Evidence map›Paper›PMID 31988269›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney Disease.

Donald E Wesson, Jerry M Buysse, David A Bushinsky

Registry-linked trialOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07473713 (Veverimer to Decrease Net Acid Excretion and Bone Resorption in Adults With Osteopenia), which is not on this map. Cited by 96 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 2 pooled it
15.3field-weighted citation impact, top 1% of its field
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.

NCT07473713 phase1recruitingnot on this mapstarted 2026, after this paper: background citation

Veverimer to Decrease Net Acid Excretion and Bone Resorption in Adults With Osteopenia: a Dose-finding Randomized Controlled Trial

TypeinterventionalSponsorTufts Medical CenterRan2026 to 2028Enrolled60ConditionsOsteopeniaArmsveverimer daily, veverimer every other day, Placebo
3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 2 syntheses or guidelines pooled it, 183 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Effects of veverimer on serum bicarbonate and physical function in diabetic patients with chronic kidney disease and metabolic acidosis: subgroup analysis from a randomized, controlled trial.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022
    Trial
  5. Trial
  6. Trial
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

36 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Donald E WessonBaylor Scott & White Health and Wellness Center, Dallas, Texas; Donald.wesson@BSWHealth.org.
Jerry M BuysseFFV Consulting, Los Altos, California; and.
David A BushinskyDivision of Nephrology, University of Rochester School of Medicine, Rochester, New York.
Bryan College · USUniversity of Rochester · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retrospective analyses and single-center prospective studies identify chronic metabolic acidosis as an independent and modifiable risk factor for progression of CKD. In patients with CKD, untreated chronic metabolic acidosis often leads to an accelerated reduction in GFR. Mechanisms responsible for this reduction include adaptive responses that increase acid excretion but lead to a decline in kidney function. Metabolic acidosis in CKD stimulates production of intrakidney paracrine hormones including angiotensin II, aldosterone, and endothelin-1 (ET-1) that mediate the immediate benefit of increased kidney acid excretion, but their chronic upregulation promotes inflammation and fibrosis. Chronic metabolic acidosis also stimulates ammoniagenesis that increases acid excretion but also leads to ammonia-induced complement activation and deposition of C3 and C5b-9 that can cause tubule-interstitial damage, further worsening disease progression. These effects, along with acid accumulation in kidney tissue, combine to accelerate progression of kidney disease. Treatment of chronic metabolic acidosis attenuates these adaptive responses; reduces levels of angiotensin II, aldosterone, and ET-1; reduces ammoniagenesis; and diminishes inflammation and fibrosis that may lead to slowing of CKD progression.

Indexed as

Disease ProgressionAcid-Base EquilibriumAcidosisAdaptation, PhysiologicalAldosteroneAngiotensin IIBiomarkersEndothelin-1FemaleFollow-Up StudiesGlomerular Filtration RateHumansKidney Failure, ChronicMaleProspective StudiesRenal Insufficiency, ChronicAldosteroneAngiotensin IIBiomarkersEndothelin-1aldosteroneangiotensinchronic kidney diseasechronic metabolic acidosisendothelinprogression of chronic renal failure

Identifiers

PMID31988269
PMCPMC7062220
OpenAlexW3003235058

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.