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IgA肾病:急性肾衰竭、急性肾小管坏死及感染后急性肾小球肾炎的特征。

IgA nephropathy: acute renal failure, acute tubular necrosis, and features of postinfectious acute glomerulonephritis.

作者信息

Mazzarolo-Cruz H M, Penna D de O, Saldanha L B, Kanashiro E H, Cruz J, Malheiro P S, Marcondes M

机构信息

Nephrology Division, São Paulo University Medical School, Brazil.

出版信息

Ren Fail. 1992;14(4):533-9. doi: 10.3109/08860229209047662.

Abstract

From 1976 to 1987 on our Nephrological Unit, 57 patients with IgA nephropathy (IgAN) proven by renal biopsies were found. Three of those presented with acute tubular necrosis (ATN) and glomerulitis, without extrarenal predisposing cause in two; and showed, as prominent manifestation, a severe acute renal failure syndrome (ARFS), needing dialytic treatment. All three had hematuria, which was macroscopic in two and microscopic in one. Thus the prevalence of the association of glomerulitis and ATN was about 5.2%. There was complete recovery of renal functions in all three patients, but the usual symptomatology of IgAN. Two patients presented polymorphonuclear neutrophils infiltration of glomerular capillaries and in one of them, electron-dense deposits on the epithelial side of glomerular basement membrane ("humps") were observed, as well as those identified in the mesangial area. The glomerular polymorphonuclear neutrophils infiltration and endothelial cells proliferation (cases 1 and 3), the presence of "humps" (case 1), high antistreptolysin O (ASO) titers (cases 1 and 2), and low serum complement levels (case 1), suggest the possibility that antigens able to cause postinfectious glomerulonephritis (streptococcal or not) could induce in some individuals, by another immunopathogenetic route, mixed histopathological and clinical features of IgAN and postinfectious glomerulonephritis.

摘要

1976年至1987年期间,在我们的肾脏病科,发现了57例经肾活检证实的IgA肾病(IgAN)患者。其中3例出现急性肾小管坏死(ATN)和肾小球炎,2例无肾外诱发因素;并表现为严重的急性肾衰竭综合征(ARFS)这一突出表现,需要透析治疗。3例均有血尿,其中2例为肉眼血尿,1例为镜下血尿。因此,肾小球炎与ATN并存的发生率约为5.2%。所有3例患者的肾功能均完全恢复,但具有IgAN的常见症状。2例患者出现肾小球毛细血管多形核中性粒细胞浸润,其中1例在肾小球基底膜上皮侧观察到电子致密沉积物(“驼峰”),系膜区也有此类沉积物。肾小球多形核中性粒细胞浸润和内皮细胞增殖(病例1和3)、“驼峰”的存在(病例1)、抗链球菌溶血素O(ASO)高滴度(病例1和2)以及低血清补体水平(病例1),提示能够引起感染后肾小球肾炎(无论是否由链球菌引起)的抗原可能通过另一种免疫发病机制,在某些个体中诱发IgAN和感染后肾小球肾炎混合的组织病理学和临床特征。

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