Evidence map›Paper›PMID 22688746›Full record

ReviewNature reviews. Nephrology2012

An update on primary hyperoxaluria.

Bernd Hoppe

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04571359 (Relationship of Spot Urine Oxalate to Creatinine Ratio and 24 Hours Urinary Oxalate Excretion in Patients With Urolithiasis), which is not on this map. Cited by 158 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 2 pooled it
13.2field-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.

NCT04571359 completednot on this mapstarted 2019, after this paper: background citation

Relationship of Spot Urine Oxalate to Creatinine Ratio and 24 Hours Urinary Oxalate Excretion in Patients With Urolithiasis

Typeobservational_patient_registrySponsorAga Khan UniversityRan2019 to 2019Enrolled62ConditionsUrolithiasis, HyperoxaluriaArmsOxalate to creatinine ratio
3 · Its place in the literature

Who cites it

158 citing papers in PubMed, 2 syntheses or guidelines pooled it, 307 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Review
  9. Article
  10. Article
  11. Urolithiasis in patients with cancer.Nature reviews. Urology · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Hyperoxaluria by the AGXT gene: a case report.Journal of medical case reports · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Observational
  20. Article

98 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

1 author at 1 institution in 1 country.

Bernd HoppeUniversity Hospital, Department of Pediatric and Adolescent Medicine, Division of Pediatric Nephrology, Cologne, Germany. bernd.hoppe@uk-koeln.de
University Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The autosomal recessive inherited primary hyperoxalurias types I, II and III are caused by defects in glyoxylate metabolism that lead to the endogenous overproduction of oxalate. Type III primary hyperoxaluria was first described in 2010 and further types are likely to exist. In all forms, urinary excretion of oxalate is strongly elevated (>1 mmol/1.73 m(2) body surface area per day; normal <0.5 mmol/1.73 m(2) body surface area per day), which results in recurrent urolithiasis and/or progressive nephrocalcinosis. All entities can induce kidney damage, which is followed by reduced oxalate elimination and consequent systemic deposition of calcium oxalate crystals. Systemic oxalosis should be prevented, but diagnosis is all too often missed or delayed until end-stage renal disease (ESRD) occurs; this outcome occurs in >30% of patients with primary hyperoxaluria type I. The fact that such a large proportion of patients have such poor outcomes is particularly unfortunate as ESRD can be delayed or even prevented by early intervention. Treatment options for primary hyperoxaluria include alkaline citrate, orthophosphate, or magnesium. In addition, pyridoxine treatment can be used to normalize or reduce oxalate excretion in about 30% of patients with primary hyperoxaluria type I. Time on dialysis should be short to avoid overt systemic oxalosis. Transplantation methods depend on the type of primary hyperoxaluria and on the particular patient, but combined liver and kidney transplantation is the method of choice in patients with primary hyperoxaluria type I and isolated kidney transplantation is the preferred method in those with primary hyperoxaluria type II. To the best of our knowledge, progression to ESRD has not yet been reported in any patient with primary hyperoxaluria type III.

Indexed as

Alcohol OxidoreductasesAngiotensinogenFluid TherapyGenetic TherapyHumansHyperoxaluria, PrimaryKidney TransplantationLiver TransplantationMutationOxo-Acid-LyasesRenal DialysisTransaminases4-hydroxy-2-oxoglutarate aldolaseAGT protein, humanAlanine-glyoxylate transaminaseAlcohol OxidoreductasesAngiotensinogenglyoxylate reductaseOxo-Acid-LyasesTransaminases

Identifiers

PMID22688746
OpenAlexW2072848717

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.