Coto E, Sanz de Castro S, Aguado S, Alvarez J, Arias M, Menéndez M J, López-Larrea C
Laboratorio de Genética Molecular, Hospital Central de Asturias, Oviedo, Spain.
J Med Genet. 1995 Jun;32(6):442-5. doi: 10.1136/jmg.32.6.442.
We studied 17 large families affected by adult dominant polycystic kidney disease (ADPKD). Ultrasonographic analysis was performed on all the family members. DNA microsatellite markers closely linked to PKD1 on 16p13.3 were analysed, and linkage of the disease to this locus was determined. Families showing a negative linkage value were evaluated for linkage to the PKD2 locus on 4q. Five of the 17 families showed negative linkage for the 16p13.3 markers. In these families significant linkage to 4q was obtained. Renal cysts developed at an earlier age in PKD1 mutation carriers, and end stage renal failure occurred at an older age in people affected with PKD2. Analysis of large families with ADPKD in a Spanish population indicates that this is a genetically heterogeneous disorder, but mutations at only two loci are responsible for the development of the disease in most if not all the families. Clinicopathological differences between both forms of the disease occur, with subjects with ADPKD2 having a better prognosis than those with mutations at PKD1.
我们研究了17个受成人显性多囊肾病(ADPKD)影响的大家族。对所有家庭成员进行了超声分析。分析了与16p13.3上的PKD1紧密连锁的DNA微卫星标记,并确定了该疾病与该位点的连锁关系。对显示负连锁值的家族评估其与4q上PKD2位点的连锁关系。17个家族中有5个对16p13.3标记显示负连锁。在这些家族中,获得了与4q的显著连锁。PKD1突变携带者的肾囊肿在较早年龄出现,而PKD2患者的终末期肾衰竭在较晚年龄发生。对西班牙人群中患有ADPKD的大家族的分析表明,这是一种基因异质性疾病,但在大多数(如果不是全部)家族中,只有两个位点的突变导致了该疾病的发生。两种形式的疾病存在临床病理差异,ADPKD2患者的预后比PKD1突变患者更好。