ArticleAmerican journal of translational research2015
Activation of the calcium-sensing receptor before renal ischemia/reperfusion exacerbates kidney injury.
Article in American journal of translational research, 2015. 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, 15 citations in OpenAlex.
- The calcium-sensing receptor in inflammation: Recent updates.Frontiers in physiology · 2022Review
- Surgery for Renal Hyperparathyroidism in the Era of Cinacalcet: A Single-Center Experience.Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society · 2021Article
- In vitro/vivo drug release and anti-diabetic cardiomyopathy properties of curcumin/PBLG-PEG-PBLG nanoparticles.International journal of nanomedicine · 2018Article
- Non-invasive approaches in the diagnosis of acute rejection in kidney transplant recipients, part II: omics analyses of urine and blood samples.Clinical kidney journal · 2017Review
- Collaborative analysis of multi-gigapixel imaging data using Cytomine.Bioinformatics (Oxford, England) · 2016Article
- Comparative expression of the extracellular calcium-sensing receptor in the mouse, rat, and human kidney.American journal of physiology. Renal physiology · 2016Article
- Mesenchymal Stromal Cell Therapy in Ischemia/Reperfusion Injury.Journal of immunology research · 2015Review
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Activation of the calcium-sensing receptor (CaSR) by ischemia/reperfusion (I/R) favours apoptosis in cardiomyocytes, hepatocytes and neurons. Its role in renal I/R is unknown. We investigated the impact of pharmacological preactivation of the CaSR on kidney structure and function in a murine model of bilateral renal 30-min ischemia and 48-hour reperfusion, and in a 6-year cohort of kidney transplant recipients (KTR). C57BL/6J mice were administered daily with CaSR agonist, R-568, or with vehicle for 48 hours. Evaluation of serum urea and creatinine levels, renal histology and urine metabolome by nuclear magnetic resonance showed that R-568 was not nephrotoxic per se. Following I/R, serum urea and creatinine levels increased higher in R-568-treated animals than in controls. Jablonski's score was significantly greater in R-568-treated kidneys, which showed a higher rate of cell proliferation and apoptosis in comparison to controls. Next, we retrospectively identified 36 patients (10.7% of our cohort) who were treated by CaSR agonist, cinacalcet, at the time of kidney transplantation (KTx). After matching these to 61 KTR upon type of donor, cold ischemic time, residual diuresis, and donor age, we observed that delayed graft function, i.e. need for dialysis in the first week after KTx, occurred in 42 and 23% of cinacalcet-treated and control groups, respectively (p≤0.05). These data suggest that pharmacological preactivation of the CaSR before renal I/R exacerbates kidney injury.
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Identifiers
25755835PMC4346530W106265864What OpenQuestion holds
Registered trials
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