Department of Nephrology, Hemodialysis and Renal Transplantation, University Hospital, Brest, France; Univ Brest, F-29200 Brest, France; National Institute for Research in Health Science (INSERM) UMR 1078, "Genetics, Genomics and Biotechnologies," Brest, France.
National Institute for Research in Health Science (INSERM) UMR 1078, "Genetics, Genomics and Biotechnologies," Brest, France; Department of Molecular Genetics, University Hospital, Brest, France.
Kidney Int. 2020 Aug;98(2):476-487. doi: 10.1016/j.kint.2020.02.022. Epub 2020 Mar 23.
Monoallelic mutations of DNAJB11 were recently described in seven pedigrees with atypical clinical presentations of autosomal dominant polycystic kidney disease. DNAJB11 encodes one of the main cofactors of the endoplasmic reticulum chaperon BiP, a heat-shock protein required for efficient protein folding and trafficking. Here we conducted an international collaborative study to better characterize the DNAJB11-associated phenotype. Thirteen different loss-of-function variants were identified in 20 new pedigrees (54 affected individuals) by targeted next-generation sequencing, whole-exome sequencing or whole-genome sequencing. Amongst the 77 patients (27 pedigrees) now in total reported, 32 reached end stage kidney disease (range, 55-89 years, median age 75); without a significant difference between males and females. While a majority of patients presented with non-enlarged polycystic kidneys, renal cysts were inconsistently identified in patients under age 45. Vascular phenotypes, including intracranial aneurysms, dilatation of the thoracic aorta and dissection of a carotid artery were present in four pedigrees. We accessed Genomics England 100,000 genomes project data, and identified pathogenic variants of DNAJB11 in nine of 3934 probands with various kidney and urinary tract disorders. The clinical diagnosis was cystic kidney disease for eight probands and nephrocalcinosis for one proband. No additional pathogenic variants likely explaining the kidney disease were identified. Using the publicly available GnomAD database, DNAJB11 genetic prevalence was calculated at 0.85/10.000 individuals. Thus, establishing a precise diagnosis in atypical cystic or interstitial kidney disease is crucial, with important implications in terms of follow-up, genetic counseling, prognostic evaluation, therapeutic management, and for selection of living kidney donors.
DNAJB11 的单等位基因突变最近在七个常染色体显性遗传多囊肾病的非典型临床表型的家系中被描述。DNAJB11 编码内质网伴侣 BiP 的主要辅助因子之一,BiP 是一种热休克蛋白,对于有效的蛋白质折叠和运输是必需的。在这里,我们进行了一项国际合作研究,以更好地描述 DNAJB11 相关表型。通过靶向下一代测序、全外显子组测序或全基因组测序,在 20 个新的家系(54 个受累个体)中鉴定出 13 种不同的功能丧失变体。在总共报告的 77 名患者(27 个家系)中,32 名患者达到终末期肾病(范围为 55-89 岁,中位年龄为 75 岁);男性和女性之间没有显著差异。虽然大多数患者表现为非增大性多囊肾病,但在 45 岁以下的患者中,肾脏囊肿不一致地被发现。在四个家系中存在血管表型,包括颅内动脉瘤、胸主动脉扩张和颈动脉夹层。我们访问了英国基因组学 10 万基因组计划的数据,并在 3934 名有各种肾脏和泌尿道疾病的先证者中鉴定出 DNAJB11 的致病性变体。其中 8 名先证者的临床诊断为囊性肾病,1 名先证者的诊断为肾钙质沉着症。未发现其他可能解释肾脏疾病的致病性变体。使用公开可用的 GnomAD 数据库,计算出 DNAJB11 的遗传患病率为 0.85/10000 人。因此,在非典型囊性或间质性肾病中做出精确诊断至关重要,这对随访、遗传咨询、预后评估、治疗管理以及选择活体肾脏供体具有重要意义。