Acute kidney injury
Acute kidney injury (AKI) is a rapid deterioration in kidney function that can impair glomerular filtration and disturb fluid, electrolyte, and metabolic homeostasis.
Acute kidney injury (AKI) is a rapid deterioration in kidney function that can impair glomerular filtration and disturb fluid, electrolyte, and metabolic homeostasis. It is commonly evaluated using changes in serum creatinine level, estimated glomerular filtration rate, urine output, and related markers such as proteinuria or urine albumin-to-creatinine ratio. AKI may occur in association with sepsis, diabetes, rhabdomyolysis, surgery, transplantation, drug exposure, or renal ischemia-reperfusion injury.
The publication contexts supplied here examine AKI as both a clinical outcome and a biologically heterogeneous syndrome. The mechanisms under investigation include altered hemodynamics, endothelial dysfunction, inflammation, oxidative stress, reactive oxygen species, mitochondrial injury, apoptosis, and ferroptosis. Experimental work has also explored whether mesenchymal stem/stromal cells and mitochondrial transfer can modify the oxidative stress–inflammation axis, while clinical studies have focused on risk prediction using albuminuria, perioperative variables, machine learning, and adverse-event databases.
Rebuilt from PubMed 10 Sept 2026 · no new papers today
Where the papers sit
9 papers study acute kidney injury directly. Those 9 are one subject: Acute Kidney Injury Risk. Risk stratification centers on albuminuria, hemodynamics, hyperchloremia, creatine kinase, polypharmacy and CKD. Experimental work also tests endothelial and mitochondrial protection after ischemia-reperfusion. No way of splitting those 9 scores better than chance.
Recent Findings on acute kidney injury
A study in pregnant rats used renal ischemia-reperfusion as an experimental model of AKI to investigate whether the injury produces sustained endothelial dysfunction in peripheral, extrarenal vascular tissues and whether this dysfunction contributes to adverse pregnancy outcomes. It specifically examined delayed conception and sildenafil as potential approaches to prevent or mitigate the vascular consequences observed after renal ischemia-reperfusion 42530300Jul.
A prospective study of patients undergoing elective, isolated coronary artery bypass grafting evaluated whether the preoperative urine albumin-to-creatinine ratio predicts postoperative AKI and decline in kidney function. The analysis was designed to assess the magnitude of risk across clinically relevant urine albumin-to-creatinine ratio strata, linking proteinuria-related measures with postoperative renal outcomes 42598516Aug.
In adults with rhabdomyolysis and serum creatine kinase concentrations of at least 1000 IU/L within 72 hours of hospital admission, investigators examined the relationship between creatine kinase level, AKI, renal outcomes, and mortality. The study therefore addressed whether the biochemical severity of muscle injury, represented by creatine kinase, is associated with kidney injury and subsequent clinical outcomes 42287721Jun.
A pharmacovigilance and clinical safety analysis explored adverse drug events across single-drug exposure and combinations of two or three drugs. AKI was evaluated alongside gastrointestinal bleeding and opioid-related adverse events, placing kidney injury within a broader framework of potentially interacting medication-associated harms 42471477Jul.
A prediction-model study after orthotopic heart transplantation investigated whether perioperative hemodynamic indices could identify patients at risk of moderate-to-severe AKI. The model incorporated hemodynamic parameters in the context of major transplantation-related physiological stress, with the objective of improving early recognition of postoperative kidney injury 42264774Jun.
In elderly patients undergoing bipolar plasmakinetic transurethral resection of the prostate, a prospective observational study examined perioperative hyperchloremia and its association with AKI. The clinical setting included exposure to 0.9% saline irrigation, and the work addressed whether chloride disturbances during prostate resection are related to postoperative renal dysfunction 42189243May.
Another study developed and validated a machine-learning model for postoperative AKI in surgical patients with pre-existing chronic kidney disease. The use of SHAP-based explainability was intended to clarify the contribution of individual predictors, extending the AKI literature’s emphasis on estimated glomerular filtration rate, comorbidity, and perioperative risk stratification to patients with chronic renal impairment 42157597May.
A disproportionality analysis of the U.S. Food and Drug Administration Adverse Event Reporting System evaluated the potential association between dipeptidyl peptidase-4 inhibitor use and AKI in patients with diabetes mellitus. The study addressed a relationship described as controversial and used spontaneous-reporting data to investigate whether this class of antidiabetic drugs is disproportionately reported with AKI 42049410Apr.
Experimental research on ischemia-reperfusion injury investigated connexin 43-dependent mitochondrial transfer from mesenchymal stem/stromal cells. The proposed mechanism involved activation of PGC1α and disruption of the oxidative stress–inflammation axis, building on the reported anti-inflammatory potential of mesenchymal stem/stromal cells in AKI. The work also relates AKI to reactive oxygen species, mitochondrial biology, inflammation, and renal tubular cellular models such as HK-2 cells 42476966Jul.
Collectively, these publications extend the identified themes of diabetes and kidney-injury risk, hemodynamic prediction after heart transplantation, and perioperative hyperchloremia during prostate resection. They also open related areas not fully represented by those clusters, including pregnancy-associated vascular consequences of renal ischemia-reperfusion, rhabdomyolysis-associated AKI, medication combinations and pharmacovigilance, explainable machine learning in patients with chronic kidney disease, and cell-based modulation of oxidative and inflammatory injury.
Written from 9 PubMed abstracts, each one cited by PMID above. Published: 2026-09-02. Drafted by language models from published abstracts; not medical advice.