BACKGROUND: Neuromyopathy was reported to be a problem among live donor familial Mediterranean fever (FMF) amyloid kidney transplant recipients. We aimed to address this issue on a long-term basis. METHODS: 14 FMF amyloid live donor kidney transplant recipients with a mean post-transplant follow-up period of 82.43 +/- 50.1 months in comparison to a control group of 19 non-amyloid renal transplant patients were subjected to thorough neurological examination, laboratory and electrophysiologic studies. RESULTS: Both groups were comparable with regard to mean serum creatinine levels cyclosporine doses (p > 0.05), however trough cyclosporine levels were significantly lower in the amyloidotics than the controls (p = 0.04). Serum creatine phosphokinase was comparable in both groups (p = 0.59). The amyloid patients showed significantly increased polyphasic motor unit potentials and abnormal interference patterns in the biceps brachii muscle (p = 0.03) and the abductor polices brevis muscle (p = 0.05). Multivariate analysis showed a significant level for biceps myopathy in amyloidotics (p = 0.001). Both groups attained no difference with regard to median nerve conduction velocity. CONCLUSION: Electrophysiologically evidenced neuromyopathy is more liable to occur in long-term live donor FMF amyloidotic kidney transplant recipients than in the other non-amyloidotic kidney transplant recipients even with no clinical manifestations or high creatine phosphokinase levels. Copyright 2004 S. Karger AG, Basel
BACKGROUND:Neuromyopathy was reported to be a problem among live donorfamilial Mediterranean fever (FMF) amyloid kidney transplant recipients. We aimed to address this issue on a long-term basis. METHODS: 14 FMF amyloid live donor kidney transplant recipients with a mean post-transplant follow-up period of 82.43 +/- 50.1 months in comparison to a control group of 19 non-amyloid renal transplant patients were subjected to thorough neurological examination, laboratory and electrophysiologic studies. RESULTS: Both groups were comparable with regard to mean serum creatinine levels cyclosporine doses (p > 0.05), however trough cyclosporine levels were significantly lower in the amyloidotics than the controls (p = 0.04). Serum creatine phosphokinase was comparable in both groups (p = 0.59). The amyloid patients showed significantly increased polyphasic motor unit potentials and abnormal interference patterns in the biceps brachii muscle (p = 0.03) and the abductor polices brevis muscle (p = 0.05). Multivariate analysis showed a significant level for biceps myopathy in amyloidotics (p = 0.001). Both groups attained no difference with regard to median nerve conduction velocity. CONCLUSION: Electrophysiologically evidenced neuromyopathy is more liable to occur in long-term live donorFMF amyloidotic kidney transplant recipients than in the other non-amyloidotic kidney transplant recipients even with no clinical manifestations or high creatine phosphokinase levels. Copyright 2004 S. Karger AG, Basel