Knoers N, van den Ouweland A, Dreesen J, Verdijk M, Monnens L A, van Oost B A
Department of Human Genetics, University of Nijmegen, The Netherlands.
Pediatr Nephrol. 1993 Oct;7(5):685-8. doi: 10.1007/BF00852579.
Congenital nephrogenic diabetes insipidus (NDI) is an X-linked inherited disorder characterized by renal resistance to the antidiuretic hormonal action of arginine vasopressin. The disease gene has been assigned to the subtelomeric region of the X chromosome long arm by demonstrating close linkage between NDI and several X-chromosomal DNA markers. The finding of closely linked genetic markers is useful in the diagnosis of NDI. Receptor studies in patients have indicated that NDI might be due to the absence or an abnormality of the adenylate cyclase-bound vasopressin type 2 receptor. This assumption was supported by the discovery of functional vasopressin V2 receptor activity in somatic cell hybrid cell lines that carried at least the distal part of the human X chromosome long arm. Definite evidence for a V2 receptor defect being the cause of NDI was found in a recent study demonstrating point mutations in the V2 receptor gene from affected individuals. Direct mutation analysis is now applicable for accurate carrier detection and early (prenatal) diagnosis.
先天性肾性尿崩症(NDI)是一种X连锁遗传性疾病,其特征为肾脏对精氨酸加压素的抗利尿激素作用产生抵抗。通过证明NDI与几种X染色体DNA标记物之间存在紧密连锁,该疾病基因已被定位到X染色体长臂的亚端粒区域。紧密连锁的遗传标记物的发现有助于NDI的诊断。对患者的受体研究表明,NDI可能是由于与腺苷酸环化酶结合的血管加压素2型受体缺失或异常所致。在携带人类X染色体长臂至少远端部分的体细胞杂交细胞系中发现功能性血管加压素V2受体活性,支持了这一假设。最近一项研究在受影响个体的V2受体基因中发现了点突变,从而找到了V2受体缺陷是NDI病因的确切证据。直接突变分析现在可用于准确的携带者检测和早期(产前)诊断。