Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (771 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; acute kidney tubular necrosis; and other less severe conditions.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Acute Kidney Injuries; Kidney Injuries, Acute; Kidney Injury, Acute; Acute Renal Injury; Acute Renal Injuries; Renal Injuries, Acute; Renal Injury, Acute; Kidney Failure, Acute.
Where it fits in the MeSH classification
- Broader topics
- Renal Insufficiency
- Narrower topics
- Kidney Tubular Necrosis, Acute
Related concepts
- Acute Kidney Tubular Necrosis
Research landscape
PubMed indexes 65,249 records tagged with the MeSH heading “Acute Kidney Injury” (counts retrieved 2026-11-04). 18,938 of them (29.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 20,139 records.
Reviews account for 9,600 records (14.7%) and meta-analyses for 1,003. Randomized controlled trials number 1,372 (2.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 20,139 |
| 2000-2009 | 7,362 |
| 2010-2019 | 18,810 |
| 2020 onward | 18,938 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 9,600 | 14.7% |
| Meta-analyses | 1,003 | 1.5% |
| Randomized controlled trials | 1,372 | 2.1% |
Method: PubMed query "Acute Kidney Injury"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in kidney, urology and women's health
Kidney, urinary and reproductive health research uses lab markers (such as creatinine), imaging, symptom scores and registry data on pregnancy and birth. Findings about pregnancy are especially sensitive to who was studied and when in pregnancy exposure occurred. Nothing on this page is advice about treatment, fertility or pregnancy; speak to a qualified clinician. Check the population, the outcome measured and whether the study accounted for other health differences between groups.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Cefazolin for Methicillin-Susceptible Staphylococcus aureus Bacteremia | 2026 | Randomized controlled trial Design not recorded in structured metadata | 12 | cc by PMID 42308484 · DOI · PMC7619232 |
| Gut microbiota and sepsis-associated acute kidney injury: a narrative review | 2026 | Review article Design not recorded in structured metadata | 2 | cc by PMID 42311675 · DOI · PMC13268904 |
| Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage | 2026 | Review article Design not recorded in structured metadata | 2 | cc by PMID 42253993 · DOI · PMC13236535 |
Cefazolin for Methicillin-Susceptible Staphylococcus aureus Bacteremia [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundStaphylococcus aureus bacteremia is associated with high mortality.
- Closing excerpt
- ).
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (268 words)
BackgroundStaphylococcus aureus bacteremia is associated with high mortality. Whether cefazolin or an antistaphylococcal penicillin should be preferred for the treatment of methicillin-susceptible S. aureus bacteremia is unclear.MethodsIn an ongoing international Bayesian adaptive platform trial, we conducted an open-label, randomized comparison of cefazolin with an antistaphylococcal penicillin (flucloxacillin or cloxacillin) in adult patients with penicillin-resistant, methicillin-susceptible S. aureus bacteremia. The primary outcome, which was evaluated with a hierarchical Bayesian logistic-regression model, was death from any cause within 90 days after enrollment in the platform. We assessed the posterior probability of the noninferiority of cefazolin to flucloxacillin or cloxacillin (with the criterion for noninferiority prespecified as an adjusted odds ratio of ResultsThis domain of the ongoing trial was conducted between February 17, 2022, and August 7, 2024, by which time the criterion for noninferiority had been met. Mortality at 90 days among adults who could be evaluated was 15.0% (97 deaths among 645 patients) in the cefazolin group and 17.0% (109 deaths among 642 patients) in the antistaphylococcal-penicillin group (adjusted odds ratio, 0.81; 95% credible interval, 0.59 to 1.12; probability of noninferiority, 99.2%; probability of superiority, 89.8%). Acute kidney injury occurred in 92 of 660 patients (13.9%) in the cefazolin group, as compared with 127 of 648 (19.6%) in the antistaphylococcal-penicillin group (adjusted odds ratio, 0.67; 95% credible interval, 0.50 to 0.89; probability of superiority, 99.7%).ConclusionsIn patients with methicillin-susceptible S. aureus bacteremia, cefazolin was noninferior to flucloxacillin or cloxacillin with respect to 90-day mortality and was associated with a lower incidence of acute kidney injury. (Funded by the National Health and Medical Research Council and others; SNAP ClinicalTrials.gov number, NCT05137119.).
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42308484 · DOI · PMC7619232
Gut microbiota and sepsis-associated acute kidney injury: a narrative review [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundSepsis-associated acute kidney injury (SA-AKI) carries high morbidity and mortality, yet its pathogenesis remains incompletely understood.
- Closing excerpt
- The intestine-kidney crosstalk may provide a basis for the treatment of sepsis-induced organ injury and also provide new ideas for the treatment of SA-AKI.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (275 words)
BackgroundSepsis-associated acute kidney injury (SA-AKI) carries high morbidity and mortality, yet its pathogenesis remains incompletely understood. Emerging evidence underscores the gut-kidney axis as a critical pathway in SA-AKI development.ObjectiveThis review aims to synthesize current knowledge on how sepsis-driven gut dysbiosis compromises intestinal barrier integrity and contributes to SA-AKI, and to explore potential therapeutic strategies targeting the gut microbiota.MethodsA comprehensive literature search was conducted in PubMed, Web of Science, and Scopus databases for publications between 2005 and 2026. Studies focusing on gut-kidney crosstalk mechanisms in sepsis/AKI were included. Key findings from human and animal studies were summarized.ResultsSepsis induces marked gut dysbiosis characterized by loss of microbial diversity and expansion of pathobionts. This dysbiosis compromises intestinal barrier integrity, facilitating translocation of bacterial products such as lipopolysaccharide (LPS). Upon entering circulation, these mediators activate systemic inflammation and renal signaling cascades, including the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway, leading to tubular injury and impaired renal function. Recent human metagenomic studies have identified specific microbial signatures associated with AKI, such as increased Clostridium asparagiforme and decreased Roseburia spp., alongside elevated uremic toxin-producing bacteria like Gordonibacter pamelaeae. Additionally, gut-derived metabolites including indoxyl sulfate, p-cresol sulfate, and trimethylamine N-oxide (TMAO) have been implicated in promoting renal inflammation and fibrosis. Importantly, renal dysfunction further disrupts gut homeostasis, establishing a pathological gut-kidney feedback loop. Targeting the gut-kidney axis via fecal microbiota transplantation, probiotic supplementation, or short-chain fatty acid administration may offer novel therapeutic avenues.ConclusionsSepsis induces gut microbiota dysregulation play an important role in the development of SA-AKI. The intestine-kidney crosstalk may provide a basis for the treatment of sepsis-induced organ injury and also provide new ideas for the treatment of SA-AKI.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42311675 · DOI · PMC13268904
Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Acute kidney injury (AKI) is a common clinical syndrome characterized by substantial etiologic heterogeneity, whose pathophysiology encompasses inflammatory amplification, microcirculatory dysfunction, tubular injury, and maladaptive repair.
- Closing excerpt
- This review summarizes the dynamic regulatory network of complement activation and its pathogenic mechanisms across diverse AKI etiologies, providing an integrative framework for biomarker-guided stratification and precision therapy in AKI.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (228 words)
Acute kidney injury (AKI) is a common clinical syndrome characterized by substantial etiologic heterogeneity, whose pathophysiology encompasses inflammatory amplification, microcirculatory dysfunction, tubular injury, and maladaptive repair. Evidence from preclinical models and clinical samples indicates that dysregulated complement activation represents a potential convergent mechanism of injury in multiple forms of AKI, although its relative contribution varies across etiologies. Experimental models support mechanistic and pathogenic roles for complement activation, whereas clinical evidence in many AKI settings remains largely associative, suggesting a contributory rather than universally causal role. Diverse insults, including ischemia-reperfusion injury, nephrotoxins, and sepsis, can initiate complement activation, which converges on C3 and C5, fueling inflammatory escalation and tissue injury. In addition to cytotoxicity mediated by the terminal pathway, the complement system participates in the initiation, progression, and outcome of injury by orchestrating endothelial activation, leukocyte recruitment, tubular epithelial stress, and innate immune amplification. Concurrently, dysregulation of complement regulatory proteins, persistent activation of the C5a/C5aR axis, and crosstalk with Toll-like receptor signaling and neutrophil extracellular trap (NET) formation further amplify the damaging effects, thereby exacerbating AKI progression. Moreover, complement activation exhibits pronounced spatiotemporal heterogeneity, with its pathogenic effects shaped by the renal compartment, injury stage, and persistence of activation. This review summarizes the dynamic regulatory network of complement activation and its pathogenic mechanisms across diverse AKI etiologies, providing an integrative framework for biomarker-guided stratification and precision therapy in AKI.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42253993 · DOI · PMC13236535
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Impact of diabetes on the effects of sodium glucose co-transporter-2 inhibitors on kidney outcomes: collaborative meta-analysis of large placebo-controlled trials [4]
- Research article Comparison of machine learning and logistic regression models in predicting acute kidney injury: A systematic review and meta-analysis [5]
- Research article Acute kidney injury and adverse renal events in patients receiving SGLT2-inhibitors: A systematic review and meta-analysis [6]
- Research article Rates, predictors, and mortality of sepsis-associated acute kidney injury: a systematic review and meta-analysis [7]
- Research article Risk factors and prognosis for COVID-19-induced acute kidney injury: a meta-analysis [8]
- Research article Comparative accuracy of biomarkers for the prediction of hospital-acquired acute kidney injury: a systematic review and meta-analysis [9]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Pregnancy-related acute kidney injury in the African continent: where do we stand? A systematic review
Ahmed Saad Shalaby, Rasha Samir Shemies · Journal of Nephrology 2022 · CC BY 4.0
References
- Staphylococcus aureus Network Adaptive Platform (SNAP) Trial Group, Lee TC, Barina LA, Walls G, Goodman AL, Yahav D, et al.. Cefazolin for Methicillin-Susceptible Staphylococcus aureus Bacteremia. . 2026. PMID 42308484 · DOI · PMC7619232
- Zhang H, Fan B, Ma R, Jiang R, Qin Z, Qu X, et al.. Gut microbiota and sepsis-associated acute kidney injury: a narrative review. . 2026. PMID 42311675 · DOI · PMC13268904
- Yi D, Yang R, Guo Y, Zhou H, Luan J. Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage. . 2026. PMID 42253993 · DOI · PMC13236535
- Nuffield Department of Population Health Renal Studies Group, SGLT2 inhibitor Meta-Analysis Cardio-Renal Trialists' Consortium. Impact of diabetes on the effects of sodium glucose co-transporter-2 inhibitors on kidney outcomes: collaborative meta-analysis of large placebo-controlled trials. Lancet. 2022. PMID 36351458 · DOI · PMC7613836
- Song X, Liu X, Liu F, Wang C. Comparison of machine learning and logistic regression models in predicting acute kidney injury: A systematic review and meta-analysis. Int J Med Inform. 2021. PMID 33991886 · DOI
- Menne J, Dumann E, Haller H, Schmidt BMW. Acute kidney injury and adverse renal events in patients receiving SGLT2-inhibitors: A systematic review and meta-analysis. PLoS Med. 2019. PMID 31815931 · DOI · PMC6901179
- Liu J, Xie H, Ye Z, Li F, Wang L. Rates, predictors, and mortality of sepsis-associated acute kidney injury: a systematic review and meta-analysis. BMC Nephrol. 2020. PMID 32736541 · DOI · PMC7393862
- Lin L, Wang X, Ren J, Sun Y, Yu R, Li K, et al.. Risk factors and prognosis for COVID-19-induced acute kidney injury: a meta-analysis. BMJ Open. 2020. PMID 33172950 · DOI · PMC7656886
- Pan HC, Yang SY, Chiou TT, Shiao CC, Wu CH, Huang CT, et al.. Comparative accuracy of biomarkers for the prediction of hospital-acquired acute kidney injury: a systematic review and meta-analysis. Crit Care. 2022. PMID 36371256 · DOI · PMC9652605
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.