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Published on: May 14, 2013
Minimal-change glomerulopathy and glomerular visceral epithelial hyperplasia associated with alpha-interferon therapy
A Traynor1, T Kuzel, E Samuelson
1Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.
Insights
A patient with T-cell lymphoma developed kidney failure after interferon treatment, showing podocyte damage. Treatment with prednisone improved kidney function, suggesting lymphokine-mediated nephrotoxicity.
Area of Science:
- Nephrology
- Oncology
- Immunology
Background:
- Cutaneous T-cell lymphoma (CTCL) is a rare type of non-Hodgkin lymphoma.
- Alpha-interferon is a common treatment for CTCL, but can have side effects.
Observation:
- A 44-year-old man with CTCL experienced complete skin regression after alpha-interferon therapy.
- Concurrently, he developed acute renal failure, characterized by nephrotic-range proteinuria, interstitial nephritis, and minimal-change nephropathy.
Findings:
- Renal biopsy revealed significant proliferation of visceral epithelial cells (podocytes).
- Discontinuation of alpha-interferon and initiation of prednisone therapy led to significant improvement in renal function and proteinuria.
Implications:
- This case highlights a potential link between lymphoproliferative disorders and interferon-induced nephrotoxicity.
- Podocyte injury may play a crucial role in the pathogenesis of this condition.
- Further research is warranted to understand lymphokine-mediated effects on renal function in lymphoma patients.
Abstract:
A 44-year-old man was diagnosed with cutaneous T-cell lymphoma characterized by a proliferation of CD4-positive cells. In response to alpha-interferon therapy, he experienced rapid regression of his cutaneous disease. This improvement was associated with development of renal failure, characterized by nephrotic-range proteinuria with interstitial nephritis and minimal-change nephropathy. The remarkable finding of renal biopsy was marked proliferation of visceral epithelial cells (podocytes). Renal disease improved significantly in response to discontinuation of interferon and initiation of prednisone therapy. Nephrotic range proteinuria regressed, but never completely resolved. This case is illustrative of the probable role for lymphokine-mediated nephrotoxicity in the setting of lymphoproliferative disease.
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