Study of neuromyopathy in amyloid kidney transplant patients.
Neuromuscular status of amyloid and control groups of kidney transplant recipients was assessed through complete neurological examination, assay for serum levels of muscle enzymes (CPK and LDH), electromyography and nerve conduction velocity studies. Neuromyopathic findings were detected in both groups but without severe disabling clinical manifestations. These findings were more prominent in the amyloid group, evidenced by a more significant increase in polyphasicity detected by electromyography and longer prolongation of terminal latency measured in the median nerve. From this study, we concluded that amyloid kidney transplant recipients are more prone to neuromyopathy than the general kidney transplant population, which is mostly due to the amyloidosis itself and/or the colchicine therapy.
Sobh
M
M
Urology and Nephrology Center, University of Mansoura, Egypt.
Refaie
A
A
El-Tantawy
A E
AE
Saad
M
M
Said
E
E
Arif
S
S
El-Sherif
A
A
Ghoneim
M
M
D000686:Amyloidosis / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D003078:Colchicine / Q000627:therapeutic use; D003402:Creatine Kinase / Q000097:blood; D016572:Cyclosporine / Q000627:therapeutic use; D004576:Electromyography; D019054:Evoked Potentials, Motor; D006074:Gout Suppressants / Q000627:therapeutic use; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007674:Kidney Diseases / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D016030:Kidney Transplantation; D007770:L-Lactate Dehydrogenase / Q000097:blood; D009468:Neuromuscular Diseases / Q000209:etiology* / Q000503:physiopathology
D006074:Gout Suppressants; D007166:Immunosuppressive Agents; D016572:Cyclosporine; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D003078:Colchicine