Uric acid nephropathy occurs when excessive uric acid production or inadequate excretion leads to uric acid crystal deposition in the renal tubules and interstitium. Acute uric acid nephropathy (tumor lysis syndrome) involves massive release of purine nucleotides from rapid tumor cell death during chemotherapy for high-grade hematologic malignancies (acute leukemias, Burkitt lymphoma), overwhelming the kidney's ability to excrete uric acid. Uric acid is relatively insoluble in acidic urine (pH less than 5.5), and crystals precipitate in the concentrated, acidic environment of the distal tubules and collecting ducts, causing intratubular obstruction, tubular injury, and acute oliguric renal failure. Chronic uric acid nephropathy involves gradual deposition of monosodium urate crystals in the renal medullary interstitium, causing a chronic tubulointerstitial nephritis with slowly progressive renal insufficiency. The nurse monitors serum uric acid levels (target less than 8 mg/dL in at-risk patients), monitors urine output hourly (oliguria indicates obstruction), maintains aggressive IV hydration (target urine output 2-3 mL/kg/hour), administers allopurinol (xanthine oxidase inhibitor preventing new uric acid production) or rasburicase (recombinant urate oxidase that enzymatically converts uric acid to the more soluble allantoin), monitors...