Evidence map›Paper›PMID 35046512›Full record

ReviewHypertension research : official journal of the Japanese Society of Hypertension2022

Impact of hyperuricemia on chronic kidney disease and atherosclerotic cardiovascular disease.

Hitoshi Nishizawa, Norikazu Maeda, Iichiro Shimomura

Abstract readReview
PubMed Publisher
In one paragraph

Review in Hypertension research : official journal of the Japanese Society of Hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
14.0field-weighted citation impact, top 1% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Febuxostat and renal outcomes: post-hoc analysis of a randomized trial.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Trial
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
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  11. National Prevalence, Regional Distribution, and Risk Factors for CKD in Taiwan.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
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  15. Article
  16. Article
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  19. Review
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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

3 authors at 1 institution in 1 country.

Hitoshi NishizawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, 2-2, Yamada-oka, Suita, Osaka, 565-0871, Japan. hitoshin1127@endmet.med.osaka-u.ac.jp.
Norikazu MaedaDepartment of Metabolism and Atherosclerosis, Graduate School of Medicine, Osaka University, 2-2, Yamada-oka, Suita, Osaka, 565-0871, Japan.
Iichiro ShimomuraDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, 2-2, Yamada-oka, Suita, Osaka, 565-0871, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperuricemia is caused by reduced renal/extrarenal excretion and overproduction of uric acid. It is affected by genetic predisposition related to uric acid transporters and by visceral fat accumulation due to overnutrition. The typical symptomatic complication of hyperuricemia is gout caused by monosodium urate crystals. Accumulated evidence from epidemiological studies suggests that hyperuricemia is also a risk factor for hypertension, chronic kidney disease (CKD) and atherosclerotic cardiovascular disease (CVD). However, it remains to be determined whether urate-lowering therapy for asymptomatic patients with hyperuricemia is effective in preventing CKD or CVD progression. This mini review focuses mainly on recent papers investigating the relationship between hyperuricemia and CKD or CVD and studies of urate-lowering therapy. Accumulated studies have proposed mechanisms of renal damage and atherosclerosis in hyperuricemia, including inflammasome activation, decreased nitric oxide bioavailability and oxidative stress induced by uric acid, urate crystals and xanthine oxidoreductase (XOR)-mediated reactive oxygen species. Since patients with hyperuricemia are a heterogeneous population with complex pathologies, it may be important to assess whether an outcome is the result of decreasing serum uric acid levels or an inhibitory effect on XOR. To clarify the impact of hyperuricemia on CKD and CVD progression, high-quality and detailed clinical and basic science studies of hyperuricemia and purine metabolism are needed.

Indexed as

AtherosclerosisCardiovascular DiseasesHyperuricemiaRenal Insufficiency, ChronicFemaleHumansMaleUric AcidUric AcidAtherosclerotic cardiovascular diseaseChronic kidney diseaseUric acidXanthine oxidoreductase

Identifiers

PMID35046512
OpenAlexW4206010795

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.