title: Treatment with IFN-{alpha}, -{beta}, or -{gamma} is associated with collapsing focal segmental glomerulosclerosis.
abstract: OBJECTIVE
  Treatment with IFN is rarely associated with nephrotic syndrome and renal biopsy findings of minimal-change disease or FSGS.
  
  
  METHODS
  We report 11 cases of collapsing FSGS that developed during treatment with IFN and improved after discontinuation of therapy.
  
  
  RESULTS
  The cohort consists of seven women and four men with a mean age of 48.2 yr. Ten of the 11 patients were black. Six patients were receiving IFN-alpha for hepatitis C virus infection (n = 5) or malignant melanoma (n = 1), three were receiving IFN-beta for multiple sclerosis, and two were treated with IFN-gamma for idiopathic pulmonary fibrosis. After a median and mean [corrected] duration of therapy of 4.0 and 12.6 months, respectively, patients presented with acute renal failure (mean creatinine 3.5 mg/dl) and nephrotic-range proteinuria (mean 24-hour urine protein 9.7 g). Renal biopsy revealed collapsing FSGS with extensive foot process effacement and many endothelial tubuloreticular inclusions. Follow-up was available for 10 patients, all of whom discontinued IFN. At a mean of 23.6 months, nine of 10 patients had improvement in renal function, including one with complete remission and two with partial remission. Among the seven patients with available data, mean proteinuria declined from 9.9 to 3.0 g/d. Four of the seven patients were treated with immunosuppression, and there was no detectable benefit.
  
  
  CONCLUSIONS
  Collapsing FSGS may occur after treatment with IFN-alpha, -beta, or -gamma and is typically accompanied by the ultrastructural finding of endothelial tubuloreticular inclusions. Optimal therapy includes discontinuation of IFN.
authors.affiliation: Department of Pathology, Columbia College of Physicians and Surgeons, 630 West 168th Street, VC 14-224, New York, NY 10032, USA. gsm17@columbia.edu
authors.forename: Glen S
authors.initials: GS
authors.lastname: Markowitz
authors.forename: Samih H
authors.initials: SH
authors.lastname: Nasr
authors.forename: M Barry
authors.initials: MB
authors.lastname: Stokes
authors.forename: Vivette D
authors.initials: VD
authors.lastname: D'Agati
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced; D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000009:adverse effects*; D000998:Antiviral Agents / Q000009:adverse effects*; D001706:Biopsy; D005260:Female; D005923:Glomerulosclerosis, Focal Segmental / Q000139:chemically induced* / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D006526:Hepatitis C / Q000188:drug therapy; D006801:Humans; D054990:Idiopathic Pulmonary Fibrosis / Q000188:drug therapy; D007155:Immunologic Factors / Q000009:adverse effects*; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016898:Interferon-alpha / Q000009:adverse effects*; D016899:Interferon-beta / Q000009:adverse effects*; D007371:Interferon-gamma / Q000009:adverse effects*; D007668:Kidney / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008545:Melanoma / Q000188:drug therapy; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000188:drug therapy; D011507:Proteinuria / Q000139:chemically induced; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D000998:Antiviral Agents; D007155:Immunologic Factors; D007166:Immunosuppressive Agents; D016898:Interferon-alpha; D016899:Interferon-beta; D007371:Interferon-gamma