TY - JOUR
T1 - Long-term follow-up of polyneuropathy in diabetic kidney transplant recipients
AU - Van Der Vliet, A.
AU - Navarro, X.
AU - Kennedy, W. R.
AU - Goetz, F. C.
AU - Barbosa, J. J.
AU - Sutherland, D. E R
AU - Najarian, J. S.
PY - 1988
Y1 - 1988
N2 - Nerve conduction and electromyography (EMG) of insulin-dependent (type I) diabetic patients with end-stage nephropathy was studied before and up to 10 yr after kidney transplantation (KTx). A series of nondiabetic KTx patients served as a comparison group. Motor nerve conduction velocity (NCV) was measured in the ulnar, median, peroneal, and tibial nerves; sensory NCV was measured in the median nerve. EMG was performed in the first dorsal interosseus, flexor carpi radialis, anterior tibialis, and gastrocnemius muscles. In 68 pre-KTx diabetic patients, the mean NCV was below normal in all nerves, and the mean amplitudes of the evoked muscle action potential (MAP) were low normal in the upper extremity and below normal in the lower extremity. The values of the comparison group were within the normal range. At 1 (n = 57), 5 (n = 23), and 10 (n = 10) yr after KT(x), the mean NCV of the diabetic patients remained essentially unchanged, but MAP amplitudes of all muscles had declined. EMG revealed progression of the denervation process, especially in muscles of the lower extremities. We conclude that diabetic neuropathy continues to progress by a progressive axonal loss after correction of uremia by KTx.
AB - Nerve conduction and electromyography (EMG) of insulin-dependent (type I) diabetic patients with end-stage nephropathy was studied before and up to 10 yr after kidney transplantation (KTx). A series of nondiabetic KTx patients served as a comparison group. Motor nerve conduction velocity (NCV) was measured in the ulnar, median, peroneal, and tibial nerves; sensory NCV was measured in the median nerve. EMG was performed in the first dorsal interosseus, flexor carpi radialis, anterior tibialis, and gastrocnemius muscles. In 68 pre-KTx diabetic patients, the mean NCV was below normal in all nerves, and the mean amplitudes of the evoked muscle action potential (MAP) were low normal in the upper extremity and below normal in the lower extremity. The values of the comparison group were within the normal range. At 1 (n = 57), 5 (n = 23), and 10 (n = 10) yr after KT(x), the mean NCV of the diabetic patients remained essentially unchanged, but MAP amplitudes of all muscles had declined. EMG revealed progression of the denervation process, especially in muscles of the lower extremities. We conclude that diabetic neuropathy continues to progress by a progressive axonal loss after correction of uremia by KTx.
UR - https://www.scopus.com/pages/publications/0024240860
UR - https://www.scopus.com/pages/publications/0024240860#tab=citedBy
U2 - 10.2337/diabetes.37.9.1247
DO - 10.2337/diabetes.37.9.1247
M3 - Article
C2 - 3044890
AN - SCOPUS:0024240860
SN - 0012-1797
VL - 37
SP - 1247
EP - 1252
JO - Diabetes
JF - Diabetes
IS - 9
ER -