Iron and acute kidney injury: potential biomarkers for diagnosis and therapy

Acute kidney injury (AKI) is characterized by a rapid decline in renal excretory function and is associated with increased mortality and an elevated risk of developing or progressing to chronic kidney disease (CKD), posing a significant global public health challenge. Conventional assessment relies heavily on serum creatinine (SCr) and blood urea nitrogen (BUN), which have limitations in detecting early kidney injury. This review aims to elucidate the roles of iron metabolism and ferroptosis in AKI and evaluate the potential of iron-related proteins as biomarkers and therapeutic targets.

This review summarizes the molecular mechanisms regulating iron acquisition, storage, and efflux, examines the involvement of iron dysregulation and ferroptosis in AKI pathophysiology, and discusses the potential applications of iron-related proteins in AKI diagnosis, prognostic assessment, and therapeutic intervention.

Ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, is closely implicated in the onset and progression of AKI. Dysregulated iron homeostasis contributes to oxidative stress, mitochondrial dysfunction, inflammatory responses, and renal cellular injury. Emerging evidence suggests that iron-related proteins may serve as promising biomarkers for early AKI detection and prognostic monitoring, while also providing potential molecular targets for therapeutic intervention.

Iron metabolism dysregulation and ferroptosis play important roles in AKI pathophysiology. Iron-related proteins represent promising candidates for improving early diagnosis, prognostic evaluation, and targeted treatment of AKI. Further investigation and clinical validation are needed to establish their diagnostic and therapeutic utility.