A 10-year-old boy developed acute uric acid nephropathy consequent on treatment of a lymphoblastic lymphosarcoma. Treatment resulting in rapid lysis of malignant cells causes a rise of serum uric acid levels and an increased urinary acid load which may precipitate acute renal failure in kidneys already damaged by the effects of hyperuricemia of the malignancy per se. Clinical foresight and appropriate prophylactic therapy in similar cases are recommended.The hyperuricemia commonly ob¬ served in patients with neoplástic disease is due to increased turnover of the malignant tissue or to cell lysis following chemotherapy or radiotherapy.1 Acute uric acid nephropathy may unsue. This is a well-known complication of leukemia, especially in cases of the acute lym¬ phoblastic variety during treatment.2 Reports of acute renal failure fol¬ lowing treatment of solid tumors are far fewer and have been rarely re¬ ported in the pediatrie literature.3~7 A patient with this complication is described, and the pathogenesis and means of prevention of uric acid nephropathy are discussed in brief.
Report of a CaseA 10-year-old Jewish boy of Iraqi de¬ scent was referred to our department be¬ cause of a three-week history of cough and loss of weight. On examination, he was mildly dyspneic; swelling of the face and nonpulsatile distended jugular veins indicated the presence of a superior mediastinal syndrome. There was dullness and poor air entry over the whole of the right lung. Numerous hard shotty glands were present in the left supraclavicular fossa. The liver and the spleen were not en¬ larged.Chest roentgenograms and fluoroscopy showed a large mass occupying the ante¬ rior mediastinum, extending into most of the right hemithorax and even into the left side of the chest (Figure). Laboratory investigations showed a normal blood cell count; blood sedimentation rate was 200 mm in the first hour; serum protein and electrophoretic patterns were normal, and the blood urea nitrogen level (BUN) was 22 mg/100 ml. The specific gravity of the urine was 1.014; no proteinuria was found, and amorphous urate deposits were pres¬ ent in the sediment.Biopsy of a supraclavicular node was compatible with lymphoblastic lymphosar¬ coma. Skeletal survey and bone marrow study showed no evidence of spread of the disease. Within hours of admission, the patient's dyspnea increased and hoarse¬ ness appeared. These signs were attrib¬ uted to rapid growth of the tumor with en¬ croachment on the left recurrent laryngeal nerve. Accordingly, treatment was begun with prednisone, 60 mg daily (2 mg/kg), and locally administered radio¬ therapy, 150 rads daily. The initial uric acid level was 17.5 mg/100 ml (normal val¬ ue 3.5 to 4.5 mg/100 ml in our laboratory) and therefore allopurinol, 300 mg/day; orally administered sodium bicarbonate, 2 gm/day; acetazolamide (Diamox), 0.5 gm/day; and a high fluid intake, 2.5 liters daily, half of which was given in¬ travenously, were prescribed. There was immediate alleviation of the respiratory symptoms and signs of superior ve...
