Devriendt K, Matthijs G, Van Damme B, Van Caesbroeck D, Eccles M, Vanrenterghem Y, Fryns J P, Leys A
Center for Human Genetics, University of Leuven, Belgium.
Hum Genet. 1998 Aug;103(2):149-53. doi: 10.1007/s004390050798.
We present a family with autosomal-dominant inheritance of renal insufficiency caused by renal hypoplasia in six individuals. In all affected individuals, signs of optic disk dysplasia were detected, but most patients were asymptomatic. A heterozygous missense mutation in the PAX2 gene causing a Gly75 to Ser substitution was present in all affected individuals. A second, unrelated patient presented with ocular complaints related to optic disk dysplasia, and had a history of vesico-ureteral reflux. A heterozygous hexanucleotide duplication in the PAX2 gene was detected leading to the duplication of GluThr at positions 74 and 75. The mutations in these two families are the first mutations in the PAX2 gene that do not lead to a truncated protein. Mechanistically, these mutations are expected to result in abnormal folding of the PAX2 protein. These observations further expand the spectrum of clinical features associated with PAX2 mutations, and suggest that a distinct genetic disorder can be identified in patients with renal dysplasia through a careful eye examination. As the ocular manifestations in this syndrome are variable anomalies of retinal and optic disk dysplasia, we prefer the term "papillo-renal syndrome".
我们报告了一个家族,其中6名个体因肾发育不全而呈常染色体显性遗传的肾功能不全。在所有受影响的个体中,均检测到视盘发育异常的体征,但大多数患者无症状。所有受影响个体中均存在PAX2基因的杂合错义突变,导致甘氨酸75被丝氨酸取代。另一名无亲缘关系的患者出现与视盘发育异常相关的眼部症状,并有膀胱输尿管反流病史。检测到PAX2基因的杂合六核苷酸重复,导致第74和75位的谷氨酸-苏氨酸重复。这两个家族中的突变是PAX2基因中首次出现的不会导致截短蛋白的突变。从机制上讲,这些突变预计会导致PAX2蛋白异常折叠。这些观察结果进一步扩大了与PAX2突变相关的临床特征谱,并表明通过仔细的眼部检查,可以在肾发育异常的患者中识别出一种独特的遗传疾病。由于该综合征的眼部表现是视网膜和视盘发育异常的可变异常,我们更喜欢“乳头-肾综合征”这个术语。