ReviewNephron2023
Acute Kidney Injury and Diastolic Dysfunction: Opportunity for Targeted Intervention?
Review in Nephron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 1 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsAcute kidney injury (AKI) is common, results in nonrenal sequelae, and predisposes patients to long-term cardiovascular disease. The long-term systemic effects of AKI remain unclear. Sex is an important biological variable in ischemia-reperfusion AKI, and the protective role of estrogen has stymied the inclusion of both sexes in preclinical AKI studies. ITF2357 is a nonspecific histone deacetylase inhibitor that has been shown to improve cardiac outcomes in murine models of hypertension. Here, we review recent work that provides new insight into our understanding of cardiovascular sequelae following AKI.
methodsAdult male and female C57BL/6J mice underwent 25 min (males) and 34 min (females) of bilateral ischemia-reperfusion AKI or sham procedure. A male treatment arm received chow containing the nonspecific histone deacetylase inhibitor ITF2357 starting 3 days after AKI. Serial renal function, echocardiograms, and blood pressure assessments were performed throughout the 1-year study; renal histology and cardiac and plasma metabolomics were evaluated at 1 year.
resultsMeasured glomerular filtration rates throughout the 1-year study showed that the female model of AKI matched the male model. Untreated males developed depressed diastolic function after AKI, whereas females and males treated with ITF2357 maintained normal diastolic function. Both untreated males and females developed hypertension after AKI; males treated with ITF2357 remained normotensive.
conclusionsIschemic AKI results in long-term cardiovascular sequelae with sex as an important biological variable in outcomes. Histone deacetylase inhibition affects cardiovascular outcomes after AKI.
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Registered trials
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