ArticleAmerican journal of physiology. Renal physiology2017
Aliskiren increases aquaporin-2 expression and attenuates lithium-induced nephrogenic diabetes insipidus.
Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Lithium effects on renal functioning: an expert opinion and management algorithm.International journal of bipolar disorders · 2026Article
- Brief early life angiotensin-converting enzyme inhibition attenuates the diuretic response to saline loading in sheep with solitary functioning kidney.Clinical science (London, England : 1979) · 2023Article
- Inhibiting the urokinase-type plasminogen activator receptor system recovers STZ-induced diabetic nephropathy.Journal of cellular and molecular medicine · 2019Article
- Aquaporins in Renal Diseases.International journal of molecular sciences · 2019Review
- Inhibition of IL-1β by Aliskiren Improved Renal AQP2 Expression and Urinary Concentration Defect in Ureteral Obstruction and Release.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The direct renin inhibitor aliskiren has been shown to be retained and persist in medullary collecting ducts even after treatment is discontinued, suggesting a new mechanism of action for this drug. The purpose of the present study was to investigate whether aliskiren regulates renal aquaporin expression in the collecting ducts and improves urinary concentrating defect induced by lithium in mice. The mice were fed with either normal chow or LiCl diet (40 mmol·kg dry food
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Registered trials
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