Anthracycline-induced cardiorenal toxicity: from molecular mechanisms to clinical management

In oncology clinics, anthracyclines remain a cornerstone of cancer therapy. However, their clinical benefits are accompanied by substantial toxicities. As cumulative exposure increases and patient survival improves, the incidence of treatment-related adverse effects also increases, particularly those affecting the heart and kidneys. Rather than existing in isolation, these two forms of damage often interact: impaired cardiac function can accelerate renal injury through hemodynamic changes and neuroendocrine activation, whereas renal dysfunction further exacerbates cardiac injury via toxin accumulation and inflammation. This interaction leads to the well-recognized cardiorenal vicious cycle, which substantially limits the safe use of anthracyclines in clinical practice. Although dexrazoxane is currently the only approved cardioprotective agent, its renoprotective effect remains limited. Moreover, there are no clear guidelines or standardized strategies for preventing or managing anthracycline-induced cardiorenal toxicity. Therefore, a deeper understanding of the underlying mechanisms, along with effective monitoring and intervention strategies, is crucial for optimizing anthracycline therapy and improving patient survival. This review explores the pathological basis, molecular mechanisms, risk factors, monitoring approaches, and treatment strategies related to anthracycline-induced cardiorenal toxicity. It aims to develop a comprehensive strategy to protect both cardiac and renal function and to provide a scientific foundation for the development of safer and more effective cancer treatment regimens.