Evidence map›Paper›PMID 27339448›Full record

ReviewClinical and experimental nephrology2017

Time to target uric acid to retard CKD progression.

Takanori Kumagai, Tatsuru Ota, Yoshifuru Tamura, Wen Xiu Chang, Shigeru Shibata, Shunya Uchida

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03425708 (Study on the Effect of Hyperuricaemia on Chronic Renal Disease and Intervention), which is not on this map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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.

NCT03425708 phase4unknown statusnot on this map

Study on the Effect of Hyperuricaemia on Chronic Renal Disease and Intervention

TypeinterventionalSponsorThe Affiliated Hospital of Xuzhou Medical UniversityRan2017 to 2018Enrolled400ConditionsHyperuricemia, Chronic Renal DiseaseArms20mg Febuxostat, 40mg Febuxostat
3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Takanori KumagaiDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605, Japan.
Tatsuru OtaDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605, Japan.
Yoshifuru TamuraDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605, Japan.
Wen Xiu ChangDepartment of Nephrology, Tianjin First Central Hospital, Tianjin, China.
Shigeru ShibataDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605, Japan.
Shunya UchidaDepartment of Internal Medicine, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo, 173-8605, Japan. s_uchida@netjoy.ne.jp.
Teikyo University · JPTianjin First Center Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uric acid (UA) remains a possible risk factor of chronic kidney disease (CKD) but its potential role should be elucidated given a fact that multidisciplinary treatments assure a sole strategy to inhibit the progression to end-stage renal disease (ESRD). In clinical setting, most observational studies showed that elevation of serum uric acid (SUA) independently predicts the incidence and the development of CKD. The meta-analysis showed that SUA-lowering therapy with allopurinol may retard the progression of CKD but did not reach conclusive results due to small-sized studies. Larger scale, randomized placebo-controlled trials to assess SUA-lowering therapy are needed. Our recent analysis by propensity score methods has shown that the threshold of SUA should be less than 6.5 mg/dL to abrogate ESRD. In animal models an increase in SUA by the administration of oxonic acid, uricase inhibitor, or nephrectomy can induce glomerular hypertension, arteriolosclerosis including afferent arteriolopathy and tubulointerstitial fibrosis. The ever-growing discoveries of urate transporters prompt us to learn UA metabolism in the kidney and intestine. One example is that the intestinal ABCG2 may play a compensatory role at face of decreased renal clearance of UA in nephrectomized rats, the trigger of which is not a uremic toxin but SUA itself. This review will summarize the recent knowledge on the relationship between SUA and the kidney and try to draw a conclusion when and how to treat asymptomatic hyperuricemia accompanied by CKD. Finally we will address a future perspective on UA study including a Mendelian randomization approach.

Indexed as

AnimalsBiomarkersDisease ProgressionGenetic Predisposition to DiseaseGout SuppressantsHumansHyperuricemiaKidneyMendelian Randomization AnalysisOrganic Anion TransportersRandomized Controlled Trials as TopicRenal Insufficiency, ChronicRisk FactorsUric AcidBiomarkersGout SuppressantsOrganic Anion Transportersurate transporterUric AcidABCG2AllopurinolBenzbromaroneChronic kidney diseaseEnd-stage renal diseaseFebuxostatHyperuricemiaMendelian randomization approachPropensity score analysisSerum uric acidUrate transporter

Identifiers

PMID27339448
OpenAlexW2462733001

What OpenQuestion holds

Textmetadata
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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.