Literature DB >> 32631624

Clinical spectrum, prognosis and estimated prevalence of DNAJB11-kidney disease.

Vinh T Huynh1, Marie-Pierre Audrézet2, John A Sayer3, Albert C Ong4, Siriane Lefevre1, Valoris Le Brun5, Aurore Després5, Sarah R Senum6, Fouad T Chebib6, Miguel Barroso-Gil3, Chirag Patel7, Andrew J Mallett8, Himanshu Goel9, Amali C Mallawaarachchi10, Albertien M Van Eerde11, Eléonore Ponlot12, Marc Kribs13, Yannick Le Meur14, Peter C Harris6, Emilie Cornec-Le Gall15.   

Abstract

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.
Copyright © 2020 International Society of Nephrology. All rights reserved.

Entities:  

Keywords:  DNAJB11; chronic kidney disease; genetics; polycystic kidney disease; prognosis

Mesh:

Substances:

Year:  2020        PMID: 32631624     DOI: 10.1016/j.kint.2020.02.022

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  8 in total

1.  Monoallelic pathogenic ALG5 variants cause atypical polycystic kidney disease and interstitial fibrosis.

Authors:  Hugo Lemoine; Loann Raud; François Foulquier; John A Sayer; Baptiste Lambert; Eric Olinger; Siriane Lefèvre; Bertrand Knebelmann; Peter C Harris; Pascal Trouvé; Aurore Desprès; Gabrielle Duneau; Marie Matignon; Anais Poyet; Noémie Jourde-Chiche; Dominique Guerrot; Sandrine Lemoine; Guillaume Seret; Miguel Barroso-Gil; Coralie Bingham; Rodney Gilbert; Yannick Le Meur; Marie-Pierre Audrézet; Emilie Cornec-Le Gall
Journal:  Am J Hum Genet       Date:  2022-07-26       Impact factor: 11.043

Review 2.  Genetics, pathobiology and therapeutic opportunities of polycystic liver disease.

Authors:  Paula Olaizola; Pedro M Rodrigues; Francisco J Caballero-Camino; Laura Izquierdo-Sanchez; Patricia Aspichueta; Luis Bujanda; Nicholas F Larusso; Joost P H Drenth; Maria J Perugorria; Jesus M Banales
Journal:  Nat Rev Gastroenterol Hepatol       Date:  2022-05-13       Impact factor: 73.082

3.  Monoallelic IFT140 pathogenic variants are an important cause of the autosomal dominant polycystic kidney-spectrum phenotype.

Authors:  Sarah R Senum; Ying Sabrina M Li; Katherine A Benson; Giancarlo Joli; Eric Olinger; Sravanthi Lavu; Charles D Madsen; Adriana V Gregory; Ruxandra Neatu; Timothy L Kline; Marie-Pierre Audrézet; Patricia Outeda; Cherie B Nau; Esther Meijer; Hamad Ali; Theodore I Steinman; Michal Mrug; Paul J Phelan; Terry J Watnick; Dorien J M Peters; Albert C M Ong; Peter J Conlon; Ronald D Perrone; Emilie Cornec-Le Gall; Marie C Hogan; Vicente E Torres; John A Sayer; Peter C Harris
Journal:  Am J Hum Genet       Date:  2021-12-09       Impact factor: 11.043

4.  Epidemiology of autosomal-dominant polycystic liver disease in Olmsted county.

Authors:  Tatsuya Suwabe; Alanna M Chamberlain; Jill M Killian; Bernard F King; Adriana V Gregory; Charles D Madsen; Xiaofang Wang; Timothy L Kline; Fouad T Chebib; Marie C Hogan; Patrick S Kamath; Peter C Harris; Vicente E Torres
Journal:  JHEP Rep       Date:  2020-08-04

5.  More dissimilarities than affinities between DNAJB11-PKD and ADPKD.

Authors:  Isabella Pisani; Marco Allinovi; Viviana Palazzo; Paola Zanelli; Micaela Gentile; Maria Teresa Farina; Sara Giuliotti; Paolo Cravedi; Marco Delsante; Umberto Maggiore; Enrico Fiaccadori; Lucio Manenti
Journal:  Clin Kidney J       Date:  2022-01-31

6.  Biallelic Mutations in DNAJB11 are Associated with Prenatal Polycystic Kidney Disease in a Turkish Family.

Authors:  Esra Arslan Ateş; Ayberk Turkyilmaz; Kenan Delil; Ceren Alavanda; Mehmet Ali Söylemez; Bilgen Bilge Geçkinli; Pinar Ata; Ahmet Arman
Journal:  Mol Syndromol       Date:  2021-04-01

Review 7.  The Evolving Role of Diagnostic Genomics in Kidney Transplantation.

Authors:  Jacqueline Soraru; Aron Chakera; Nikky Isbel; Amali Mallawaarachichi; Natasha Rogers; Peter Trnka; Chirag Patel; Andrew J Mallett
Journal:  Kidney Int Rep       Date:  2022-05-25

8.  Exosomal DNAJB11 promotes the development of pancreatic cancer by modulating the EGFR/MAPK pathway.

Authors:  Xiaoli Yin; Xiaodong Tan; Peng Liu; Fuqiang Zu; Hui Chen
Journal:  Cell Mol Biol Lett       Date:  2022-10-08       Impact factor: 8.702

  8 in total

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