ReviewPediatric nephrology (Berlin, Germany)2018
A review of the role of immune cells in acute kidney injury.
Review in Pediatric nephrology (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
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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.
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Who cites it
76 citing papers in PubMed, 115 citations in OpenAlex.
- Avidity-controlled biotherapeutic delivery systems for the treatment of ischemia-reperfusion acute kidney injury.bioRxiv : the preprint server for biology · 2026Article
- The Influence of SGLT2 Inhibitors on the Immune System and Inflammatory Processes in Kidney Transplantation.International journal of molecular sciences · 2026Review
- Systemic immune-inflammation index (SII): a predictor of mortality risk in pediatric acute kidney injury.Pediatric research · 2026Article
- The role of protein prenylation in kidney diseases: Molecular basis and therapeutic implications.Molecular biology reports · 2026Review
- Effects of Folate and Fructose Intakes on Renal Cytokines and Fibrosis in an Adenine-Induced Mouse Model of Chronic Kidney Disease.International journal of molecular sciences · 2026Article
- Biodegradable ROS-Responsive TPCD Nanoparticles Mitigate Cisplatin-Induced Acute Kidney Injury via Synergistic Antioxidant and Immunomodulatory Actions.International journal of nanomedicine · 2026Article
- Diagnostic PANoptosis-related genes in acute kidney injury: bioinformatics, machine learning, and validation.Annals of medicine · 2025Article
- Review
- Effect of sevoflurane-based or propofol-based anesthesia on acute kidney injury after surgery for gastric cancer: a retrospective propensity score-matched analysis.BMC anesthesiology · 2025Article
- Modulatory role of radioprotective 105 in mitigating oxidative stress and ferroptosis via the HO-1/SLC7A11/GPX4 axis in sepsis-mediated renal injury.Cell death discovery · 2025Article
- Article
- Advances in Nano-Immunomodulatory Systems for the Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- ET-3/ETBR Mediates NaCirculation research · 2025Article
- Article
- Remote limb ischemic pre-conditioning prevents renal Ischemia/reperfusion injury in rats by modulating oxidative stress and TNF-α/NF-κB/TGF-/βapelin signaling pathway.Molecular biology reports · 2024Article
- CD8 + CD103 + iTregs protect against ischemia-reperfusion-induced acute kidney Injury by inhibiting pyroptosis.Apoptosis : an international journal on programmed cell death · 2024Article
- Combined Plasma Olink Proteomics and Transcriptomics Identifies CXCL1 and TNFRSF12A as Potential Predictive and Diagnostic Inflammatory Markers for Acute Kidney Injury.Inflammation · 2024Article
- Crosstalk among proximal tubular cells, macrophages, and fibroblasts in acute kidney injury: single-cell profiling from the perspective of ferroptosis.Human cell · 2024Article
- Traditional Chinese Medicine and renal regeneration: experimental evidence and future perspectives.Chinese medicine · 2024Review
- Mesoscale size-promoted targeted therapy for acute kidney injury through combined RONS scavenging and inflammation alleviation strategy.Materials today. Bio · 2024Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a systemic disease occurring commonly in patients who are critically ill. Etiologies of AKI can be septic or aseptic (nephrotoxic, or ischemia-reperfusion injury). Recent evidence reveals that innate and adaptive immune responses are involved in mediating damage to renal tubular cells and in recovery from AKI. Dendritic cells, monocytes/macrophages, neutrophils, T lymphocytes, and B lymphocytes all contribute to kidney injury. Conversely, M2 macrophages and regulatory T cells are essential in suppressing inflammation, tissue remodeling and repair following kidney injury. AKI itself confers an increased risk for developing infection owing to increased production and decreased clearance of cytokines, in addition to dysfunction of immune cells themselves. Neutrophils are the predominant cell type rendered dysfunctional by AKI. In this review, we describe the bi-directional interplay between the immune system and AKI and summarize recent developments in this field of research.
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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.