ArticleCommunications biology2020
Urinary phosphate-containing nanoparticle contributes to inflammation and kidney injury in a salt-sensitive hypertension rat model.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Effect of the phosphate binder sucroferric oxyhydroxide in dialysis patients on endogenous calciprotein particles, inflammation, and vascular cells.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Trial
- Integrated morphological and transcriptomic analysis of bone disorders in aldosterone-salt hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Identifying Novel Therapeutic Opportunities for Dilated Cardiomyopathy: A Bioinformatics Approach to Drug Repositioning and Herbal Medicine Prediction.Current pharmaceutical biotechnology · 2026Article
- Hypertension inhibition by Dubosiella newyorkensis via reducing pentosidine synthesis.NPJ biofilms and microbiomes · 2025Article
- Possible contribution of phosphate to the pathogenesis of chronic kidney disease in dolphins.Scientific reports · 2023Article
- High Intake of Sodium Chloride for 28 Days Causes No Effect on Serum FGF23 Concentrations in Cats.Animals : an open access journal from MDPI · 2022Article
- Risk factors and implications associated with renal mineralization in chronic kidney disease in cats.Journal of veterinary internal medicine · 2022Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although disturbed phosphate metabolism frequently accompanies chronic kidney disease (CKD), its causal role in CKD progression remains unclear. It is also not fully understood how excess salt induces organ damage. We here show that urinary phosphate-containing nanoparticles promote kidney injury in salt-sensitive hypertension. In Dahl salt-sensitive rats, salt loading resulted in a significant increase in urinary phosphate excretion without altering serum phosphate levels. An intestinal phosphate binder sucroferric oxyhydroxide attenuated renal inflammation and proteinuria in this model, along with the suppression of phosphaturia. Using cultured proximal tubule cells, we confirmed direct pathogenic roles of phosphate-containing nanoparticles in renal tubules. Finally, transcriptome analysis revealed a potential role of complement C1q in renal inflammation associated with altered phosphate metabolism. These data demonstrate that increased phosphate excretion promotes renal inflammation in salt-sensitive hypertension and suggest a role of disturbed phosphate metabolism in the pathophysiology of hypertensive kidney disease and high salt-induced kidney injury.
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Registered trials
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