Evidence map›Paper›PMID 23739234›Full record

ArticleKidney international2013

NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy.

Felix Knauf, John R Asplin, Ignacio Granja, Insa M Schmidt, Gilbert W Moeckel, Rachel J David, Richard A Flavell, Peter S Aronson

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02684656 (Pilot Study of Lowering Plasma Oxalate With Hemodiafiltration to Reduce Systemic Inflammation in Patients With End-Stage Renal Disease), which is not on this map. Cited by 130 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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.

NCT02684656 nacompletednot on this mapstarted 2016, after this paper: background citation

Pilot Study of Lowering Plasma Oxalate With Hemodiafiltration to Reduce Systemic Inflammation in Patients With End-Stage Renal Disease (ESRD)

TypeinterventionalSponsorUniversity of Erlangen-Nürnberg Medical SchoolRan2016 to 2016Enrolled14ConditionsChronic Kidney Disease Requiring Chronic DialysisArmsHemodialysis, Hemodiafiltration
3 · Its place in the literature

Who cites it

130 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. IL-1 Inhibition and Vascular Function in CKD.Journal of the American Society of Nephrology : JASN · 2017
    Trial
  5. Review
  6. Article
  7. Article
  8. Review
  9. The role of inflammation and ROS in CaOx kidney stones.European journal of medical research · 2025
    Review
  10. Inhibition of the inflammasome ameliorates orthologous polycystic kidney disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
  12. Article
  13. Mechanisms underlying atrial fibrillation in chronic kidney disease.Journal of molecular and cellular cardiology · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Felix KnaufDepartment of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
John R Asplin
Ignacio Granja
Insa M Schmidt
Gilbert W Moeckel
Rachel J David
Richard A Flavell
Peter S Aronson
Yale University · USLink Foundation · USHoward Hughes Medical Institute · US

Funding

Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI ARONSON, PETER S. · 2008 to 2022
$16.8M
Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Roles of SLC26A6 in Renal NaCI Transport and Prevention of Oxalate UrolithiasisR37DK033793 · NIDDK · YALE UNIVERSITY · PI ARONSON, PETER S. · 1994 to 2016
$6.8M
NIDDK NIH HHS P30 DK079310NIDDK NIH HHS P30DK079310NIDDK NIH HHS R37 DK033793NIDDK NIH HHS R37DK33793NIDDK NIH HHS U24 DK059635NIDDK NIH HHS U24DK059635
6 · The paper itself

Abstract

Oxalate nephropathy with renal failure is caused by multiple disorders leading to hyperoxaluria due to either overproduction of oxalate (primary hyperoxaluria) or excessive absorption of dietary oxalate (enteric hyperoxaluria). To study the etiology of renal failure in crystal-induced kidney disease, we created a model of progressive oxalate nephropathy by feeding mice a diet high in soluble oxalate (high oxalate in the absence of dietary calcium). Renal histology was characterized by intratubular calcium-oxalate crystal deposition with an inflammatory response in the surrounding interstitium. Oxalate nephropathy was not found in mice fed a high oxalate diet that also contained calcium. NALP3, also known as cryopyrin, has been implicated in crystal-associated diseases such as gout and silicosis. Mice fed the diet high in soluble oxalate demonstrated increased NALP3 expression in the kidney. Nalp3-null mice were completely protected from the progressive renal failure and death that occurred in wild-type mice fed the diet high in soluble oxalate. NALP3 deficiency did not affect oxalate homeostasis, thereby excluding differences in intestinal oxalate handling to explain the observed phenotype. Thus, progressive renal failure in oxalate nephropathy results primarily from NALP3-mediated inflammation.

Indexed as

OxalatesAnimalsCarrier ProteinsDisease Models, AnimalDisease ProgressionFemaleGenotypeInflammasomesInflammation MediatorsKidneyMaleMiceMice, Inbred C57BLMice, KnockoutNephritisNLR Family, Pyrin Domain-Containing 3 ProteinCarrier ProteinsInflammasomesInflammation MediatorsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOxalates

Identifiers

PMID23739234
PMCPMC3772982
OpenAlexW2020675784

What OpenQuestion holds

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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.