TY - JOUR
T1 - Acute renal dysfunction during interleukin-2 treatment
T2 - Suggestion of an intrinsic renal lesion
AU - Shalmi, Craig L.
AU - Dutcher, Janice P.
AU - Feinfeld, Donald A.
AU - Chun, K. J.
AU - Saleemi, Khalid R.
AU - Freeman, Leonard M.
AU - Lynn, Robert I.
AU - Wiernik, Peter H.
PY - 1990/11
Y1 - 1990/11
N2 - Adoptive immunotherapy with interleukin-2 (IL-2) and lymphokine-acrivared killer (LAK) cells has been effective in treating some advanced malignancies in animals and humans. One complication of this treatment is a reversible, oliguric, acute renal failure, which has been ascribed to renal hypoperfusion and resultant prerenal azotemia. We serially studied renal function in 10 patients receiving high-dose regimens of recombinant interleukin-2 (rIL-2) to attempt to delineate further the nature of the renal dysfunction caused by IL-2 treatment. Renal plasma flow was computed from iodine 131 (I-131 Hippuran; Mediphysics, Paramus, NJ) orthoiodohippurate, excretion curves, and glomerular filtration rate (GFR) was determined by creatinine clearance. Studies done prior to and on day 4 of treatment showed that GFR fell in nine of 10 patients, with a mean decrease of 43% ± 8%, and renal plasma flow fell in five of the 10 patients with a mean decrease of 5% ± 10%. The average pretherapy filtration fraction was calculated to be 23% ± 1% and after 4 days of treatment, decreased to a mean value of 15 ± 2%. The BUN to creatinine ratio also declined in all patients. These findings collectively suggest that IL-2 nephrotoxicity may result from an intrarenal defect in addition to the previously described prerenal azotemia. Additionally, radionuclide studies of renal function are a reliable and reproducible noninvasive method of assessing these changes in renal function.
AB - Adoptive immunotherapy with interleukin-2 (IL-2) and lymphokine-acrivared killer (LAK) cells has been effective in treating some advanced malignancies in animals and humans. One complication of this treatment is a reversible, oliguric, acute renal failure, which has been ascribed to renal hypoperfusion and resultant prerenal azotemia. We serially studied renal function in 10 patients receiving high-dose regimens of recombinant interleukin-2 (rIL-2) to attempt to delineate further the nature of the renal dysfunction caused by IL-2 treatment. Renal plasma flow was computed from iodine 131 (I-131 Hippuran; Mediphysics, Paramus, NJ) orthoiodohippurate, excretion curves, and glomerular filtration rate (GFR) was determined by creatinine clearance. Studies done prior to and on day 4 of treatment showed that GFR fell in nine of 10 patients, with a mean decrease of 43% ± 8%, and renal plasma flow fell in five of the 10 patients with a mean decrease of 5% ± 10%. The average pretherapy filtration fraction was calculated to be 23% ± 1% and after 4 days of treatment, decreased to a mean value of 15 ± 2%. The BUN to creatinine ratio also declined in all patients. These findings collectively suggest that IL-2 nephrotoxicity may result from an intrarenal defect in addition to the previously described prerenal azotemia. Additionally, radionuclide studies of renal function are a reliable and reproducible noninvasive method of assessing these changes in renal function.
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U2 - 10.1200/JCO.1990.8.11.1839
DO - 10.1200/JCO.1990.8.11.1839
M3 - Article
C2 - 2230870
AN - SCOPUS:0025043985
SN - 0732-183X
VL - 8
SP - 1839
EP - 1846
JO - Journal of Clinical Oncology
JF - Journal of Clinical Oncology
IS - 11
ER -