Evidence map›Paper›PMID 23089270›Full record

ReviewAdvances in chronic kidney disease2012

Renal transport of uric acid: evolving concepts and uncertainties.

Ion Alexandru Bobulescu, Orson W Moe

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in chronic kidney disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 4 pooled it
6.7field-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.

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

194 citing papers in PubMed, 4 syntheses or guidelines pooled it, 386 citations in OpenAlex.

  1. Pooled it
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  4. Guideline
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  6. SGLT2 Inhibition and Uric Acid Excretion in Patients with Type 2 Diabetes and Normal Kidney Function.Clinical journal of the American Society of Nephrology : CJASN · 2022
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134 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

2 authors at 1 institution in 1 country.

Ion Alexandru BobulescuDepartments of Internal Medicine and Physiology and the Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-8856, USA. alexandru.bobulescu@utsouthwestern.edu
Orson W Moe
The University of Texas Southwestern Medical Center · US

Funding

UT Southwestern O'Brien Kidney Research Core CenterP30DK079328 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2007 to 2021
$16.9M
Klotho and Phosphate in Chronic Kidney Disease: Pathogenesis and TherapeuticsR01DK091392 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HU, MING-CHANG, MOE, ORSON W · 2011 to 2021
$3.2M
Neonatal Proximal Tubule AcidificationR01DK041612 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BAUM, MICHEL GERARD, MOE, ORSON W · 1991 to 2013
$2.7M
Protein Phosphatase Regulation of the Principal Renal Sodium Transporter NHE3K01DK090282 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BOBULESCU, ION ALEXANDRU · 2011 to 2015
$434k
Generation of High Impact Resources for Erythropoietin Receptor ResearchR21CA152977 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2010 to 2011
$407k
NCI NIH HHS R21 CA152977NIDDK NIH HHS K01 DK090282NIDDK NIH HHS P30 DK079328NIDDK NIH HHS R01 DK041612NIDDK NIH HHS R01 DK091392
6 · The paper itself

Abstract

In addition to its role as a metabolic waste product, uric acid has been proposed to be an important molecule with multiple functions in human physiologic and pathophysiologic processes and may be linked to human diseases beyond nephrolithiasis and gout. Uric acid homeostasis is determined by the balance between production, intestinal secretion, and renal excretion. The kidney is an important regulator of circulating uric acid levels by reabsorbing about 90% of filtered urate and being responsible for 60% to 70% of total body uric acid excretion. Defective renal handling of urate is a frequent pathophysiologic factor underpinning hyperuricemia and gout. Despite tremendous advances over the past decade, the molecular mechanisms of renal urate transport are still incompletely understood. Many transport proteins are candidate participants in urate handling, with URAT1 and GLUT9 being the best characterized to date. Understanding these transporters is increasingly important for the practicing clinician as new research unveils their physiologic characteristics, importance in drug action, and genetic association with uric acid levels in human populations. The future may see the introduction of new drugs that act specifically on individual renal urate transporters for the treatment of hyperuricemia and gout.

Indexed as

Biological TransportGlucose Transport Proteins, FacilitativeGoutHumansHyperuricemiaKidneyKidney Tubules, ProximalOrganic Anion TransportersOrganic Cation Transport ProteinsUncertaintyUric AcidGlucose Transport Proteins, FacilitativeOrganic Anion TransportersOrganic Cation Transport ProteinsSLC22A12 protein, humanSLC2A9 protein, humanUric Acid

Identifiers

PMID23089270
PMCPMC3619397
OpenAlexW2150866339

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.