Cisplatin-induced kidney injury is transient and associated with short-term elevation of urine interleukin-18 in patients with testicular cancer


Session type:


Alan Cameron1,Kelly McMahon2,Paul Welsh1,Ashita Waterston3,Michael Zappitelli4,Jeff White3,Patrick Mark1,Rhian Touyz1,Ninian Lang1
1University of Glasgow,2McGill University,3Beatson West of Scotland Cancer Centre,4University of Toronto



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.