Evidence map›Paper›PMID 27125746›Full record

ReviewVitamins and hormones2016

αKlotho and Chronic Kidney Disease.

J A Neyra, M C Hu

Open access · greenAbstract readReview
In one paragraph

Review in Vitamins and hormones, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
17.6field-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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Article
  6. Review
  7. Article
  8. Article
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  11. Review
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  15. Review
  16. Klotho in Clinical Nephrology: Diagnostic and Therapeutic Implications.Clinical journal of the American Society of Nephrology : CJASN · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Micturition defects and altered bladder function in theAmerican journal of clinical and experimental urology · 2020
    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

2 authors at 1 institution in 1 country.

J A NeyraUniversity of Texas Southwestern Medical Center, Dallas, TX, United States; Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States.
M C HuUniversity of Texas Southwestern Medical Center, Dallas, TX, United States; Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States. Electronic address: ming-chang.hu@utsouthwestern.edu.
Southwestern Medical Center · US

Funding

Klotho: Therapeutic Agent for Ischemia Reperfusion Induced Acute Kidney InjuryR01DK092461 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HU, MING-CHANG · 2011 to 2021
$3.7M
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
NIDDK NIH HHS R01 DK091392NIDDK NIH HHS R01 DK092461
6 · The paper itself

Abstract

Alpha-Klotho (αKlotho) protein is encoded by the gene, Klotho, and functions as a coreceptor for endocrine fibroblast growth factor-23. The extracellular domain of αKlotho is cleaved by secretases and released into the circulation where it is called soluble αKlotho. Soluble αKlotho in the circulation starts to decline in chronic kidney disease (CKD) stage 2 and urinary αKlotho in even earlier CKD stage 1. Therefore soluble αKlotho is an early and sensitive marker of decline in kidney function. Preclinical data from numerous animal experiments support αKlotho deficiency as a pathogenic factor for CKD progression and extrarenal CKD complications including cardiac and vascular disease, hyperparathyroidism, and disturbed mineral metabolism. αKlotho deficiency induces cell senescence and renders cells susceptible to apoptosis induced by a variety of cellular insults including oxidative stress. αKlotho deficiency also leads to defective autophagy and angiogenesis and promotes fibrosis in the kidney and heart. Most importantly, prevention of αKlotho decline, upregulation of endogenous αKlotho production, or direct supplementation of soluble αKlotho are all associated with attenuation of renal fibrosis, retardation of CKD progression, improvement of mineral metabolism, amelioration of cardiac function and morphometry, and alleviation of vascular calcification in CKD. Therefore in rodents, αKlotho is not only a diagnostic and prognostic marker for CKD but the enhancement of endogenous or supplement of exogenous αKlotho are promising therapeutic strategies to prevent, retard, and decrease the comorbidity burden of CKD.

Indexed as

Renal Insufficiency, ChronicAnimalsBiomarkersCardiovascular DiseasesEpigenesis, GeneticFibroblast Growth Factor-23Fibroblast Growth FactorsGene Expression RegulationGlucuronidaseHumansKidneyKlotho ProteinsMineralsBiomarkersFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsMineralsCardiovascular diseaseChronic kidney diseaseFGF23HyperphosphatemiaKlothoUremic cardiomyopathyVascular calcification

Identifiers

PMID27125746
PMCPMC5658019
OpenAlexW2302700424

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.