Evidence map›Paper›PMID 26723865›Full record

ArticleThe Journal of urology2016

Assessment of Urinary Inhibitor or Promoter Activity in Uric Acid Nephrolithiasis.

Steeve Doizi, Kathy Rodgers, John Poindexter, Khashayar Sakhaee, Naim M Maalouf

Open access · greenAbstract read
In one paragraph

Article in The Journal of urology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.0field-weighted citation impact, top 21% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 10 citations in OpenAlex.

  1. Article
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

5 authors at 1 institution in 1 country.

Steeve DoiziCharles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas.
Kathy RodgersCharles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas.
John PoindexterCharles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas.
Khashayar SakhaeeDivision of Mineral Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Naim M MaaloufDivision of Mineral Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: naim.maalouf@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

UT Southwestern Center for Translational Medicine (UL1/KL2/TL1)UL1TR001105 · NCATS · UT SOUTHWESTERN MEDICAL CENTER · PI TOTO, ROBERT DANIEL · 2013 to 2017
$24.5M
UT-Southwestern Clinical and Translational Alliance for Research (UT-STAR) (TL1)UL1TR000451 · NCATS · UT SOUTHWESTERN MEDICAL CENTER · PI TOTO, ROBERT DANIEL · 2012 to 2012
$6.3M
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
NCATS NIH HHS UL1 TR000451NCATS NIH HHS UL1 TR001105NIDDK NIH HHS R01 DK081423
6 · The paper itself

Abstract

purposeWe assessed decreased inhibitor activity or increased promoter activity in the urine of idiopathic uric acid stone formers compared to nonstone formers independent of urinary pH. MATERIALS AND

methodsA total of 30 idiopathic uric acid stone formers, and 9 obese and 12 lean nonstone formers collected 24-hour urine while on a metabolic diet. Three urine aliquots per subject were used to assess spontaneous nucleation (de novo crystal formation), crystal growth using a 0.1 mg/ml anhydrous uric acid seed and steady-state uric acid solubility (the maximum amount of uric acid dissolvable in urine) using a 5 mg/ml uric acid seed. All experiments were performed for 6 hours at a constant pH of 5.0. Uric acid concentration was measured in filtered aliquots at 0, 3 and 6 hours.

resultsAt baseline 24-hour urinary pH was significantly lower and uric acid saturation was significantly higher in idiopathic uric acid stone formers. No significant spontaneous nucleation developed and similar uric acid steady-state solubility was reached in the 3 groups. Idiopathic uric acid stone formers and lean nonstone formers showed a similar decrease in uric acid concentration during crystal growth. Obese nonstone formers started with a higher uric acid concentration and consequently demonstrated a greater decrease in the uric acid concentration for crystal growth.

conclusionsThis study suggests that there is no significant difference between idiopathic uric acid stone formers and nonstone formers in promoter or inhibitor activity in whole urine against uric acid stone formation when urine pH is maintained constant. The findings suggest that uric acid stone formation is dictated by high urinary saturation with respect to uric acid, which is driven primarily by low urine pH.

Indexed as

CrystallizationAdultAgedFemaleHumansHydrogen-Ion ConcentrationKidney CalculiMaleMiddle AgedUric AcidUrineUric Acidcrystallizationhydrogen-ion concentrationkidney calculiuric acidurine

Identifiers

PMID26723865
PMCPMC5514291
OpenAlexW2206087060

What OpenQuestion holds

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Registered trials

None linked

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.