Finer Gal, Birk Ohad, Landau Daniel
Department of Pediatrics, Soroka University Medical Center, Ben Gurion University of the Negev, Beer Sheva, Israel.
Harefuah. 2004 Jul;143(7):466-70, 552.
Autosomal recessive polycystic kidney disease (ARPKD) is a severe renal disease. Kidneys and liver may be affected clinically but at a varying severity, ranging from a Potter-like syndrome, systemic hypertension and variable renal dysfunction to portal hypertension due to hepatic fibrosis. Most ARPKD cases are caused by mutations in the gene PKHD1. Specific mutations in patients from various ethnic backgrounds have been described, most cases being compound heterozygotes. The genotype-phenotype correlation has not been sufficiently studied.
a) Clinical characterization of ARPKD patients in Southern Israel. b) Establishment of a genetic method for prenatal diagnosis of the disease.
Clinical data of all ARPKD cases diagnosed in our institution was retrospectively analyzed. DNA samples were collected from the patients, parents and siblings. Linkage analysis was used to verify individual genetic status.
Eighteen ARPKD patients from 7 extended Bedouin families were identified (perinatal manifestation = 9; neonatal = 2; infantile = 2; juvenile = 5). The family trees in all cases were highly suggestive of a founder effect, implying that affected individuals were very likely to harbor identical mutations on both ARPKD alleles. Inter- and intra-familial phenotypic variability was found in several families. Linkage analysis using polymorphic markers specific to the chromosome 6p-PKHD1 locus was established in our laboratory and was found to be reliable, thereby assisting in prenatal diagnosis in known ARPKD families.
Phenotypic variability exists in ARPKD, even among families with supposedly homozygous mutations in the PKHD1 gene. We have established a reliable method for prenatal diagnosis of the disease by linkage analysis, thus enabling future diagnosis in families at risk.
常染色体隐性多囊肾病(ARPKD)是一种严重的肾脏疾病。肾脏和肝脏在临床上可能会受到影响,但严重程度各不相同,范围从波特样综合征、系统性高血压和不同程度的肾功能不全到肝纤维化导致的门静脉高压。大多数ARPKD病例是由PKHD1基因突变引起的。已经描述了来自不同种族背景患者的特定突变,大多数病例为复合杂合子。基因型与表型的相关性尚未得到充分研究。
a)对以色列南部ARPKD患者进行临床特征分析。b)建立该疾病的产前诊断遗传方法。
对在我们机构诊断的所有ARPKD病例的临床数据进行回顾性分析。从患者、父母和兄弟姐妹中收集DNA样本。使用连锁分析来验证个体遗传状态。
确定了来自7个大家庭的18例ARPKD患者(围产期表现=9例;新生儿期=2例;婴儿期=2例;青少年期=5例)。所有病例的家族谱系都高度提示存在奠基者效应,这意味着受影响个体很可能在两个ARPKD等位基因上携带相同的突变。在几个家庭中发现了家族间和家族内的表型变异性。我们实验室建立了使用6号染色体p-PKHD1位点特异性多态性标记的连锁分析方法,发现该方法可靠,从而有助于已知ARPKD家族的产前诊断。
ARPKD存在表型变异性,即使在PKHD1基因假定为纯合突变的家族中也是如此。我们通过连锁分析建立了一种可靠的疾病产前诊断方法,从而能够对有风险的家庭进行未来诊断。