ArticlePloS one2012
Sirolimus induced phosphaturia is not caused by inhibition of renal apical sodium phosphate cotransporters.
Article in PloS one, 2012. 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, 19 citations in OpenAlex.
- [Pattern of biochemical markers of mineral and bone disorders in kidney transplant recipients: real-world data].Problemy endokrinologii · 2023Article
- Rapamycin treatment induces tubular proteinuria: role of megalin-mediated protein reabsorption.Frontiers in pharmacology · 2023Article
- Lack of PTEN in osteocytes increases circulating phosphate concentrations by decreasing intact fibroblast growth factor 23 levels.Scientific reports · 2020Article
- The tripartite interaction of phosphate, autophagy, and αKlotho in health maintenance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Therapeutic Use of mTOR Inhibitors in Renal Diseases: Advances, Drawbacks, and Challenges.Oxidative medicine and cellular longevity · 2018Review
- mTOR Regulates Endocytosis and Nutrient Transport in Proximal Tubular Cells.Journal of the American Society of Nephrology : JASN · 2017Article
- Roles of mTOR complexes in the kidney: implications for renal disease and transplantation.Nature reviews. Nephrology · 2016Review
- Inorganic Phosphate Activates the AKT/mTORC1 Pathway and Shortens the Life Span of an α‑Klotho-Deficient Model.Journal of the American Society of Nephrology : JASN · 2016Article
- Mammalian target of rapamycin signaling inhibition ameliorates vascular calcification via Klotho upregulation.Kidney international · 2015Article
- Renal phosphate transporters.Current opinion in nephrology and hypertension · 2014Review
- mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The vast majority of glomerular filtrated phosphate is reabsorbed in the proximal tubule. Posttransplant phosphaturia is common and aggravated by sirolimus immunosuppression. The cause of sirolimus induced phosphaturia however remains elusive. Male Wistar rats received sirolimus or vehicle for 2 or 7 days (1.5mg/kg). The urine phosphate/creatinine ratio was higher and serum phosphate was lower in sirolimus treated rats, fractional excretion of phosphate was elevated and renal tubular phosphate reabsorption was reduced suggesting a renal cause for hypophosphatemia. PTH was lower in sirolimus treated rats. FGF 23 levels were unchanged at day 2 but lower in sirolimus treated rats after 7 days. Brush border membrane vesicle phosphate uptake was not altered in sirolimus treated groups or by direct incubation with sirolimus. mRNA, protein abundance, and subcellular transporter distribution of NaPi-IIa, Pit-2 and NHE3 were not different between groups but NaPi-IIc mRNA expression was lower at day 7. Transcriptome analyses revealed candidate genes that could be involved in the phosphaturic response. Sirolimus caused a selective renal phosphate leakage, which was not mediated by NaPi-IIa or NaPi-IIc regulation or localization. We hypothesize that another mechanism such as a basolateral phosphate transporter may be responsible for the sirolimus induced phosphaturia.
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