Biomarkers for Early Detection of Cisplatin-Induced Nephrotoxicity

Nephrotoxicity is a common complication during antineoplastic therapy, particularly when platinum-based medications are used. Early detection of this condition is crucial for improving risk stratification and management, thereby enhancing decision-making in kidney disease treatment. However, traditional biomarkers for renal assessment lack sensitivity in identifying early or subclinical damage, underscoring the need for novel and more precise markers. This study aimed to investigate the effectiveness of urinary KIM-1, clusterin, nephrin, and serum cystatin C in detecting nephrotoxicity associated with platinum-based therapies. A total of 43 patients with different oncological diseases participated in the prospective study, divided into two groups based on the nephrotoxic potential of the administered drugs: patients treated with cisplatin (high-risk group for nephrotoxicity) and patients treated with oxaliplatin/carboplatin (low-to-moderate risk group for nephrotoxicity). The results showed that nephrotoxicity, determined as a decrease in eGFR of >10 mL/min/1.73 m² at the sixth month after initiation of platinum-based therapy, occurred in 54.3% of cases, with 80% of these attributable to cisplatin-based therapy. Conventional renal biomarkers, such as the serum creatinine and urine albumin-creatinine ratio, have shown controversial results in the course of the study. In contrast, the patients treated with cisplatin, as well as those who developed nephrotoxicity, showed significant increases in the mean values of cystatin C (p < 0.001, respectively, p < 0.001), urinary KIM-1 (p = 0.005, respectively, p = 0.002), and urinary clusterin (p = 0.001, respectively, p = 0.001). Among the group with a low to moderate risk of nephrotoxicity including those treated with oxaliplatin/carboplatin, no statistically significant changes over time were observed in any of the biomarkers. These findings suggest that the aforementioned biomarkers can be used for the early detection of cisplatin-induced eGFR decline.