Intestinal paracellular phosphate absorption resists dietary adaptation but is upregulated in CKD

Clicks: 27
ID: 324752
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #37 of 152 articles by views in nephrology dialysis transplantation

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 152 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Abstract Background and hypothesis The paracellular absorption of phosphate (Pi) contributes the bulk of intestinal absorption under conditions of high dietary Pi availability. Here, we hypothesized that dietary Pi content and reduced renal function affect intestinal paracellular Pi transport. Methods Wildtype male mice received low (<0.1%, LP) or high (1.2%, HP) diet for 7 days. Urine, blood, intestinal segments and kidneys were collected and analyzed for urinary and plasma concentrations of Pi and Ca2+, plasma levels of Pi-regulating hormones, evaluation of trans- and paracellular Pi transport across jejunum and ileum and intestinal claudin expression. Additionally, wildtype male mice underwent sham operation or 5/6 nephrectomy followed by 14 days of HP diet to mimic the pathophysiological features of CKD and intestinal Pi transport was assessed. Results Mice displayed the expected systemic adaptation to LP/HP diets but showed no differences in ileal paracellular Pi transport upon different dietary Pi. The protein expression of several barrier-associated claudins (claudin-3, -4 and -7) was upregulated upon HP diet, specifically in the ileum. 5/6 nephrectomized mice showed the expected disturbed mineral metabolism, lacked downregulation of active intestinal Pi transport, and showed higher ileal paracellular Pi transport. Claudin-3 and claudin-7 were mislocalized in the ileum. In human intestinal cells, the uremic toxin p-cresol enhanced Pi permeability. Conclusion Changes in dietary Pi intake do not alter paracellular Pi fluxes. In a mouse model of CKD, active intestinal Pi transport is not downregulated despite hyperphosphatemia and paracellular Pi fluxes elevated. The loss of junctional barrier integrity might be driven driven by uremic toxins such as p-cresol and could contribute to systemic phosphate imbalance in CKD. Our findings highlight the intestinal epithelial tight junction (TJ) and uremic toxins as potential therapeutic targets to prevent disturbed phosphate homeostasis in CKD.
Reference Key
openalex_W7202286185 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Zsuzsa Radványi, Laurine Lang, Nati Hernando, Carsten A. Wagner
Are you one of these authors? Claim your profile
Journal nephrology dialysis transplantation
Year 2026
DOI
10.1093/ndt/gfag185
URL
https://doi.org/10.1093/ndt/gfag185
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.