阿尔波特综合征
IV型胶原
肾小球基底膜
病理
基底膜
镜下血尿
突变
遗传连锁
肾小球肾炎
医学
遗传学
生物
基因
肾
内科学
蛋白尿
层粘连蛋白
细胞外基质
作者
Henny H. Lemmink,W Nillesen,Toshio Mochizuki,Cornelis H. Schröder,Han G. Brunner,Bernard A. van Oost,L.A.H. Monnens,H.J.M. Smeets
摘要
Benign familial hematuria (BFH) is characterized by autosomal dominant inheritance, thinning of the glomerular basement membrane (GBM) and normal renal function. It is frequent in patients with persistent microscopic hematuria, but cannot be clinically differentiated from the initial stages of Alport syndrome, a severe GBM disorder which progresses to renal failure. We present here linkage of benign familial hematuria with the COL4A3 and COL4A4 genes at 2q35-37 (Zmax = 3.58 at theta = 0.0). Subsequently, a glycine to glutamic acid substitution was identified in the collagenous region of the COL4A4 gene. We conclude that type IV collagen defects cause both benign hematuria and Alport syndrome. Furthermore, our data suggest that BFH patients can be carriers of autosomal recessive Alport syndrome.
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