ArticlePloS one2018
The aquaporin 5 -1364A/C promoter polymorphism impacts on resolution of acute kidney injury in pneumonia evoked ARDS.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- The Aquaporin 5 -1364A/C Promoter Polymorphism Is Associated With Cytomegalovirus Infection Risk in Kidney Transplant Recipients.Frontiers in immunology · 2019Trial
- AI-Supported, Integrative Prediction of Postoperative Delirium: Protocol for the CONFUSED Study.JMIR research protocols · 2026Article
- Exploring Aquaporins in Human Studies: Mechanisms and Therapeutic Potential in Critical Illness.Life (Basel, Switzerland) · 2024Review
- Aquaporins in sepsis- an update.Frontiers in immunology · 2024Review
- Aquaporin Expression and Regulation in Clinical and Experimental Sepsis.International journal of molecular sciences · 2023Review
- Aquaporin-5 Dynamic Regulation.International journal of molecular sciences · 2023Review
- Article
- Protectin DX promotes epithelial injury repair and inhibits fibroproliferation partly via ALX/PI3K signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Hypotheses about sub-optimal hydration in the weeks before coronavirus disease (COVID-19) as a risk factor for dying from COVID-19.Medical hypotheses · 2020Article
- Article
- DNA methylation of a NF-κB binding site in the aquaporin 5 promoter impacts on mortality in sepsis.Scientific reports · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAquaporin 5 (AQP5) expression impacts on cellular water transport, renal function but also on key mechanisms of inflammation and immune cell migration that prevail in sepsis and ARDS. Thus, the functionally relevant AQP5 -1364A/C promoter single nucleotide polymorphism could impact on the development and resolution of acute kidney injury (AKI). Accordingly, we tested the hypothesis that the AQP5 promoter -1364A/C polymorphism is associated with AKI in patients suffering from pneumonia evoked ARDS.
methodsThis prospective study included 136 adult patients of Caucasian ethnicity with bacterially evoked pneumonia resulting in ARDS. Blood sampling was performed within 24 hours of ICU admission and patients were genotyped for the AQP5 promoter -1364A/C single nucleotide polymorphism. The development of an AKI and the cumulative net fluid balance was described over a 30-day observation period and compared between the AA and AC/CC genotypes, and between survivors and non-survivors.
resultsIncidence of an AKI upon admission did not differ in AA (58%) and AC/CC genotype carriers (60%; p = 0.791). However, on day 30, homozygous AA genotypes (57%) showed an increased prevalence of AKI compared to AC/CC genotypes (24%; p = 0.001). Furthermore, the AA genotype proved to be a strong, independent risk factor for predicting AKI persistence (odds-ratio: 3.35; 95%-CI: 1.2-9.0; p = 0.017). While a negative cumulative fluid balance was associated with increased survival (p = 0.001) the AQP5 promoter polymorphism had no impact on net fluid balance (p = 0.96).
conclusionsIn pneumonia evoked ARDS, the AA genotype of the AQP5 promoter polymorphism is associated with a decreased recovery rate from AKI and this is independent of fluid balance. Consequently, the role of AQP5 in influencing AKI likely rests in factors other than fluid balance.
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