Paul Binu M, Consugar Mark B, Ryan Lee Moonnoh, Sundsbak Jamie L, Heyer Christina M, Rossetti Sandro, Kubly Vickie J, Hopp Katharina, Torres Vicente E, Coto Eliecer, Clementi Maurizio, Bogdanova Nadja, de Almeida Edgar, Bichet Daniel G, Harris Peter C
Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.
Kidney Int. 2014 Feb;85(2):383-92. doi: 10.1038/ki.2013.227. Epub 2013 Jun 12.
Mutations to PKD1 and PKD2 are associated with autosomal dominant polycystic kidney disease (ADPKD). The absence of apparent PKD1/PKD2 linkage in five published European or North American families with ADPKD suggested a third locus, designated PKD3. Here we re-evaluated these families by updating clinical information, re-sampling where possible, and mutation screening for PKD1/PKD2. In the French-Canadian family, we identified PKD1: p.D3782_V3783insD, with misdiagnoses in two individuals and sample contamination explaining the lack of linkage. In the Portuguese family, PKD1: p.G3818A segregated with the disease in 10 individuals in three generations with likely misdiagnosis in one individual, sample contamination, and use of distant microsatellite markers explaining the linkage discrepancy. The mutation PKD2: c.213delC was found in the Bulgarian family, with linkage failure attributed to false positive diagnoses in two individuals. An affected son, but not the mother, in the Italian family had the nonsense mutation PKD1: p.R4228X, which appeared de novo in the son, with simple cysts probably explaining the mother's phenotype. No likely mutation was found in the Spanish family, but the phenotype was atypical with kidney atrophy in one case. Thus, re-analysis does not support the existence of a PKD3 in ADPKD. False positive diagnoses by ultrasound in all resolved families shows the value of mutation screening, but not linkage, to understand families with discrepant data.
PKD1和PKD2的突变与常染色体显性多囊肾病(ADPKD)相关。在已发表的五个欧洲或北美ADPKD家族中,未发现明显的PKD1/PKD2连锁关系,这表明存在第三个基因座,命名为PKD3。在此,我们通过更新临床信息、尽可能重新采样以及对PKD1/PKD2进行突变筛查,对这些家族进行了重新评估。在法裔加拿大家族中,我们鉴定出PKD1:p.D3782_V3783insD,两名个体存在误诊,样本污染解释了连锁关系缺失的原因。在葡萄牙家族中,PKD1:p.G3818A在三代中的10名个体中与疾病共分离,一名个体可能存在误诊、样本污染以及使用了距离较远的微卫星标记解释了连锁差异。在保加利亚家族中发现了PKD2:c.213delC突变,连锁失败归因于两名个体的假阳性诊断。意大利家族中,一名患病儿子而非母亲携带无义突变PKD1:p.R4228X,该突变可能是儿子新发的,单纯囊肿可能解释了母亲的表型。在西班牙家族中未发现可能的突变,但该家族的表型不典型,有一例出现肾萎缩。因此,重新分析不支持ADPKD中存在PKD3。在所有已解决的家族中,超声检查出现的假阳性诊断表明,突变筛查对于理解数据存在差异的家族具有价值,但连锁分析则不然。