Amelioration of nerve conduction velocity following simultaneous kidney/pancreas transplantation is due to the glycaemic control provided by the pancreas.
Diabetic polyneuropathy is a common, disabling chronic complication of diabetes mellitus. Previous studies have suggested that combined pancreas-kidney transplantation can ameliorate nerve conduction. The relative contribution of the correction of hyperglycaemia and uraemia on nerve function is still a matter of debate. Nerve conduction velocity (NCV) was assessed before and after simultaneous pancreas and kidney transplantation, and before and after pancreas graft failure in five insulin-dependent diabetic (IDDM) patients affected by severe diabetic polyneuropathy. Sensory and motor NCV were recorded in five nerves and expressed as a cumulative index for each patient. Metabolic control was evaluated by fasting blood glucose and glycosylated haemoglobin levels. NCV index was below normal values before transplant: -3.8 +/- 0.7 (normal value: 0.89), improved 1 and 2 years after transplant: -3.1 +/- 1.3 and -2.6 +/- 0.9 (p = 0.0019), stabilised until pancreas failure and deteriorated to pre-transplant values 2 years after pancreas graft failure: -3.6 +/- 1.0 (p = 0.034). Fasting blood glucose levels worsened after pancreas graft failure. HbA1c levels, in the normal range during functioning pancreas graft (6.6 +/- 0.6%), deteriorated after its failure (8.0 +/- 0.6%, p = 0.04). Kidney function was preserved. These data support a positive effect of pancreas transplantation per se on NCV in IDDM subjects with diabetic polyneuropathy, thus demonstrating that metabolic control provided by a self-regulated source of insulin not only halts but also ameliorates nerve function, even if polyneuropathy is advanced.
Martinenghi
S
S
Department of Medicine, University of Milan, San Raffaele Scientific Institute, Italy.
Comi
G
G
Galardi
G
G
Di Carlo
V
V
Pozza
G
G
Secchi
A
A
D000328:Adult; D001786:Blood Glucose / Q000032:analysis / Q000378:metabolism; D003404:Creatinine / Q000032:analysis / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000503:physiopathology; D005215:Fasting; D005260:Female; D005500:Follow-Up Studies; D006442:Glycated Hemoglobin / Q000032:analysis / Q000378:metabolism; D006084:Graft Rejection / Q000503:physiopathology; D006085:Graft Survival / Q000502:physiology; D006801:Humans; D007003:Hypoglycemia / Q000503:physiopathology*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007223:Infant; D007328:Insulin / Q000627:therapeutic use; D016030:Kidney Transplantation; D008297:Male; D009431:Neural Conduction / Q000502:physiology*; D010179:Pancreas / Q000503:physiopathology*; D016035:Pancreas Transplantation / Q000276:immunology
D001786:Blood Glucose; D003404:Creatinine; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin