The efficacy of interleukin‐1 antagonist
drugs in combination with colchicine in patients with FMF‐AA with colchicine resistance after kidney transplantation: A study with histopathologic evidence. Issue 6 (13th April 2021)

• Record Type: Journal Article
• Authors: Simsek, Cenk; Karatas, Murat; Tatar, Erhan; Yildirim, Ali Murat; Alkan, Funda Tasli; Uslu, Adam
• Is Part Of: Clinical transplantation. Volume 35:Issue 6(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-04-13
• Subjects: colchicine -- FMF‐amyloidosis -- IL‐1 antagonist -- kidney transplantation; Transplantation of organs, tissues, etc -- Periodicals; 617.95
• DOI: 10.1111/ctr.14309
• Languages: English
• ISSNs: 0902-0063

Abstract

Abstract: Background: The efficacy of anti‐interleukin‐1 (IL‐1) drugs in kidney transplant patients with FMF‐AA who developed colchicine resistance has not been clearly demonstrated. Method: Thirty nine kidney transplant recipients with FMF‐AA were evaluated. Group 1 consisted of patients who were in remission after transplantation with colchine and Group 2 included those who developed colchicine resistance. Results: The mean follow‐up of the patients was 88.5 ± 61.9 months. Following the treatment with IL‐1 antagonists; serum Amyloid A (SAA) averages (79.4 ± 35.3 mg/L) as well as the average number of hospitalizations per month due to FMF episodes (1.4 ± 0.5 times/month) decreased significantly (26.6 ± 25.9 mg/L and 0.1 ± 0.3 times/month) ( p < .001). Rates of death with a functional graft were 30% and 0% in group 1 and 2 ( p = .086). Biopsy‐proven AA amyloidosis recurrence in the allograft was observed in 11 of 19 (58%) and seven of nine (78%) patients in group 1 and 2, respectively. Interestingly, glomerular amyloid deposition was not present in the vast majority of biopsies. De novo vasculer amyloid deposition was observed during treatment. Conclusion: IL‐1 antagonist drug and colchicine combination almost completely prevented acute FMF attacks in kidney transplant patients with colchicine resistance. However, amyloid accumulation did not cease during IL‐1 antagonist drug treatment.