ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS2022
Tolvaptan Improves Contrast-Induced Acute Kidney Injury.
Article in Journal of the renin-angiotensin-aldosterone system : JRAAS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- The impact of tolvaptan on the incidence of contrast-induced acute kidney injury and long-term prognosis in high-risk patients after coronary intervention.Renal failure · 2025Trial
- Roxadustat attenuates contrast-induced acute kidney injury potentially mediated via the Nrf2/HO-1 signaling pathway.Renal failure · 2026Article
- ClpP deficiency attenuates contrast-induced HK-2 cell injury through changes associated with mitochondrial dynamics and apoptosis.PloS one · 2026Article
- Research progress on risk factors and early predictors of contrast-induced nephropathy.American journal of translational research · 2026Review
- Multiparametric Evaluation of Drug-Induced Acute Kidney Injury Using Preclinical 7T Magnetic Resonance Imaging in Rat Models.Metabolites · 2025Article
- Transcriptional activation of PINK1 by MyoD1 mediates mitochondrial homeostasis to induce renal calcification in pediatric nephrolithiasis.Cell death discovery · 2024Article
- Sodium selenite attenuates inflammatory response and oxidative stress injury by regulating the Nrf2/ARE pathway in contrast-induced acute kidney injury in rats.BMC nephrology · 2024Article
- Signal pathways involved in contrast-induced acute kidney injury.Frontiers in physiology · 2024Review
Corrections and comments
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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
objectiveContrast-induced acute kidney injury (CI-AKI) is a serious side effect of contrast media use. The purpose of this study was to investigate the role and mechanism of tolvaptan (TOL) in CI-AKI.
methods24 Wistar male rats were randomly divided into 4 groups (
resultsTOL could significantly reduce the serum level of urea nitrogen, creatinine, and neutrophil gelatinase-associated lipocalin and decrease serum Cys-C and urine KIM-1 in CI-AKI rats. The result above meant that TOL could improve kidney injury and reduce tubular cell apoptosis in CI-AKI rats. In addition, TOL contributed to a reduction of oxidative stress level by downregulating myeloperoxidase level and increasing the activities of superoxide dismutase and glutathione peroxidase in the kidney tissue of CI-AKI rats. After the pretreatment of TOL, the expression of proapoptotic proteins cleaved-caspase 3 and BAX, as well as mitochondrial fusion proteins DRP1 and MFN2 was downregulated, while the expression of Bcl-2 and PINK1 was upregulated in the kidney tissue of CI-AKI rats. Further, TOL could activate the Nrf2 signaling pathway, and the Nrf2 inhibitor ML385 reversed the effect of TOL on CI-AKI.
conclusionTOL can improve CI-AKI by activating the Nrf2/HO-1 signaling pathway, inhibiting oxidative stress response, and reducing tubular cell apoptosis.
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