Hyperuricemia & Tumor Lysis Syndrome

Key Features

Complication of treatment-associated tumor lysis of hematologic as well as rapidly proliferating malignancies
May be worsened by thiazide diuretic use
Rapid increase in serum uric acid can cause acute urate nephropathy from uric acid crystallization
To prevent urate nephropathy, serum uric acid must be reduced before chemotherapy

Laboratory tests (serum uric acid, phosphorus, calcium, electrolytes [particularly, potassium and sodium], creatinine) should be monitored following initiation of chemotherapy

Prevention of hyperuricemia, hyperphosphatemia and hyperkalemia are most important
- The American Society of Clinical Oncology guidelines recommend aggressive hydration before, during, and after chemotherapy to help keep urine flowing and facilitate excretion of uric acid and phosphorus
- Bicarbonate infusions are no longer recommended
Treatment for hyperuricemia
- Allopurinol
  - Blocks the enzyme xanthine oxidase and therefore the formation of uric acid from purine breakdown
  - Dosage: 100 mg/m² every 8 hours orally (maximum 800 mg/day) with dose adjustments for impaired kidney function given before starting chemotherapy
- Rasburicase
  - Dosage: 0.1–0.2 mg/kg/day intravenously for 1–7 days
  - Indicated for patients at high risk for developing tumor lysis syndrome or in whom hyperuricemia develops despite treatment with allopurinol
  - May be considered for patients with baseline elevated uric acid who are being treated with venetoclax (Bcl-2 inhibitor) for chronic lymphocytic leukemia who have large lymph nodes [≥ 10 cm] or nodes ≥ 5 cm accompanied by white blood cell counts > 25,000/mcL [25 × 10⁹/L]
  - Cannot be given to patients with known glucose 6-phosphate dehydrogenase (G6PD) deficiency nor can it be given to pregnant or lactating women
Elevated potassium or phosphorus levels need to be promptly treated (see Hyperkalemia and Hyperphosphatemia)