Contrast-induced acute kidney injury: from pathophysiology to risk prediction and prevention strategies

Area of Science:

• Nephrology
• Radiology
• Molecular Biology

Background:

• Contrast-induced acute kidney injury (CI-AKI) is a significant cause of hospital-acquired kidney damage, increasing mortality and morbidity.
• Iodinated contrast media (ICM) are increasingly used in diagnostics, necessitating a thorough understanding of CI-AKI.
• Despite decreased incidence, CI-AKI remains a critical clinical challenge.

Purpose of the Study:

• To review the complex pathophysiology of CI-AKI, including novel mechanisms like ferroptosis and neutrophil extracellular traps (NETs).
• To clarify procedural controversies regarding contrast administration routes and their impact on CI-AKI risk.
• To highlight emerging biomarkers and risk stratification models for CI-AKI management.

Main Methods:

• Literature review integrating molecular pathogenesis, procedural aspects, and biomarker research.
• Analysis of recent discoveries in CI-AKI mechanisms, including cellular pathways and molecular targets.
• Evaluation of existing risk stratification tools and their clinical utility.

Main Results:

• CI-AKI pathophysiology involves vasoconstriction, oxidative stress, hypoxia, inflammation, tubular toxicity, ferroptosis, and NETs.
• MicroRNAs (e.g., miR-30c, miR-21) show potential as biomarkers and therapeutic targets.
• Patient comorbidities and procedural complexity, not solely the route of administration, dictate CI-AKI risk.

Conclusions:

• Understanding CI-AKI's multifaceted pathogenesis is crucial for effective prevention strategies.
• Emerging biomarkers and refined risk models enhance patient stratification and management.
• Further research into novel mechanisms and targeted therapies is warranted to mitigate CI-AKI.