Evidence map›Paper›PMID 37509715›Full record

ReviewBiomedicines2023

The Potential Influence of Uremic Toxins on the Homeostasis of Bones and Muscles in Chronic Kidney Disease.

Kuo-Chin Hung, Wei-Cheng Yao, Yi-Lien Liu, Hung-Jen Yang, Min-Tser Liao, Keong Chong, Ching-Hsiu Peng, Kuo-Cheng Lu

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.

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  19. Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice.International journal of molecular sciences · 2024
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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

8 authors at 4 institutions in 1 country.

Kuo-Chin HungDivision of Nephrology, Department of Medicine, Min-Sheng General Hospital, Taoyuan City 330, Taiwan.ORCID 0000-0001-9023-8925
Wei-Cheng YaoDepartment of Anesthesiology, Min-Sheng General Hospital, Taoyuan City 330, Taiwan.
Yi-Lien LiuDepartment of Family Medicine, Min-Sheng General Hospital, Taoyuan City 330, Taiwan.
Hung-Jen YangDepartment of General Medicine, Min-Sheng General Hospital, Taoyuan City 330, Taiwan.
Min-Tser LiaoDepartment of Pediatrics, Taoyuan Armed Forces General Hospital Hsinchu Branch, Hsinchu City 300, Taiwan.
Keong ChongDivision of Endocrinology and Metabolism, Department of Medicine, Min-Sheng General Hospital, Taoyuan City 330, Taiwan.
Ching-Hsiu PengDivision of Nephrology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, and School of Medicine, Tzu Chi University, Hualien 970, Taiwan.ORCID 0000-0001-6293-144X
Kuo-Cheng LuDivision of Nephrology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, and School of Medicine, Tzu Chi University, Hualien 970, Taiwan.ORCID 0000-0002-7062-8560
Min Sheng General Hospital · TWFu Jen Catholic University · TWTri-Service General Hospital · TWTzu Chi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with chronic kidney disease (CKD) often experience a high accumulation of protein-bound uremic toxins (PBUTs), specifically indoxyl sulfate (IS) and p-cresyl sulfate (pCS). In the early stages of CKD, the buildup of PBUTs inhibits bone and muscle function. As CKD progresses, elevated PBUT levels further hinder bone turnover and exacerbate muscle wasting. In the late stage of CKD, hyperparathyroidism worsens PBUT-induced muscle damage but can improve low bone turnover. PBUTs play a significant role in reducing both the quantity and quality of bone by affecting osteoblast and osteoclast lineage. IS, in particular, interferes with osteoblastogenesis by activating aryl hydrocarbon receptor (AhR) signaling, which reduces the expression of Runx2 and impedes osteoblast differentiation. High PBUT levels can also reduce calcitriol production, increase the expression of Wnt antagonists (SOST, DKK1), and decrease klotho expression, all of which contribute to low bone turnover disorders. Furthermore, PBUT accumulation leads to continuous muscle protein breakdown through the excessive production of reactive oxygen species (ROS) and inflammatory cytokines. Interactions between muscles and bones, mediated by various factors released from individual tissues, play a crucial role in the mutual modulation of bone and muscle in CKD. Exercise and nutritional therapy have the potential to yield favorable outcomes. Understanding the underlying mechanisms of bone and muscle loss in CKD can aid in developing new therapies for musculoskeletal diseases, particularly those related to bone loss and muscle wasting.

Indexed as

bone losschronic kidney diseaseindoxyl sulfatesarcopeniauremic toxins

Identifiers

PMID37509715
PMCPMC10377042
OpenAlexW4385213254

What OpenQuestion 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 OpenQuestion graph.