Investigations on the subclinical and clinical nephrotoxicity of interferon alpha-2B in patients with myeloproliferative syndromes.

Since the introduction of interferon alpha-2b (IFN alpha-2b) into clinical oncology there have been several reports dealing with acute renal failure during therapy with this new type of anticancer drug. We investigated 58 patients (pts) with myeloproliferative syndromes (56 pts with chronic myelogenous leukemia, 2 pts with essential thrombocythemia) who were treated with 4 x 10(6) IU IFN alpha-2b each day subcutaneously. In order to assess the nephrotoxic potential we used the following noninvasive methods: 1. Analysis of the excretion of 4 urinary enzymes (LDH, LAP, GGT, NAG), 2. Determination of the excretion of protein, albumin, alpha-1-microglobulin immunoglobulin G (Ig G), 3. serum creatinine. The investigations were done every 2 weeks and took 70 weeks. We found an increase in the excretion of all 4 enzymes which remained stable during the whole observation period, protein excretion was pathological in about 20% of all pts and reached values of up to 9.07 g/L alpha-1-microglobulin was excreted in pathological amounts in about 20% of all pts during the whole observation period, albumin was found in pathological quantities in about 15% of all pts and Ig G was pathologically increased in the urine in about 10% of the pts. Serum creatinine rose in 5-10% of the pts up to 1.5 mg/dL. In conclusion, IFN alpha-2b is capable of inducing combined glomerular and tubular damage. Therefore, avoiding additional nephrotoxic insults is desirable.