Evidence map›Paper›PMID 35884889›Full record

ArticleBiomedicines2022

Analysis of Purine Metabolism to Elucidate the Pathogenesis of Acute Kidney Injury in Renal Hypouricemia.

Daisuke Miyamoto, Nana Sato, Koji Nagata, Yukinao Sakai, Hitoshi Sugihara, Yuki Ohashi, Blanka Stiburkova, Ivan Sebesta, Kimiyoshi Ichida, Ken Okamoto

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
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  9. Review
  10. SLC2A9 rs16890979 reduces uric acid absorption by kidney organoids.Frontiers in cell and developmental biology · 2023
    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

10 authors at 5 institutions in 2 countries.

Daisuke MiyamotoDepartment of Nephrology, Graduate School of Medicine, Nippon Medical School, Tokyo 113-8603, Japan.ORCID 0000-0002-1863-3370
Nana SatoDepartment of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan.
Koji NagataDepartment of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan.ORCID 0000-0002-4704-0603
Yukinao SakaiDepartment of Nephrology, Graduate School of Medicine, Nippon Medical School, Tokyo 113-8603, Japan.ORCID 0000-0002-8558-0571
Hitoshi SugiharaDepartment of Endocrinology, Diabetes, and Metabolism, Graduate School of Medicine, Nippon Medical School, Tokyo 113-8603, Japan.
Yuki OhashiDepartment of Pathophysiology, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan.
Blanka StiburkovaDepartment of Pediatrics and Adolescent Medicine, First Faculty of Medicine, Charles University and General University Hospital, 11000 Prague, Czech Republic.
Ivan SebestaInstitute of Rheumatology, Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital, 11000 Prague, Czech Republic.
Kimiyoshi IchidaDepartment of Pathophysiology, Tokyo University of Pharmacy and Life Sciences, Tokyo 192-0392, Japan.
Ken OkamotoDepartment of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo 113-8657, Japan.ORCID 0000-0003-2760-5344
Nippon Medical School · JPThe University of Tokyo · JPCharles University · CZJikei University School of Medicine · JPTokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal hypouricemia is a disease caused by the dysfunction of renal urate transporters. This disease is known to cause exercise-induced acute kidney injury, but its mechanism has not yet been established. To analyze the mechanism by which hypouricemia causes renal failure, we conducted a semi-ischemic forearm exercise stress test to mimic exercise conditions in five healthy subjects, six patients with renal hypouricemia, and one patient with xanthinuria and analyzed the changes in purine metabolites. The results showed that the subjects with renal hypouricemia had significantly lower blood hypoxanthine levels and increased urinary hypoxanthine excretion after exercise than healthy subjects. Oxidative stress markers did not differ between healthy subjects and hypouricemic subjects before and after exercise, and no effect of uric acid as a radical scavenger was observed. As hypoxanthine is a precursor for adenosine triphosphate (ATP) production via the salvage pathway, loss of hypoxanthine after exercise in patients with renal hypouricemia may cause ATP loss in the renal tubules and consequent tissue damage.

Indexed as

acute kidney injuryhypouricemiaxanthinuria

Identifiers

PMID35884889
PMCPMC9312704
OpenAlexW4283769541

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.