Immune checkpoint inhibitors (ICI) have been approved by the Food and Drug Administration (FDA) for use in many solid tumors and hematological malignancies. Immune-related adverse events (irAEs) are potential side effects that can arise during or after treatment with ICI therapy. We describe a case of ICI-induced Fanconi syndrome in a 58-year-old man with extensive-stage small-cell lung cancer (ES-SCLC), who had disease progression after initial chemotherapy and radiation. He was started on nivolumab and ipilimumab as second-line treatment. Three weeks into the therapy, he developed abdominal pain with grade 3 transaminitis and required steroids and mycophenolate for presumed autoimmune hepatitis. Subsequently, he presented with worsening abdominal pain and was found to have an enlarging right adrenal mass. Laboratory work-up revealed a white blood cell (WBC) count of 17 K/µL, aspartate aminotransferase (AST)/alanine aminotransferase (ALT) 99/210 U/L, direct bilirubin 2.8 mg/dL, blood urea nitrogen (BUN) 43 mg/dL, Cr 2.31 mg/dL (baseline: 1.1 mg/dL), phosphorus 2.3 mg/dL, and glucose 303 mg/dL with metabolic acidosis. There was no evidence of urinary tract obstruction. Urinary findings were notable for glucosuria (>500 mg/dL), fractional excretion of phosphorus and uric acid of 56% (normal range 10%-20%) and 75% (normal range 7%-10%), respectively. He was started on intravenous (IV) bicarbonate and methylprednisolone. Fanconi syndrome with proximal tubular damage secondary to ICI therapy was diagnosed. He was discharged on oral bicarbonate and steroid taper. On follow-up after four weeks, his renal function recovered to baseline.