Institute of Human Genetics, Klinikum rechts der Isar, Technical University of Munich, School of Medicine, Munich, Germany.
Department of Nephrology, Klinikum rechts der Isar, Technical University of Munich, School of Medicine, Munich, Germany.
Eur J Hum Genet. 2023 Jun;31(6):674-680. doi: 10.1038/s41431-023-01331-x. Epub 2023 Mar 16.
Individuals with congenital anomalies of the kidney and urinary tract (CAKUT) show a broad spectrum of malformations. CAKUT can occur in an isolated fashion or as part of a syndromic disorder and can lead to end-stage kidney failure. A monogenic cause can be identified in ~12% of affected individuals. This study investigated a single-center CAKUT cohort analyzed by exome sequencing (ES). Emphasis was placed on the question whether diagnostic yield differs between certain CAKUT phenotypes (e.g., bilateral kidney affection, unilateral kidney affection or only urinary tract affection). 86 unrelated individuals with CAKUT were categorized according to their phenotype and analyzed by ES to identify a monogenic cause. Prioritized variants were rated according to the recommendations of the American College of Medical Genetics and Genomics and the Association for Clinical Genomic Science. Diagnostic yields of different phenotypic categories were compared. Clinical data were collected using a standardized questionnaire. In the study cohort, 7/86 individuals had a (likely) pathogenic variant in the genes PAX2, PBX1, EYA1, or SALL1. Additionally, in one individual, a 17q12 deletion syndrome (including HNF1B) was detected. 64 individuals had a kidney affection, which was bilateral in 36. All solved cases (8/86, 9%) had bilateral kidney affection (diagnostic yield in subcohort: 8/36, 22%). Although the diagnostic yield in CAKUT cohorts is low, our single-center experience argues, that, in individuals with bilateral kidney affection, monogenic burden is higher than in those with unilateral kidney or only urinary tract affection.
患有先天性肾和尿路异常(CAKUT)的个体表现出广泛的畸形。CAKUT 可以孤立发生,也可以作为综合征疾病的一部分,并且可能导致终末期肾衰竭。约 12%的受影响个体可确定为单基因病因。本研究通过外显子组测序(ES)调查了一个单中心 CAKUT 队列。重点是确定特定 CAKUT 表型(例如双侧肾脏受累、单侧肾脏受累或仅尿路受累)之间的诊断效果是否存在差异。根据其表型将 86 名无亲缘关系的 CAKUT 个体进行分类,并通过 ES 进行分析以确定单基因病因。根据美国医学遗传学和基因组学学院以及临床基因组科学协会的建议,对优先变体进行了评分。比较了不同表型类别的诊断效果。使用标准化问卷收集临床数据。在研究队列中,7/86 名个体在 PAX2、PBX1、EYA1 或 SALL1 基因中具有(可能)致病性变异。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。86 名个体中有 7 名患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。86 名个体中有 7 名患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。7 名个体患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。86 名个体中有 7 名患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。7 名个体患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。7 名个体患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。7 名个体患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。7 名个体患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。7 名个体患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。此外,在一名个体中,检测到 17q12 缺失综合征(包括 HNF1B)。7 名个体患有(可能)致病变体,其中包括 PAX2、PBX1、EYA1 或 SALL1。
在 CAKUT 队列中,诊断效果较低,但我们的单中心经验表明,在双侧肾脏受累的个体中,单基因负担高于单侧肾脏或仅尿路受累的个体。