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Tumor lysis syndrome causes hyperuricemia, hyperphosphatemia, secondary hypocalcemia, and AKI. The priorities are to protect the kidneys and prevent calcium phosphate precipitation. Immediate, high-rate isotonic IV fluids increase renal perfusion and solute clearance; diuretics are considered only after euvolemia is achieved and urine output is adequate. Rasburicase rapidly degrades existing uric acid and should be continued/initiated for elevated levels. Hyperphosphatemia is addressed with dietary restriction and non–calcium-based binders (e.g., sevelamer) to reduce intestinal phosphate absorption; adding calcium can worsen calcium phosphate deposition unless the patient has symptomatic hypocalcemia (tetany, seizures, arrhythmia). Routine urine alkalinization is no longer recommended because it can promote calcium phosphate crystallization and complicate rasburicase efficacy. Dialysis (hemodialysis or CRRT) is indicated for refractory electrolyte abnormalities, fluid overload, or worsening uremia despite medical care. APRN tasks include TLS order set activation, Q6–8h labs (K, Ca, Phos, uric acid, creatinine), telemetry, medication review to avoid nephrotoxins, and early nephrology consultation with clear thresholds for escalation.