Evidence map›Paper›PMID 25045326›Full record

ArticleClinical reviews in bone and mineral metabolism2011

Uric Acid Nephrolithiasis: A Systemic Metabolic Disorder.

Michael R Wiederkehr, Orson W Moe

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

Article in Clinical reviews in bone and mineral metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06335537 (Impact of Sodium Bicarbonate on 24-hour Urine Parameters in Hypocitriuric and Uric Acid Stone Formers), which is not on this map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 45% 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.

NCT06335537 phase1recruitingnot on this mapstarted 2025, after this paper: background citation

Impact of Sodium Bicarbonate on 24-hour Urine Parameters in Hypocitriuric and Uric Acid Stone Formers

TypeinterventionalSponsorUniversity of California, IrvineRan2025 to 2026Enrolled100ConditionsUric Acid StonesArmsPotassium citrate, Sodium bicarbonate
3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. SGLT2 inhibitors and nephrolithiasis risk: a meta-analysis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
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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.

Michael R WiederkehrDivision of Nephrology, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX 75246, USA.
Orson W MoeDepartment of Internal Medicine, Division of Nephrology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8885, USA, Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX, USA, Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Baylor University Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Pathogenesis of Uric Acid Nephrolithiasis: The Multifaceted Role of Renal LipidsR01DK081423 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MAALOUF, NAIM M, MOE, ORSON W · 2009 to 2023
$6.1M
NIDDK NIH HHS R01 DK081423
6 · The paper itself

Abstract

Uric acid nephrolithiasis is characteristically a manifestation of a systemic metabolic disorder. It has a prevalence of about 10% among all stone formers, the third most common type of kidney stone in the industrialized world. Uric acid stones form primarily due to an unduly acid urine; less deciding factors are hyperuricosuria and a low urine volume. The vast majority of uric acid stone formers have the metabolic syndrome, and not infrequently, clinical gout is present as well. A universal finding is a low baseline urine pH plus insufficient production of urinary ammonium buffer. Persons with gastrointestinal disorders, in particular chronic diarrhea or ostomies, and patients with malignancies with a large tumor mass and high cell turnover comprise a less common but nevertheless important subset. Pure uric acid stones are radiolucent but well visualized on renal ultrasound. A 24 h urine collection for stone risk analysis provides essential insight into the pathophysiology of stone formation and may guide therapy. Management includes a liberal fluid intake and dietary modification. Potassium citrate to alkalinize the urine to a goal pH between 6 and 6.5 is essential, as undissociated uric acid deprotonates into its much more soluble urate form.

Indexed as

Acid urineAlkalineAmmoniumGoutHyperuricosuriaMetabolic syndromepHPotassium citrateUric acid nephrolithiasisUrine buffer

Identifiers

PMID25045326
PMCPMC4100778
OpenAlexW2090806259

What OpenQuestion holds

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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.