Evidence map›Paper›PMID 22359229›Full record

ReviewCurrent rheumatology reports2012

Regulation of uric acid excretion by the kidney.

Michael S Lipkowitz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 5 pooled it
6.9field-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

109 citing papers in PubMed, 5 syntheses or guidelines pooled it, 215 citations in OpenAlex.

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49 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.

Michael S LipkowitzNephrology and Hypertension, Georgetown University Medical Center, Washington, DC 20007, USA. michael.s.lipkowitz@gunet.georgetown.edu
Georgetown University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been known for many years that the kidney plays a major role in uric acid homeostasis, as more than 70% of urate excretion is renal. Furthermore, hyperuricemia in gout is most commonly the result of relative urate underexcretion, as the kidney has enormous capacity for urate reabsorption. A clear understanding of the mechanisms of renal handling of urate has been hampered by the differences between humans and animal models. The power of human genetics and genome-wide association studies has now provided new insight into the molecular mechanisms of urate transport by identifying the transporters that have critical roles in urate transport. This review surveys the new evidence for a molecular model of urate transport in the renal proximal tubule and uses these data to refute the popular four-component model for urate transport that has long been in vogue. It also discusses data that help us understand the relation of diuretics to hyperuricemia, losartan-induced uricosuria, variations in uric acid levels in hyperglycemia, and the effects of dairy diets on serum urate levels. In the end, several of these clinical findings are explained, and the remaining gaps in our knowledge will become evident.

Indexed as

GoutHumansHyperuricemiaKidneyOrganic Anion TransportersOrganic Cation Transport ProteinsUric AcidOrganic Anion TransportersOrganic Cation Transport ProteinsUric Acid

Identifiers

PMID22359229
OpenAlexW1977802778

What OpenQuestion holds

Textmetadata
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.