Acute kidney injury and energy metabolism

Acute kidney injury (AKI) predominantly affects hospitalized patients, particularly those in intensive care units, and has emerged as a significant global public health concern. Several factors, including severe cardiovascular disease, surgery-induced renal ischemia, nephrotoxic drugs, and sepsis, contribute to the development of AKI. Despite the implementation of various clinical strategies to prevent or treat AKI, its morbidity and mortality remain high, and there are no clinically effective therapeutic agents available. The limitations of traditional renal function markers (such as urine output, serum creatinine, and urea nitrogen levels), including their delayed response and insensitivity, underscore the urgent need for novel early biomarkers to facilitate the timely diagnosis of AKI. The proximal tubular epithelial cells in the kidney play a central role in both the onset and progression of AKI. These cells are highly metabolically active and have a substantial energy demand, primarily relying on fatty acid oxidation to meet their energy needs. Acylcarnitines are crucial in transporting fatty acids from the cytoplasm into the mitochondrial matrix for beta-oxidation, which generates energy essential for maintaining cellular function and viability. This review aims to summarize the current understanding of AKI, including its triggers, classification, underlying mechanisms, and potential biomarkers. Special emphasis is placed on the role of fatty acid and carnitine metabolism in AKI, with the goal of providing a theoretical foundation for future investigations into AKI mechanisms and the identification of early diagnostic biomarkers.