Cisplatin re-challenge following recovery from carboplatin-induced, biopsy-proven acute tubular necrosis in a 57-year-old patient with squamous-transformed non-small cell lung cancer: a case report.

内容摘要

Cisplatin-based chemotherapy remains a key treatment option for advanced non-small cell lung cancer (NSCLC), particularly in patients with squamous histology or those who develop histologic transformation after resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). Squamous transformation represents an uncommon but clinically challenging resistance mechanism, often associated with limited therapeutic options and continued reliance on platinum-based regimens. However, prior platinum-associated acute tubular necrosis (ATN), particularly when histologically confirmed, frequently precludes further use of platinum in clinical practice. This creates a critical therapeutic dilemma in which effective treatment options are limited; however, re-administration of platinum agents is considered high-risk. Evidence regarding the safety of cisplatin re-challenge after recovery from biopsy-proven ATN is extremely limited, leaving clinicians without clear guidance. We describe the case of a 57-year-old Japanese man who developed squamous transformation after osimertinib treatment and subsequently experienced carboplatin-induced biopsy-proven ATN following the first cycle of chemoimmunotherapy. Serum creatinine increased from 0.76 to 1.55 mg/dL, with a decline in estimated glomerular filtration rate (eGFR) from 83.82 to 37.83 mL/min/1.73 m2. Renal function recovered within 1 month after the ATN episode, and cisplatin-based therapy was initiated 3 months after creatinine recovered to 0.91 mg/dL with an eGFR of 67.40 mL/min/1.73 m2 and creatinine clearance of 83.60 mL/min/1.73 m2, exceeding the predefined eligibility threshold of 80 mL/min/1.73 m2. During the first cycle, severe gastrointestinal toxicity led to dehydration-associated acute kidney injury (AKI), with creatinine peaking at 2.46 mg/dL and eGFR declining to 22.71 mL/min/1.73 m2, but renal function improved after prompt hydration, electrolyte replacement, and treatment modification. This case suggests that cisplatin re-challenge should be considered in carefully selected patients after recovery from biopsy-proven platinum-associated ATN, when clinically necessary. Importantly, our findings highlight that even in the setting of recurrent AKI, treatment continuation may be feasible under strict multidisciplinary management, including intensive hydration, electrolyte correction, and close nephrology involvement. Rather than demonstrating general safety, this case provides a clinically relevant framework for risk assessment and management in situations where therapeutic options are limited. However, these observations were derived from a single case and should be interpreted with caution.