Paths to organ damage and risk factors in AKI

Acute kidney injury (AKI) is a multifactorial syndrome with a complex pathophysiology including different inflammatory cells and mediators. Current research focuses on identifying key contributing pathways, determining high-risk groups, characterizing AKI sub-phenotypes and investigating strategies for therapeutic interventions.

Key advances

• Experimental models and kidney biopsy samples from patients with acute kidney injury (AKI) suggest that T cell and neutrophil infiltration hinder kidney recovery and might be therapeutic targets to prevent post-AKI transition to chronic kidney disease.

• Osteopontin produced by tubule cells seems to contribute to the development of AKI-associated acute lung injury by mediating vascular leakage and inflammation through binding to its receptor CD44 in the lung.

• An updated risk score based on eight pre-procedural parameters has potential to identify patients at high risk of developing contrast-associated AKI after percutaneous coronary intervention.

• An intervention programme for cardiologists, which included clinical decision support with audit and feedback, was effective at reducing the incidence of AKI after coronary interventions (time-adjusted absolute risk reduction of 2.3%).

• In patients with cancer treated with immune checkpoint inhibitors (ICIs), the risk of ICI-associated AKI (ICI-AKI) was highest in patients with impaired kidney function at baseline, those receiving proton pump inhibitors or those with extrarenal immune-related adverse events; two-thirds of patients recovered kidney function after ICI-AKI.