Literature DB >> 27708066

Long-term renal outcome in children with OCRL mutations: retrospective analysis of a large international cohort.

Marcin Zaniew1,2, Arend Bökenkamp3, Marcin Kolbuc1, Claudio La Scola4, Federico Baronio5, Anna Niemirska6, Maria Szczepanska7, Julia Bürger8, Angela La Manna9, Monika Miklaszewska10, Anna Rogowska-Kalisz11, Jutta Gellermann12, Argyroula Zampetoglou13, Anna Wasilewska14, Magdalena Roszak15, Jerzy Moczko15, Aleksandra Krzemien16, Dariusz Runowski6, Grzegorz Siten17, Iga Zaluska-Lesniewska18, Patrizia Fonduli19, Franca Zurrida19, Fabio Paglialonga20, Zoran Gucev21, Dusan Paripovic22, Rina Rus23, Valerie Said-Conti24, Lisa Sartz25, Woo Yeong Chung26, Se Jin Park27, Jung Won Lee28, Yong Hoon Park29, Yo Han Ahn30, Przemyslaw Sikora2,31, Constantinos J Stefanidis13, Velibor Tasic21, Martin Konrad8, Franca Anglani32, Maria Addis33, Hae Il Cheong34, Michael Ludwig35, Detlef Bockenhauer36.   

Abstract

Background: Lowe syndrome (LS) and Dent-2 disease (DD2) are disorders associated with mutations in the OCRL gene and characterized by progressive chronic kidney disease (CKD). Here, we aimed to investigate the long-term renal outcome and identify potential determinants of CKD and its progression in children with these tubulopathies.
Methods: Retrospective analyses were conducted of clinical and genetic data in a cohort of 106 boys (LS: 88 and DD2: 18). For genotype-phenotype analysis, we grouped mutations according to their type and localization. To investigate progression of CKD we used survival analysis by Kaplan-Meier method using stage 3 CKD as the end-point.
Results: Median estimated glomerular filtration rate (eGFR) was lower in the LS group compared with DD2 (58.8 versus 87.4 mL/min/1.73 m2, P < 0.01). CKD stage II-V was found in 82% of patients, of these 58% and 28% had moderate-to-severe CKD in LS and DD2, respectively. Three patients (3%), all with LS, developed stage 5 of CKD. Survival analysis showed that LS was also associated with a faster CKD progression than DD2 (P < 0.01). On multivariate analysis, eGFR was dependent only on age (b = -0.46, P < 0.001). Localization, but not type of mutations, tended to correlate with eGFR. There was also no significant association between presence of nephrocalcinosis, hypercalciuria, proteinuria and number of adverse clinical events and CKD. Conclusions: CKD is commonly found in children with OCRL mutations. CKD progression was strongly related to the underlying diagnosis but did not associate with clinical parameters, such as nephrocalcinosis or proteinuria.
© The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

Entities:  

Keywords:  Dent-2 disease; Lowe syndrome; OCRL; chronic kidney disease; nephrocalcinosis

Mesh:

Substances:

Year:  2018        PMID: 27708066     DOI: 10.1093/ndt/gfw350

Source DB:  PubMed          Journal:  Nephrol Dial Transplant        ISSN: 0931-0509            Impact factor:   5.992


  15 in total

Review 1.  The 5-phosphatase OCRL in Lowe syndrome and Dent disease 2.

Authors:  Maria Antonietta De Matteis; Leopoldo Staiano; Francesco Emma; Olivier Devuyst
Journal:  Nat Rev Nephrol       Date:  2017-07-03       Impact factor: 28.314

Review 2.  Phosphoinositides in the kidney.

Authors:  Leopoldo Staiano; Maria Antonietta De Matteis
Journal:  J Lipid Res       Date:  2018-10-12       Impact factor: 5.922

3.  Dent disease in Poland: what we have learned so far?

Authors:  Marcin Zaniew; Małgorzata Mizerska-Wasiak; Iga Załuska-Leśniewska; Piotr Adamczyk; Katarzyna Kiliś-Pstrusińska; Adam Haliński; Jan Zawadzki; Beata S Lipska-Ziętkiewicz; Krzysztof Pawlaczyk; Przemysław Sikora; Michael Ludwig; Maria Szczepańska
Journal:  Int Urol Nephrol       Date:  2017-08-16       Impact factor: 2.370

4.  Lowe syndrome patient cells display mTOR- and RhoGTPase-dependent phenotypes alleviated by rapamycin and statins.

Authors:  Kayalvizhi Madhivanan; Swetha Ramadesikan; Wen-Chieh Hsieh; Mariana C Aguilar; Claudia B Hanna; Robert L Bacallao; R Claudio Aguilar
Journal:  Hum Mol Genet       Date:  2020-06-27       Impact factor: 6.150

5.  Dent-2 disease with a Bartter-like phenotype caused by the Asp631Glu mutation in the OCRL gene.

Authors:  Eleni Drosataki; Sevasti Maragkou; Kleio Dermitzaki; Ioanna Stavrakaki; Dimitra Lygerou; Helen Latsoudis; Christos Pleros; Ioannis Petrakis; Ioannis Zaganas; Kostas Stylianou
Journal:  BMC Nephrol       Date:  2022-05-12       Impact factor: 2.585

6.  Splicing Analysis of Exonic OCRL Mutations Causing Lowe Syndrome or Dent-2 Disease.

Authors:  Lorena Suarez-Artiles; Ana Perdomo-Ramirez; Elena Ramos-Trujillo; Felix Claverie-Martin
Journal:  Genes (Basel)       Date:  2018-01-04       Impact factor: 4.096

7.  A 3D Renal Proximal Tubule on Chip Model Phenocopies Lowe Syndrome and Dent II Disease Tubulopathy.

Authors:  Sindhu Naik; Andrew R Wood; Maté Ongenaert; Paniz Saidiyan; Edo D Elstak; Henriëtte L Lanz; Jan Stallen; Richard Janssen; Elizabeth Smythe; Kai S Erdmann
Journal:  Int J Mol Sci       Date:  2021-05-19       Impact factor: 5.923

8.  Whole-genome sequencing revealed an interstitial deletion encompassing OCRL and SMARCA1 gene in a patient with Lowe syndrome.

Authors:  Bixia Zheng; Qiuxia Chen; Chunli Wang; Wei Zhou; Ying Chen; Guixia Ding; Zhanjun Jia; Aihua Zhang; SongMing Huang
Journal:  Mol Genet Genomic Med       Date:  2019-08-03       Impact factor: 2.183

9.  The phosphoinositide 3-kinase inhibitor alpelisib restores actin organization and improves proximal tubule dysfunction in vitro and in a mouse model of Lowe syndrome and Dent disease.

Authors:  Marine Berquez; Jonathan R Gadsby; Beatrice Paola Festa; Richard Butler; Stephen P Jackson; Valeria Berno; Alessandro Luciani; Olivier Devuyst; Jennifer L Gallop
Journal:  Kidney Int       Date:  2020-09-09       Impact factor: 10.612

Review 10.  Genetics and phenotypic heterogeneity of Dent disease: the dark side of the moon.

Authors:  Lisa Gianesello; Dorella Del Prete; Franca Anglani; Lorenzo A Calò
Journal:  Hum Genet       Date:  2020-08-29       Impact factor: 4.132

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