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Molecular Mechanisms and Biomarkers Associated with Chemotherapy-Induced AKI
Letizia De Chiara1, Gianmarco Lugli1,2, Gianluca Villa3
1Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, 50139 Florence, Italy.
Abstract:
Acute kidney injury (AKI) is a life-threatening condition characterized by a rapid and transient decrease in kidney function. AKI is part of an array of conditions collectively defined as acute kidney diseases (AKD). In AKD, persistent kidney damage and dysfunction lead to chronic kidney disease (CKD) over time. A variety of insults can trigger AKI; however, chemotherapy-associated nephrotoxicity is increasingly recognized as a significant side effect of chemotherapy. New biomarkers are urgently needed to identify patients at high risk of developing chemotherapy-associated nephrotoxicity and subsequent AKI. However, a lack of understanding of cellular mechanisms that trigger chemotherapy-related nephrotoxicity has hindered the identification of effective biomarkers to date. In this review, we aim to (1) describe the known and potential mechanisms related to chemotherapy-induced AKI; (2) summarize the available biomarkers for early AKI detection, and (3) raise awareness of chemotherapy-induced AKI.
Insights
Chemotherapy can cause acute kidney injury (AKI), a serious condition. Understanding its mechanisms and identifying new biomarkers are crucial for early detection and patient risk assessment.
Area of Science:
- Nephrology
- Oncology
- Pharmacology
Background:
- Acute kidney injury (AKI) is a critical condition involving rapid kidney function decline.
- Chemotherapy-associated nephrotoxicity is a growing concern, potentially leading to chronic kidney disease (CKD).
- Current understanding of chemotherapy-induced AKI mechanisms is limited, hindering biomarker development.
Purpose of the Study:
- To review the mechanisms of chemotherapy-induced AKI.
- To summarize current biomarkers for early AKI detection.
- To increase awareness of chemotherapy-related kidney damage.
Main Methods:
- Literature review of existing studies on chemotherapy-induced nephrotoxicity.
- Analysis of cellular mechanisms contributing to AKI.
- Compilation of data on established and emerging AKI biomarkers.
Main Results:
- Chemotherapy poses a significant risk for AKI, necessitating further research into underlying mechanisms.
- Early detection of AKI is challenged by a lack of specific biomarkers.
- Further investigation into cellular pathways is vital for identifying effective biomarkers.
Conclusions:
- Chemotherapy-induced AKI is a serious clinical issue requiring better diagnostic tools.
- Identifying novel biomarkers is essential for managing patients undergoing chemotherapy.
- Enhanced understanding of mechanisms will improve AKI prediction and prevention.
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