ArticleOxidative medicine and cellular longevity2018
Urinary Mitochondrial DNA Identifies Renal Dysfunction and Mitochondrial Damage in Sepsis-Induced Acute Kidney Injury.
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05458063 (The Effectiveness of the Urine Mitochondrial Deoxyribonucleic Acid and, Serum Beta 2 Microglobulin as a Biomarker of Renal Function Impairment in Critically Ill Surgical Patients), which is not on this map. Cited by 44 papers, 2 of them syntheses that pooled it.
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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.
The Effectiveness of the Urine Mitochondrial Deoxyribonucleic Acid and, Serum Beta 2 Microglobulin as a Biomarker of Renal Function Impairment in Critically Ill Surgical Patients
Who cites it
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations.Mitochondrion · 2021Pooled it
- Rates, predictors, and mortality of sepsis-associated acute kidney injury: a systematic review and meta-analysis.BMC nephrology · 2020Pooled it
- IgA nephropathy is associated with elevated urinary mitochondrial DNA copy numbers.Scientific reports · 2019Trial
- Efficacy of nicotiflorin in ameliorating septic acute kidney injury: the role of PINK1/parkin in mitochondrial restoration and oxidative stress reduction.Renal failure · 2026Article
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- Predictive value of miR-151a-3p for the onset of sepsis-induced acute kidney injury and its functional role during disease development.BMC immunology · 2026Article
- Transcriptomics reveal dysregulated genes during folic acid-induced acute injury and fibrosis in kidney and their attenuation by antioxidantAmerican journal of physiology. Cell physiology · 2026Article
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- NMR-based urinary biomarkers in pediatric primary mitochondrial disorders and chronic kidney disease: shared mitochondrial dysfunction, diverging biosignatures.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Temporal dynamics of IgG-mediated immunometabolic dysfunction: from acute obesity to chronic aging.Frontiers in immunology · 2025Review
- Mitochondrial dysfunction in acute and post-acute phases of COVID-19 and risk of non-communicable diseases.npj metabolic health and disease · 2024Review
- Irisin-Encapsulated Mitochondria-Targeted Biomimetic Nanotherapeutics for Alleviating Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cell-free DNA in patients with sepsis: long term trajectory and association with 28-day mortality and sepsis-associated acute kidney injury.Frontiers in immunology · 2024Article
- Effects of cell-free DNA on kidney disease and intervention strategies.Frontiers in pharmacology · 2024Review
- Melatonin attenuates sepsis-induced acute kidney injury by promoting mitophagy through SIRT3-mediated TFAM deacetylation.Autophagy · 2024Article
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Dynamics of Urinary Extracellular DNA in Urosepsis.Biomolecules · 2023Article
- The protective effect of H151, a novel STING inhibitor, in renal ischemia-reperfusion-induced acute kidney injury.American journal of physiology. Renal physiology · 2023Article
- Mitofilin Heterozygote Mice Display an Increase in Myocardial Injury and Inflammation after Ischemia/Reperfusion.Antioxidants (Basel, Switzerland) · 2023Article
- BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils.The Journal of clinical investigation · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent animal studies have shown that mitochondrial dysfunction initiates and accelerates renal injury in sepsis, but its role in sepsis remains unknown. Mitochondrial stress or dying cells can lead to fragmentation of the mitochondrial genome, which is considered a surrogate marker of mitochondrial dysfunction. Therefore, we evaluated the efficiency of urinary mitochondrial DNA (UmtDNA) as a marker of renal dysfunction during sepsis-induced acute kidney injury (AKI).
methodsWe isolated DNA from plasma and urine of patients. mtDNA levels were quantified by quantitative PCR. Sepsis patients were divided into no AKI, mild AKI, and severe AKI groups according to RIFLE criteria. Additionally, cecal ligation and puncture (CLP) was established in rats to evaluate the association between UmtDNA and mitochondrial function.
resultsA total of 52 (49.5%) developed AKI among enrolled sepsis patients. Increased systemic mtDNA did not correlate with systemic inflammation or acute renal dysfunction in sepsis patients, while AKI did not have an additional effect on circulating mtDNA levels. In contrast, UmtDNA was significantly enriched in severe AKI patients compared with that in the mild AKI or no AKI group, positively correlated with plasma creatinine, urinary neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1, and inversely with the estimated glomerular filtration rate. Additionally, UmtDNA increased in rats following CLP-induced sepsis. UmtDNA was predictive of AKI development and correlated with plasma creatinine and blood urea nitrogen in the rat sepsis model. Finally, the UmtDNA level was inversely correlated with the cortical mtDNA copy number and relative expression of mitochondrial gene in the kidney.
conclusionAn elevated UmtDNA level correlates with mitochondrial dysfunction and renal injury in sepsis patients, indicating renal mitochondrial injury induced by sepsis. Therefore, UmtDNA may be regarded as a valuable biomarker for the occurrence of AKI and the development of mitochondria-targeted therapies following sepsis-induced AKI.
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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.