Arg913Gln variation of SLC12A3 gene is associated with diabetic nephropathy in type 2 diabetes and Gitelman syndrome: a systematic review

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Abstract

Background

Diabetic nephropathy is a global common cause of chronic kidney disease and end-stage renal disease. A lot of research has been conducted in biomedical sciences, which has enhanced understanding of the pathophysiology of diabetic nephropathy and has expanded the potential available therapies. An increasing number of evidence suggests that genetic alterations play a major role in development and progression of diabetic nephropathy. This systematic review was focused on searching an association between Arg913Gln variation in SLC12A3 gene with diabetic nephropathy in individuals with Type 2 Diabetes and Gitelman Syndrome.

Methods

An extensive systematic review of the literature was completed using PubMed, EBSCO and Cochrane Library, from their inception to January 2018. The PRISMA guidelines were followed and the search strategy ensured that all possible studies were identified to compile the review. Inclusion criteria for this review were: 1) Studies that analyzed the SLC12A3 gene in individuals with Type 2 Diabetes and Gitelman Syndrome. 2) Use of at least one analysis investigating the association between the Arg913Gln variation of SLC12A3 gene with diabetic nephropathy. 3) Use of a case–control or follow-up design. 4) Investigation of type 2 diabetes mellitus in individuals with Gitelman’s syndrome, with a history of diabetic nephropathy.

Results

The included studies comprised 2106 individuals with diabetic nephropathy. This review shows a significant genetic association in most studies in the Arg913Gln variation of SLC12A3 gene with the diabetic nephropathy, pointing out that the mutations of this gene could be a key predictor of end-stage renal disease.

Conclusions

The results showed in this systematic review contribute to better understanding of the association between the Arg913Gln variation of SLC12A3 gene with the pathogenesis of diabetic nephropathy in individuals with T2DM and GS.

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Most cited references 42

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Decline in estimated glomerular filtration rate and subsequent risk of end-stage renal disease and mortality.

Josef Coresh, Tanvir Turin, Kunihiro Matsushita … (2014)

The established chronic kidney disease (CKD) progression end point of end-stage renal disease (ESRD) or a doubling of serum creatinine concentration (corresponding to a change in estimated glomerular filtration rate [GFR] of −57% or greater) is a late event. To characterize the association of decline in estimated GFR with subsequent progression to ESRD with implications for using lesser declines in estimated GFR as potential alternative end points for CKD progression. Because most people with CKD die before reaching ESRD, mortality risk also was investigated. Individual meta-analysis of 1.7 million participants with 12,344 ESRD events and 223,944 deaths from 35 cohorts in the CKD Prognosis Consortium with a repeated measure of serum creatinine concentration over 1 to 3 years and outcome data. Transfer of individual participant data or standardized analysis of outputs for random-effects meta-analysis conducted between July 2012 and September 2013, with baseline estimated GFR values collected from 1975 through 2012. End-stage renal disease (initiation of dialysis or transplantation) or all-cause mortality risk related to percentage change in estimated GFR over 2 years, adjusted for potential confounders and first estimated GFR. The adjusted hazard ratios (HRs) of ESRD and mortality were higher with larger estimated GFR decline. Among participants with baseline estimated GFR of less than 60 mL/min/1.73 m2, the adjusted HRs for ESRD were 32.1 (95% CI, 22.3-46.3) for changes of −57% in estimated GFR and 5.4 (95% CI, 4.5-6.4) for changes of −30%. However, changes of −30% or greater (6.9% [95% CI, 6.4%-7.4%] of the entire consortium) were more common than changes of −57% (0.79% [95% CI, 0.52%-1.06%]). This association was strong and consistent across the length of the baseline period (1 to 3 years), baseline estimated GFR, age, diabetes status, or albuminuria. Average adjusted 10-year risk of ESRD (in patients with a baseline estimated GFR of 35 mL/min/1.73 m2) was 99% (95% CI, 95%-100%) for estimated GFR change of −57%, was 83% (95% CI, 71%-93%) for estimated GFR change of −40%, and was 64% (95% CI, 52%-77%) for estimated GFR change of −30% vs 18% (95% CI, 15%-22%) for estimated GFR change of 0%. Corresponding mortality risks were 77% (95% CI, 71%-82%), 60% (95% CI, 56%-63%), and 50% (95% CI, 47%-52%) vs 32% (95% CI, 31%-33%), showing a similar but weaker pattern. Declines in estimated GFR smaller than a doubling of serum creatinine concentration occurred more commonly and were strongly and consistently associated with the risk of ESRD and mortality, supporting consideration of lesser declines in estimated GFR (such as a 30% reduction over 2 years) as an alternative end point for CKD progression.

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George L. Bakris, Rajiv K. Agarwal, Juliana C N Chan … (2015)

Steroidal mineralocorticoid receptor antagonists, when added to a renin-angiotensin system blocker, further reduce proteinuria in patients with chronic kidney disease but may be underused because of a high risk of adverse events.

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John M. Miller, Thang V. Pham, Phuong-Mai T Pham … (2007)

Hypomagnesemia has been reported to occur at an increased frequency among patients with type 2 diabetes compared with their counterparts without diabetes. Despite numerous reports linking hypomagnesemia to chronic diabetic complications, attention to this issue is poor among clinicians. This article reviews the literature on the metabolism of magnesium, incidence of hypomagnesemia in patients with type 2 diabetes, implicated contributing factors, and associated complications. Hypomagnesemia occurs at an incidence of 13.5 to 47.7% among patients with type 2 diabetes. Poor dietary intake, autonomic dysfunction, altered insulin metabolism, glomerular hyperfiltration, osmotic diuresis, recurrent metabolic acidosis, hypophosphatemia, and hypokalemia may be contributory. Hypomagnesemia has been linked to poor glycemic control, coronary artery diseases, hypertension, diabetic retinopathy, nephropathy, neuropathy, and foot ulcerations. The increased incidence of hypomagnesemia among patients with type 2 diabetes presumably is multifactorial. Because current data suggest adverse outcomes in association with hypomagnesemia, it is prudent to monitor magnesium routinely in this patient population and treat the condition whenever possible.

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Author and article information

Contributors

Eduardo De la Cruz-Cano: eduardocano239@gmail.com

Cristina del C. Jiménez-González: cristina.jimenezgonzalez1@gmail.com

Vicente Morales-García: almostmaster@live.com.mx

Conny Pineda-Pérez: nutripineda@hotmail.com

Juan G. Tejas-Juárez: juan.tejas@ujat.mx

Francisco J. Rendón-Gandarilla: fjrgandarilla@gmail.com

Silvia Jiménez-Morales: sjimenez@inmegen.gob.mx

José A. Díaz-Gandarilla: (52) 9933581500 Ext.6900 , diazgandarilla123@gmail.com

Journal

Journal ID (nlm-ta): BMC Nephrol

Journal ID (iso-abbrev): BMC Nephrol

Title: BMC Nephrology

Publisher: BioMed Central (London )

ISSN (Electronic): 1471-2369

Publication date (Electronic): 28 October 2019

Publication date PMC-release: 28 October 2019

Publication date Collection: 2019

Volume: 20

Electronic Location Identifier: 393

Affiliations

[1 ]GRID grid.441115.4, División Académica Multidisciplinaria de Comalcalco, , Universidad Juárez Autónoma de Tabasco, ; C. P. 86650 Comalcalco, Tabasco Mexico

[2 ]ISNI 0000 0004 1791 0836, GRID grid.415745.6, Secretaría de Salud, Hospital General de Comalcalco, Departamento de Laboratorio de Análisis Clínicos, ; C.P. 86300 Comalcalco, Tabasco Mexico

[3 ]GRID grid.441115.4, División Académica de Ciencias de la Salud, , Universidad Juárez Autónoma de Tabasco, ; C.P. 86100 Villahermosa, Tabasco Mexico

[4 ]ISNI 0000 0004 0627 7633, GRID grid.452651.1, Instituto Nacional de Medicina Genómica (INMEGEN), Laboratorio Genómica del Cáncer, ; Periférico Sur No. 4809, Col. Arenal Tepepan, Deleg. Tlalpan, C.P. 14610 Ciudad de México, Mexico

[5 ]Universidades para el Bienestar Benito Juárez García, Medicina Integral y Salud Comunitaria, Juan R. Escudero, Guerrero, C.P. 39940 Mexico

Article

Publisher ID: 1590

DOI: 10.1186/s12882-019-1590-9

PMC ID: 6819471

PubMed ID: 31660880

SO-VID: 832899f3-6bd6-42f8-ae12-f4ad6d5adf80

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 24 January 2018

Date accepted : 14 October 2019

Custom metadata

ScienceOpen disciplines: Nephrology

Keywords: diabetic nephropathy,type 2 diabetes mellitus,gitelman syndrome,slc12a3 gene

Data availability:

ScienceOpen disciplines: Nephrology

Keywords: diabetic nephropathy, type 2 diabetes mellitus, gitelman syndrome, slc12a3 gene

Arg913Gln variation of SLC12A3 gene is associated with diabetic nephropathy in type 2 diabetes and Gitelman syndrome: a systematic review

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Abstract

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Background

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Results

Conclusions

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Karger: Nephrology

Most cited references 42

Decline in estimated glomerular filtration rate and subsequent risk of end-stage renal disease and mortality.

Effect of Finerenone on Albuminuria in Patients With Diabetic Nephropathy: A Randomized Clinical Trial.

Hypomagnesemia in patients with type 2 diabetes.

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