Cisplatin-induced kidney injury is transient and associated with short-term elevation of urine interleukin-18 in patients with testicular cancer
Session type: Poster / e-Poster / Silent Theatre session
Cisplatin causes acute kidney injury (AKI) but changes in urinary AKI biomarkers are not well defined clinically. We investigated short- and intermediate-term AKI using novel biomarkers over 9 months in patients with testicular cancer treated with cisplatin.
Prospective observational study of men with testicular cancer in 3 groups following orchiectomy: 1) surveillance; 2) adjuvant cisplatin-based chemotherapy (1-2 cycles); 3) metastatic cisplatin-based chemotherapy (3-4 cycles). Blood and urine was collected at 6 visits: baseline, 24h, 6 weeks, 3, 6 and 9 months for renal injury markers.
27 men (median age 34y [IQR 31-40y]) were recruited: surveillance (N=10); adjuvant cisplatin (N=7); metastatic cisplatin (N=10). Urinary renal injury biomarkers (interleukin-18 [IL-18], neutrophil gelatinase-associated lipocalin [NGAL], vascular endothelial growth factor [VEGF], kidney injury molecule-1 [KIM-1], albumin/creatinine ratio [ACR]) and serum cystatin C (CysC) were elevated at 24h and 6 weeks (KIM-1) post-cisplatin in adjuvant and metastatic groups (all: P<0.05 vs. baseline). These normalized by 6 weeks (IL-18; NGAL; VEGF; ACR; CysC) and 3 months (KIM-1). eGFR was within normal range throughout.
Novel biomarkers indicate cisplatin nephrotoxicity is reversible over 3 months. Elevation of IL-18 supports a major inflammatory renal insult. This provides evidence to support investigation of anti-inflammatory drugs for cisplatin nephrotoxicity prevention.