Evidence map›Paper›PMID 41164167›Full record

ReviewFrontiers in medicine2025

Vitamin D and chronic kidney disease: mechanisms, clinical implications, and future perspectives.

Hong Wang, Tingting Yuan, Weihua Wu, Santao Ou

Abstract readReview
In one paragraph

Review in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Hong Wang *Department of Nephrology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Tingting Yuan *Department of Nephrology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Weihua WuDepartment of Nephrology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.
Santao OuDepartment of Nephrology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Vitamin D deficiency is common in chronic kidney disease (CKD). Vitamin D/vitamin D receptor (VDR) signaling intersects inflammation, oxidative stress/mitochondrial injury, fibrogenic pathways, the renin-angiotensin-aldosterone system (RAAS), and the gut-kidney axis, providing a biologic rationale for renoprotection. Methods: Narrative review; literature identified from PubMed/MEDLINE, Embase, Web of Science, and Cochrane Library (January 2000-August 2025). Adult CKD populations (non-dialysis, dialysis, transplant) were included. Outcomes covered biologic/surrogate (e.g., proteinuria, estimated glomerular filtration rate [eGFR] slope) and hard endpoints (kidney failure, major cardiovascular events, fractures, mortality). Results: Nutritional vitamin D reliably corrects deficiency and improves laboratory profiles; VDR activators (VDRAs) suppress secondary hyperparathyroidism (SHPT). However, consistent benefits on hard outcomes have not been demonstrated across CKD settings, likely reflecting heterogeneity (baseline vitamin D status, stage, co-therapies, endpoints) and formulation/dosing differences (D₃ vs. D₂; cholecalciferol vs. calcifediol; steady vs. bolus). Safety considerations (hypercalcemia/mineral imbalance) apply to active agents and high-dose bolus regimens. Conclusion: A pragmatic approach is warranted: replete deficiency with nutritional vitamin D (prefer D₃; consider calcifediol when faster repletion or persistent SHPT is relevant), avoid mega-bolus dosing, and reserve active VDRAs for clear SHPT indications with careful calcium-phosphate-parathyroid hormone (PTH) monitoring-rather than positioning vitamin D as disease-modifying therapy for unselected CKD. Future trials should enrich truly deficient, higher-risk phenotypes, standardize regimens, and prioritize event-driven hard endpoints with embedded mechanistic markers to confirm on-target biology.

Indexed as

chronic kidney diseaseinflammationrenal fibrosisvitamin Dvitamin D receptor protein

Identifiers

PMID41164167
PMCPMC12558989

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.