ArticleCritical care (London, England)2018
Kidney histopathology in lethal human sepsis.
Article in Critical care (London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Acute kidney injury and renal replacement therapy in COVID-19 patients: A systematic review and meta-analysis.International immunopharmacology · 2021Pooled it
- Article
- Urinary cell cycle arrest biomarkers TIMP-2 and IGFBP7 for the assessment of acute kidney injury in dogs with pyometra.Frontiers in veterinary science · 2026Article
- Sepsis-induced immunothrombosis: from cellular crosstalk to multiple organ dysfunction.Frontiers in immunology · 2026Review
- AMSC-EVs attenuate acute kidney injury through TXNIP-IKKα/NFκB signaling-mediated renal CX3CR1Stem cell research & therapy · 2025Article
- Sepsis-associated acute kidney injury in mice and humans elicits heterogeneous renal microvascular microRNA responses.Scientific reports · 2025Article
- Uncovering molecular markers of the microvascular endothelial response in sepsis-associated acute kidney injury: a translational study in mice and humans.Intensive care medicine experimental · 2025Article
- Complement Activation is More Pronounced in the Kidneys of Critically Ill Patients With COVID-19 Than in Those With Bacterial Sepsis.Kidney international reports · 2025Article
- Ablation of macrophage transcriptional factor FoxO1 protects against ischemia-reperfusion injury-induced acute kidney injury.Acta pharmaceutica Sinica. B · 2025Article
- Host Response Protein Biomarkers Indicative of Persistent Acute Kidney Injury in Critically Ill COVID-19 Patients.Critical care explorations · 2025Article
- Post-translational modifications in sepsis-induced acute kidney injury: mechanisms and perspectives.Frontiers in pharmacology · 2025Review
- Critical role of LncRNA in sepsis-associated acute kidney injury.Frontiers in pharmacology · 2025Review
- Obeticholic acid ameliorates sepsis-induced renal mitochondrial damage by inhibiting the NF-κb signaling pathway.Renal failure · 2024Article
- HBSP inhibits tubular cell pyroptosis and apoptosis, promotes macrophage M2 polarization, and protects LPS-induced acute kidney injury.Journal of cellular and molecular medicine · 2024Article
- The renoprotective effect of Tibolone in sepsis-induced acute kidney injury.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2024Article
- Renal tubular epithelial cells response to injury in acute kidney injury.EBioMedicine · 2024Review
- Clinical and histopathological characteristics of acute kidney injury in a cohort of brain death donors with procurement biopsies.Journal of nephrology · 2024Article
- Association between 24-hour urine volume and 28-day intensive care unit mortality in sepsis patients: a multi-center retrospective cohort study.Frontiers in medicine · 2024Article
- Regulatory networks of circRNA- centred ceRNAs in sepsis-induced acute kidney injury.Epigenetics · 2023Article
- Acute and chronic histopathological findings in renal biopsies in COVID-19.Clinical and experimental medicine · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe histopathology of sepsis-associated acute kidney injury (AKI) in critically ill patients remains an understudied area. Previous studies have identified that acute tubular necrosis (ATN) is not the only driver of sepsis-AKI. The focus of this study was to identify additional candidate processes that may drive sepsis-AKI. To do this we immunohistochemically characterized the histopathological and cellular features in various compartments of human septic kidneys.
methodsWe studied the following histopathological features: leukocyte subsets, fibroblast activation, cellular proliferation, apoptosis, and fibrin deposition in the glomerulus and the tubulointerstitium in human post-mortem kidney biopsy tissue. Biopsy tissue samples from 27 patients with sepsis-AKI were collected 33 min (range 24-150) after death in the ICU. The unaffected part of the kidneys from 12 patients undergoing total nephrectomy as a result of renal carcinoma served as controls.
resultsImmunohistochemical analysis revealed the presence of more neutrophils and macrophages in the glomeruli and more neutrophils in the tubulointerstitium of renal tissue from patients with sepsis compared to control renal tissue. Type II macrophages were predominant, with some macrophages expressing both type I and type II markers. In contrast, there were almost no macrophages found in control kidneys. The number of activated (myo)fibroblasts was low in the glomeruli of sepsis-AKI kidneys, yet this was not observed in the tubulointerstitium. Cell proliferation and fibrin deposition were more pronounced in the glomeruli and tubulointerstitium of sepsis-AKI than in control kidneys.
conclusionsThe extensive heterogeneity of observations among and within patients emphasizes the need to thoroughly characterize patients with sepsis-AKI in a large sample of renal biopsy tissue from patients with sepsis.
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