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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
Author(s) -
Simsek Cenk,
Karatas Murat,
Tatar Erhan,
Yildirim Ali Murat,
Alkan Funda Tasli,
Uslu Adam
Publication year - 2021
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/ctr.14309
Subject(s) - medicine , colchicine , gastroenterology , kidney transplantation , antagonist , transplantation , aa amyloidosis , kidney , kidney disease , familial mediterranean fever , disease , receptor
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.
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