ArticleCommunications medicine2023
Proteomic characterization of acute kidney injury in patients hospitalized with SARS-CoV2 infection.
Article in Communications medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- The significance of matrix remodeling associated 7 (MXRA7) in pathogenesis or management of renal diseases deserves more investigations.Renal failure · 2025Article
- Liquid Biopsy-Multiomics Link Adhesion Pathway Dysregulation to Kidney Injury Severity.Kidney international reports · 2025Article
- The peptidoglycan ofScience translational medicine · 2025Article
- Peripheral Transcriptomics in Acute and Long-Term Kidney Dysfunction in SARS-CoV-2 Infection.Kidney360 · 2025Article
- New approaches to acute kidney injury.Clinical kidney journal · 2024Article
- Proteomics and Incident Kidney Failure in Individuals With CKD: The African American Study of Kidney Disease and Hypertension and the Boston Kidney Biopsy Cohort.Kidney medicine · 2024Article
- Brain-wide alterations revealed by spatial transcriptomics and proteomics in COVID-19 infection.Nature aging · 2024Article
- Risk of acute kidney injury in critically-ill patients with COVID-19 compared with seasonal influenza: a retrospective cohort study.EClinicalMedicine · 2024Article
- Proteomic profiling of peripheral blood mononuclear cells reveals immune dysregulation and metabolic alterations in kidney transplant recipients with COVID-19.Frontiers in immunology · 2024Article
- Kidney Disease and Proteomics: A Recent Overview of a Useful Tool for Improving Early Diagnosis.Advances in experimental medicine and biology · 2024Article
- Multi-omics Approach in Kidney Transplant: Lessons Learned from COVID-19 Pandemic.Current transplantation reports · 2023Article
- Acyl coenzyme A binding protein (ACBP): An aging- and disease-relevant "autophagy checkpoint".Aging cell · 2023Review
- Kidney Injury in Critically Ill Patients with COVID-19 - From Pathophysiological Mechanisms to a Personalized Therapeutic Model.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2023Review
- Circulating proteins to predict COVID-19 severity.Scientific reports · 2023Article
- Multi-omics identify falling LRRC15 as a COVID-19 severity marker and persistent pro-thrombotic signals in convalescence.Nature communications · 2022Article
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Authors and funding
43 authors at 8 institutions in 4 countries.
Funding
Abstract
backgroundAcute kidney injury (AKI) is a known complication of COVID-19 and is associated with an increased risk of in-hospital mortality. Unbiased proteomics using biological specimens can lead to improved risk stratification and discover pathophysiological mechanisms.
methodsUsing measurements of ~4000 plasma proteins in two cohorts of patients hospitalized with COVID-19, we discovered and validated markers of COVID-associated AKI (stage 2 or 3) and long-term kidney dysfunction. In the discovery cohort (N = 437), we identified 413 higher plasma abundances of protein targets and 30 lower plasma abundances of protein targets associated with COVID-AKI (adjusted p < 0.05). Of these, 62 proteins were validated in an external cohort (p < 0.05, N = 261).
resultsWe demonstrate that COVID-AKI is associated with increased markers of tubular injury (NGAL) and myocardial injury. Using estimated glomerular filtration (eGFR) measurements taken after discharge, we also find that 25 of the 62 AKI-associated proteins are significantly associated with decreased post-discharge eGFR (adjusted p < 0.05). Proteins most strongly associated with decreased post-discharge eGFR included desmocollin-2, trefoil factor 3, transmembrane emp24 domain-containing protein 10, and cystatin-C indicating tubular dysfunction and injury.
conclusionsUsing clinical and proteomic data, our results suggest that while both acute and long-term COVID-associated kidney dysfunction are associated with markers of tubular dysfunction, AKI is driven by a largely multifactorial process involving hemodynamic instability and myocardial damage.
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Registered trials
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