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肾脏疾病患儿肾小球基底膜相关肽的尿排泄情况。

Urinary excretion of glomerular basement membrane-related peptides in children with renal disorders.

作者信息

Wingen A M, Schärer K, Rauterberg E W

机构信息

Institute of Immunology, University of Heidelberg, Federal Republic of Germany.

出版信息

Pediatr Nephrol. 1987 Jul;1(3):428-35. doi: 10.1007/BF00849249.

Abstract

Urinary excretion of glomerular basement membrane (GBM)-related peptides was analysed in 72 patients with a variety of renal diseases by immunoblotting using polyclonal antibodies against either collagenase or pepsin digests of human GBM. The specificity of the antibodies was verified by elution of antibodies bound to urinary GBM-related peptides on nitrocellulose blots and demonstration of reactivity of the eluted antibodies with the respective GBM digests. Furthermore, six mice immunized with urinary GBM-related peptides all developed focal linear deposits of mouse IgG along their GBM, linear and mesangial deposits of C3 in the glomeruli and serum antibodies reactive with human GBM. Monoclonal antibodies against urinary GBM-related peptides of one of the mice reacted with different peptides of the non-collagenous and collagenous domains of type IV collagen, the major structural protein of GBM. In the majority of the 75 patients' urines tested, excretion of GBM-related peptides with molecular weights of 33, 50, 80 and 150 kilodaltons (kD) was detectable. Patients with a diminished glomerular filtration rate (GFR) demonstrated excretion of the 33 kD peptide more frequently (91%) and never of the 80 kD peptide as compared with patients with normal GFR (33 kD [42%] 80 kD [87%]). The pattern of urinary GBM-related peptides was not specific for the underlying renal disease as in Alport's syndrome.

摘要

通过使用针对人肾小球基底膜(GBM)胶原酶或胃蛋白酶消化产物的多克隆抗体进行免疫印迹分析,对72例患有各种肾脏疾病的患者尿中GBM相关肽的排泄情况进行了研究。通过洗脱与硝酸纤维素印迹上尿GBM相关肽结合的抗体,并证明洗脱抗体与相应GBM消化产物的反应性,验证了抗体的特异性。此外,用尿GBM相关肽免疫的6只小鼠均在其GBM上出现了小鼠IgG的局灶性线性沉积、肾小球中C3的线性和系膜沉积以及与人GBM反应的血清抗体。针对其中一只小鼠尿GBM相关肽的单克隆抗体与IV型胶原(GBM的主要结构蛋白)非胶原和胶原结构域的不同肽发生反应。在测试的75例患者的大多数尿液中,可检测到分子量为33、50、80和150千道尔顿(kD)的GBM相关肽的排泄。与肾小球滤过率(GFR)正常的患者相比,肾小球滤过率降低(GFR)的患者更频繁地排泄33 kD肽(91%),且从未排泄80 kD肽(33 kD [42%],80 kD [87%])。尿GBM相关肽的模式不像在Alport综合征中那样对潜在的肾脏疾病具有特异性。

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