固醇、硫唑嘌呤、秋水仙碱、消炎痛、肝素、抑肽酶（特雷西洛）和硝达唑也未能减少蛋白尿。最初的蛋白尿消退36小时，没有复发，尽管线性沉积的GP芽1和芽2后7天，抗体GMB结合的羊球蛋白。在GP肾毒性肾炎模型中，抗GBM抗体沉积物显然通过目前尚不明确的机制介导对白蛋白的渗透性增加，该机制独立于补体、PMN和其他已知的炎症介质。
Immunologic mechanisms of proteinuria were investigated in guinea pigs (GP) injected with sheep antiserum (NTS) to GP glomerular basement membrane (GBM). Linear deposition of sheep gamma 1 and gamma 2 IgG led to a prompt but transient (36 hr) increase in albumin excretion from control values of 0.026 +/- 0.013 mg/hr to maximal values of 26+/-12.1 mg/rh at six hours without detectable histologic or electron microscopic changes except for decreased staining for glomerular polyanion and epithelial cell foot process fusion. GBM permeability to anionic ferritin was not increased during proteinuria. Anti-GBM antibody deposits did not fix GP C3 or C4 in vivo or in vitro. NTS-induced proteinuria was the same in guinea pigs that were normal, greater than 95% depleted of C3 through C9, genetically deficient in C4, and depleted of circulating polymorphonuclear leukocytes (PMN). Prior administration of antihistamines, steroids, azathioprine, colchicine, indomethacin, heparin, aprotinin (Trasylol), and niridazole also failed to reduced proteinuria. Initial proteinuria subsided by 36 hr, did not recur despite linear deposition of GP gemma 1 and gemma 2 after day seven, and antibody to GMB-bound sheep globlin. In the GP nephrotoxic nephritis model, anti-GBM antibody deposits apparently mediate increased permeability to albumin by a currently undefined mechanism which is independent of complement, PMN, and other know mediators of inflammation.