Pathophysiology

Patients with TLS experience a wide range of metabolic abnormalities. The massive cell lysis that occurs leads to the release of intracellular electrolytes resulting in hyperkalemia and hyperphosphatemia. High concentrations of phosphate bind to calcium leading to hypocalcemia and calcium phosphate precipitation in the renal tubule. Purine nucleic acids are also released which are subsequently metabolized to uric acid through multiple enzyme-mediated steps (Fig. 99-6). Uric acid is poorly soluble at urinary acidic pH leading to crystallization in the renal tubule. The precipitation of uric acid and calcium phosphate leads to metabolic acidosis, facilitating further uric acid crystallization. Acute renal failure may be the end result.

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