Acute renal dysfunction during interleukin-2 treatment: Suggestion of an intrinsic renal lesion

Craig L. Shalmi, Janice P. Dutcher, Donald A. Feinfeld, K. J. Chun, Khalid R. Saleemi, Leonard M. Freeman, Robert I. Lynn, Peter H. Wiernik

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)1839-1846
Number of pages8
JournalJournal of Clinical Oncology
Volume8
Issue number11
DOIs
Publication statusPublished - Nov 1990
Externally publishedYes

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ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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