ReviewPflugers Archiv : European journal of physiology2022
Metabolic mechanisms of acute proximal tubular injury.
Review in Pflugers Archiv : European journal of physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Lactate in acute kidney injury: pathobiology, risk stratification, and clinical interpretation.Renal failure · 2026Review
- Discovery urinary metabolomics of preterm neonatal acute kidney injury.Pediatric nephrology (Berlin, Germany) · 2026Observational
- Redox-Mediated Mitochondrial Dysfunction as a Common Pathogenic Axis in Acute Kidney Injury and Chronic Kidney Disease.Biomolecules · 2026Review
- Arginase-1 Expressing Macrophages Interact with Myofibroblasts to Regulate Insulin-Like Growth Factor-1-Dependent Tubule Repair.Kidney360 · 2026Article
- Single-cell analysis reveals that NRG1/3-ERBB4 signaling affects metabolic reprogramming and immune escape in Wilms tumor.Biology direct · 2026Article
- Pathophysiology and Management of Sepsis-associated Acute Kidney Injury.Clinics in chest medicine · 2026Review
- Optimization of M1 macrophage targeting using a glucosylated albumin nanoplatform for ROS scavenging and mitochondrial rescue in acute kidney injury.Journal of nanobiotechnology · 2026Article
- Selpercatinib-induced renal tubular damage resulting in symptomatic hyponatremia and polyuria: a case report.Cancer chemotherapy and pharmacology · 2026Article
- Arsenic trioxide-induced acute kidney injury: OPA1- and Drp1-mediated mitochondrial dynamics imbalance, PINK1/Parkin-dependent mitophagy, and Chuanhuang Fang III.Frontiers in molecular biosciences · 2026Article
- Osmotic Nephropathy Induced by L-Proline Stabilized Sucrose-free Intravenous Immunoglobulins: A Case Report.Kidney medicine · 2026Article
- SUL-138 mitigates accelerated endothelial aging and protects the kidney.Clinical science (London, England : 1979) · 2025Article
- Ultrastructural and Immunohistochemical Study on the Nephrotoxicity Following Intravitreal Administration of the Antifungal Agents Voriconazole and Micafungin in New Zealand White Rabbits.International journal of molecular sciences · 2025Article
- Metabolite-enhanced normothermic machine perfusion improves kidney transplant viability.JCI insight · 2025Article
- PPDPF preserves integrity of proximal tubule by modulating NMNAT activity in chronic kidney diseases.Science advances · 2025Article
- Activation of branched chain amino acid catabolism protects against nephrotoxic acute kidney injury.American journal of physiology. Renal physiology · 2025Article
- Mitochondrial dysfunction in acute kidney injury.Renal failure · 2024Review
- The impact of tubular dysfunction and its relationship with acute kidney injury in children.Pediatric nephrology (Berlin, Germany) · 2024Article
- CD44 expression in renal tubular epithelial cells in the kidneys of rats with cyclosporine-induced chronic kidney disease.Journal of toxicologic pathology · 2024Article
- Urinary Concentration of Renal Biomarkers in Healthy Term Neonates: Gender Differences in GST-pi Excretion.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Potential Biomarkers for the Earlier Diagnosis of Kidney and Liver Damage in Acute Intermittent Porphyria.Life (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage to the proximal tubule (PT) is the most frequent cause of acute kidney injury (AKI) in humans. Diagnostic and treatment options for AKI are currently limited, and a deeper understanding of pathogenic mechanisms at a cellular level is required to rectify this situation. Metabolism in the PT is complex and closely coupled to solute transport function. Recent studies have shown that major changes in PT metabolism occur during AKI and have highlighted some potential targets for intervention. However, translating these insights into effective new therapies still represents a substantial challenge. In this article, in addition to providing a brief overview of the current state of the field, we will highlight three emerging areas that we feel are worthy of greater attention. First, we will discuss the role of axial heterogeneity in cellular function along the PT in determining baseline susceptibility to different metabolic hits. Second, we will emphasize that elucidating insult specific pathogenic mechanisms will likely be critical in devising more personalized treatments for AKI. Finally, we will argue that uncovering links between tubular metabolism and whole-body homeostasis will identify new strategies to try to reduce the considerable morbidity and mortality associated with AKI. These concepts will be illustrated by examples of recent studies emanating from the authors' laboratories and performed under the auspices of the Swiss National Competence Center for Kidney Research (NCCR Kidney.ch).
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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 Socratic graph.