Evidence map›Paper›PMID 33790861›Full record

ArticleFrontiers in endocrinology2021

Metabolic Changes in Peripheral Blood Mononuclear Cells Isolated From Patients With End Stage Renal Disease.

Mehmet M Altintas, Salvatore DiBartolo, Lana Tadros, Beata Samelko, Haimanot Wasse

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06417307 (Supervised Exercise Therapy on Mitochondrial Functions of Platelet and Lymphocyte in Patients With End-Stage Renal Disease on Hemodialysis), which is not on this map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 13% 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.

NCT06417307 phase3completednot on this map

Supervised Exercise Therapy on Mitochondrial Functions of Platelet and Lymphocyte in Patients With End-Stage Renal Disease on Hemodialysis

TypeinterventionalSponsorChang Gung Memorial HospitalRan2021 to 2024Enrolled180ConditionsHemodialysis ComplicationArmsSupervised exercise training, Control group
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  6. AlteredExperimental biology and medicine (Maywood, N.J.) · 2025
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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

5 authors at 1 institution in 1 country.

Mehmet M AltintasDepartment of Internal Medicine, Division of Nephrology, Rush University Medical Center, Chicago, IL, United States.
Salvatore DiBartoloDepartment of Internal Medicine, Division of Nephrology, Rush University Medical Center, Chicago, IL, United States.
Lana TadrosDepartment of Internal Medicine, Division of Nephrology, Rush University Medical Center, Chicago, IL, United States.
Beata SamelkoDepartment of Internal Medicine, Division of Nephrology, Rush University Medical Center, Chicago, IL, United States.
Haimanot WasseDepartment of Internal Medicine, Division of Nephrology, Rush University Medical Center, Chicago, IL, United States.
Rush University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As numerous complex pathologies stem from cellular energy dysfunction, we aimed to elucidate mitochondrial function and associated stress pathologies in kidney disease in a cohort of hemodialysis patients with end-stage kidney disease (ESKD). The bioenergetics study was conducted using peripheral blood mononuclear cells (PBMCs) of ESKD patients (n = 29) and healthy controls (no ESKD, n = 10). PBMCs were isolated from whole blood and seeded into assay plates to detect changes in oxidative phosphorylation and glycolysis. The bioenergetics analysis (i.e., mitochondrial stress test) was performed using Seahorse XFe24 flux analyzer. We observed significant reduction in mitochondrial respiration in patient PBMCs in terms of fundamental bioenergetics parameters such as basal respiration, ATP turnover, maximal respiration and spare respiratory capacity. These findings were correlated with the expression levels of proteins coordinating cellular energy status and regulating mitochondrial dynamics. Our data demonstrates an association between mitochondrial oxygen consumption of PBMCs and ESKD. AMPK activity, its downstream effector PGC-1α and mitochondrial fission/fusion proteins are partially responsible for the decrease in oxidative phosphorylation of PBMCs isolated from ESKD patients. We propose a link between mitochondrial dysfunction and ESKD and a role for mitochondria as a potential site for therapeutic interventions.

Indexed as

Cell SeparationAdultAgedAged, 80 and overCarbon DioxideCase-Control StudiesCell RespirationEnergy MetabolismFemaleGlycolysisHumansKidney Failure, ChronicLactic AcidLeukocytes, MononuclearMaleMetabolic Flux AnalysisCarbon DioxideLactic AcidAMPKbioenergeticsESKDmitochondriaPBMCs

Identifiers

PMID33790861
PMCPMC8006313
OpenAlexW3135502736

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.