Abstract: FR-PO008
Cisplatin-Induced Kidney Injury Is Transient and Associated with Short-Term Elevation of Urine Interleukin-18 in Patients with Testicular Cancer
Session Information
- AKI: Clinical, Outcomes, Trials - I
October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- McMahon, Kelly, McGill University, Montreal, Quebec, Canada
- Cameron, Alan C., University of Glasgow, Glasgow, United Kingdom
- White, Jeff D., Beatson West of Scotland Cancer Centre, Glasgow, United Kingdom
- Welsh, Paul, University of Glasgow, Glasgow, United Kingdom
- Zappitelli, Michael, Toronto Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada
- Touyz, Rhian, University of Glasgow, Glasgow, United Kingdom
- Mark, Patrick B., University of Glasgow, Glasgow, United Kingdom
- Lang, Ninian N., University of Glasgow, Glasgow, United Kingdom
Background
Cisplatin causes acute kidney injury (AKI) but changes in urinary AKI biomarkers are not well defined in clinical practice. We investigated short- and medium-term AKI using novel biomarkers over 9 months in patients with testicular cancer treated with cisplatin.
Methods
Prospective observational study of men with testicular cancer in 3 groups following orchiectomy: 1) surveillance; 2) adjuvant cisplatin (1-2 cycles); 3) metastatic disease with high dose cisplatin (3-4 cycles). Blood/urine was collected at 6 visits: baseline, 24h, 6 weeks, 3, 6 and 9 months for renal injury markers.
Results
27 men (median age 34y [IQR 31-40y]) were recruited: surveillance (N=10); adjuvant cisplatin (N=7); metastatic cisplatin (N=10). Urine tubular injury markers (interleukin-18 [IL-18], neutrophil gelatinase-associated lipocalin [NGAL], vascular endothelial growth factor [VEGF], kidney injury molecule-1 [KIM-1]), urine 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. Urine IL-18 rose in both cisplatin groups at 24h (median [IQR]: adjuvant 24h 22.8 [16.4-34.7] vs. baseline 6.8 [5.7-15.9]; metastatic 24h 23.7 [20.1-36.1] vs. baseline 9.2 [7.2-11.9] pg/mg, P<0.05) and returned to baseline by 6 weeks.
Conclusion
Cisplatin nephrotoxicity is reversible over 3 months and is evident with use of novel biomarkers. Elevation of IL-18 supports a major inflammatory renal insult. This provides evidence to support investigation of anti-inflammatory drugs to prevent cisplatin toxicity.
Funding
- Government Support - Non-U.S.