ArticleMolecular and cellular biochemistry2025
Impairment of platelet mitochondrial respiration in patients with chronic kidney disease with and without diabetes.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Platelet mitochondria dysfunction in diabetes mellitus: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Effect of Imeglimin on mitochondrial function in patients with type 2 diabetes mellitus: a prospective cohort study.Frontiers in endocrinology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Chronic kidney disease (CKD) and diabetic kidney disease (DKD) are major public health problems, and their burden is growing relentlessly with the aging of the global population. Their early recognition is now a public health priority, and there is an unmet need for the identification of specific biomarkers in minimally invasive or non-invasive samples. Mitochondrial dysfunction plays a pivotal role in the development and progression of both CKD and DKD and circulating platelets have emerged as an ideal candidate for the assessment of the respiratory function. The present study assessed mitochondrial respiration in platelets isolated from the peripheral blood of patients with DKD and CKD compared to healthy controls. The study included a total number of 89 subjects, as follows: 30 DKD patients divided into three subgroups based on the urinary albumin-to-creatinine ratio (uACR): 20 normoalbuminuric, 10 microalbuminuric, and 10 macroalbuminuric, 29 CKD patients (positive controls) and 20 healthy individuals (negative controls). Platelets were isolated by differential centrifugations and a high-resolution respirometry protocol was adapted to assess mitochondrial respiration dependent on complex I (CI) and complex II (CII). A significant reduction of the CI-supported active respiration was found in the normoalbuminuric DKD patients and further decreased in the microalbuminuric DKD subgroup. Both CI and CII-dependent coupled respiration and the maximal uncoupled respiration were significantly reduced in the macroalbuminuric DKD subgroup. In conclusion, mitochondrial respiration impairment in peripheral platelets is evident from the early stages of DKD. Moreover, platelet mitochondrial respiration was more severely impaired in patients with macroalbuminuric DKD as compared to those with CKD. Further, more extensive follow-up studies are warranted to determine whether platelet respiratory mitochondrial dysfunction could serve as a peripheral biomarker for kidney mitochondrial dysfunction and/or as a prognostic tool in DKD.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.