Case Presentation: A 49-year-old male with metastatic renal cell carcinoma (RCC) involving the lungs and liver, diagnosed one month prior and with no other past medical history, presented from his outpatient oncology clinic with one week of worsening oral intake, throat pain, nausea, abdominal pain, fatigue, and confusion. He had received his first dose of nivolumab on the day of admission. Initial laboratory evaluation showed potassium 5.6 meq/L (baseline 4.1 meq/L), creatinine 2.2 mg/dL (1.0 mg/dL), bicarbonate 11 mg/dL (22 mg/dL), calcium 10.2 mg/dL (9.8 mg/dL), lactic acid 9.3 mmol/L, AST 653 U/L (63 U/L), and ALT 448 U/L (49 U/L). CT imaging demonstrated a large right renal mass invading the right adrenal gland and liver, with gastric distension concerning for gastric outlet obstruction from extrinsic compression. Within 24 hours, he developed rapidly worsening metabolic abnormalities consistent with tumor lysis syndrome (TLS), including potassium 6.4 mg/dL, phosphorus 5.7 mg/dL (baseline 2.9 mg/dL), uric acid 21 mg/dL, creatinine 2.9 mg/dL, and calcium 10.6 mg/dL, along with worsening liver function and lactic acidosis. He received aggressive intravenous fluids, intravenous sodium bicarbonate infusion, and rasburicase, but progressed to acute oliguric renal failure requiring hemodialysis. He subsequently decompensated due to a presumed upper gastrointestinal bleed causing hemorrhagic shock and atrial fibrillation with rapid ventricular response (Afib w/ RVR). He was transferred to the ICU for vasopressor support. Endoscopic intervention was deferred due to high procedural risk with minimal expected benefit. Despite maximal interventions, he continued to decline and ultimately passed away after transition to comfort care.
Discussion: TLS is usually associated with hematologic malignancies and cytotoxic therapy. Spontaneous TLS (STLS) in solid tumors is rare and has been reported infrequently in metastatic renal cell carcinoma due to its slower proliferation and limited chemosensitivity. When STLS occurs, mortality is high because metabolic abnormalities evolve quickly and are often misattributed to sepsis or organ failure. In this case, the rapid metabolic deterioration occurring within hours of the first nivolumab dose supports STLS driven by extensive tumor burden rather than an immunotherapy effect. Early recognition and management, including IV fluids, rasburicase, and timely nephrology involvement, are crucial to prevent irreversible renal injury. Hemodialysis plays a key role when hyperkalemia, hyperphosphatemia, or acidosis become refractory. The patient’s upper GI bleed and Afib w/ RVR were likely consequences of his advanced metastatic disease, impaired hepatic function, uremic platelet dysfunction, mucosal hypoperfusion, and overall critical illness, rather than direct manifestations of TLS.
Conclusions: STLS in metastatic RCC is a rare but life-threatening oncologic emergency. Early recognition and management increases the chance of survival in this high mortality condition (20-40% morality). It should be considered in hospitalized patients with bulky solid tumors who exhibit increases in uric acid, potassium, phosphate or decreases in calcium before chemo or immuno-therapy is initiated. Clinicians in acute care hospital settings (medical residents and hospital medicine clinicians), should maintain vigilance for TLS beyond hematologic malignancies, especially with patients with aggressive solid tumors such as metastatic renal cell carcinoma.