Evidence map›Paper›PMID 34750550›Full record

ReviewNature reviews. Nephrology2022

Pathophysiological mechanisms leading to muscle loss in chronic kidney disease.

Xiaonan H Wang, William E Mitch, S Russ Price

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 4 pooled it
11.4field-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

109 citing papers in PubMed, 4 syntheses or guidelines pooled it, 153 citations in OpenAlex.

  1. Pooled it
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  6. Observational
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  15. Association between serum bicarbonate and low mid-upper arm circumference in patients with non-dialysis-dependent chronic kidney disease: A cross-sectional study.Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition · 2026
    Article
  16. Muscle Matters: Poor Muscle Quality Increases Mortality Risk in Early CKD.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Article
  17. Review
  18. Article
  19. Review
  20. Article

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

3 authors at 3 institutions in 1 country.

Xiaonan H WangRenal Division, Department of Medicine, Emory University, Atlanta, GA, USA.
William E MitchNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
S Russ PriceDepartment of Biochemistry and Molecular Biology, Brody School of Medicine, East Carolina University, Greenville, NC, USA. pricest17@ecu.edu.ORCID http://orcid.org/0000-0003-0893-0723
Baylor College of Medicine · USEast Carolina University · USEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of muscle proteins is a deleterious consequence of chronic kidney disease (CKD) that causes a decrease in muscle strength and function, and can lead to a reduction in quality of life and increased risk of morbidity and mortality. The effectiveness of current treatment strategies in preventing or reversing muscle protein losses is limited. The limitations largely stem from the systemic nature of diseases such as CKD, which stimulate skeletal muscle protein degradation pathways while simultaneously activating mechanisms that impair muscle protein synthesis and repair. Stimuli that initiate muscle protein loss include metabolic acidosis, insulin and IGF1 resistance, changes in hormones, cytokines, inflammatory processes and decreased appetite. A growing body of evidence suggests that signalling molecules secreted from muscle can enter the circulation and subsequently interact with recipient organs, including the kidneys, while conversely, pathological events in the kidney can adversely influence protein metabolism in skeletal muscle, demonstrating the existence of crosstalk between kidney and muscle. Together, these signals, whether direct or indirect, induce changes in the levels of regulatory and effector proteins via alterations in mRNAs, microRNAs and chromatin epigenetic responses. Advances in our understanding of the signals and processes that mediate muscle loss in CKD and other muscle wasting conditions will support the future development of therapeutic strategies to reduce muscle loss.

Indexed as

MicroRNAsRenal Insufficiency, ChronicHumansMuscle, SkeletalMuscular AtrophyQuality of LifeMicroRNAs

Identifiers

PMID34750550
OpenAlexW3214295340

What Socratic 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 Socratic graph.