Evidence map›Paper›PMID 35351460›Full record

ReviewKidney international2022

Effects of acid on bone.

David A Bushinsky, Nancy S Krieger

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Kidney international, 2022. 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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Risks and benefits of face masks in children.Frontiers in pediatrics · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Primary Distal Renal Tubular Acidosis: Toward an Optimal Correction of Metabolic Acidosis.Clinical journal of the American Society of Nephrology : CJASN · 2024
    Review
  18. Risk factors for hip and vertebral fractures in chronic kidney disease: the CRIC study.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
    Article
  19. Article
  20. Review
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

2 authors at 2 institutions in 1 country.

David A BushinskyNephrology Division, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA. Electronic address: david_bushinsky@URMC.Rochester.edu.
Nancy S KriegerNephrology Division, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.
University of Rochester · USUniversity of Rochester Medical Center · US

Funding

Hypercalciuria and Bone Quality in the Genetic Hypercalciuric Stone-Forming RatsR01DK075462 · NIDDK · UNIVERSITY OF ROCHESTER · PI BUSHINSKY, DAVID A · 2008 to 2019
$3.8M
EFFECTS OF ACID ON BONER01AR046289 · NIAMS · UNIVERSITY OF ROCHESTER · PI BUSHINSKY, DAVID A · 2000 to 2010
$3.0M
NIAMS NIH HHS R01 AR046289NIDDK NIH HHS R01 DK075462
6 · The paper itself

Abstract

The homeostatic regulation of a stable systemic pH is of critical importance for mammalian survival. During metabolic acidosis (a reduction in systemic pH caused by a primary decrease in serum bicarbonate concentration), as seen in clinical disorders such as the later stages of chronic kidney disease, renal tubular acidosis, or chronic diarrhea, bone buffers the accumulated acid; however, this homeostatic function of the skeleton occurs at the expense of the bone mineral content and leads to decreased bone quality. During short-term studies to model acute metabolic acidosis, there is initial physiochemical bone mineral dissolution, releasing carbonate and phosphate proton buffers into the extracellular fluid. In addition, there is net proton influx into the mineral with release of bone sodium and potassium. During long-term studies to model chronic metabolic acidosis, there is also inhibition of osteoblast activity, resulting in reduced bone formation, and an increase in osteoclast activity, resulting in increased bone resorption and release of calcium and anionic proton buffers. These physicochemical and cell-mediated bone responses to metabolic acidosis, in addition to an acidosis-induced increased urine calcium excretion, without a corresponding increase in intestinal calcium absorption, induce a net loss of body calcium that is almost certainly derived from the mineral stores of bone.

Indexed as

AcidosisCalciumAnimalsBone and BonesHydrogen-Ion ConcentrationMammalsPhosphatesProtonsCalciumPhosphatesProtonsbonecalciummineral metabolism

Identifiers

PMID35351460
PMCPMC9133222
OpenAlexW4220663642

What OpenQuestion holds

Textmetadata
LicenceTDM
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.