Increased weakness after pancreas and kidney transplantation

Background. Already there is evidence that simultaneous pancreas and kidney (SPK), or pancreas after kidney (PAR) transplantation, in patients with ty pe 1 diabetes mellitus and end-stage kidney disease prevents worsening of d iabetic polyneuropathy, but neuropathic improvement is delayed and incomple te. Methods. In 85 patients with type 1 diabetes mellitus who underwent SPR or PAK transplantations, we performed sequential neuromuscular evaluations bef ore, every 3 months after, and yearly after transplantation, quantitating m uscle weakness separately from overall severity of polyneuropathy. Results. We found that, on average, the weakness subscore of the Neuropathy Impairment Score of the lower limbs [NIS(LL)-W] was significantly worse at 3, 6, 9, and 12 months (by about 5 points) than at baseline. By contrast, for these times after transplantation, a composite score of nerve conductio n abnormalities, an independent measure of severity of polyneuropathy, was not significantly worse and, in fact, was significantly improved. In multiv ariate analysis, length of hospital stay correlated with the increased weak ness. Conclusions. We conclude that: (1) increased neuromuscular impairment after transplantation is mainly due to muscle weakness and not to worsening poly neuropathy; (2) in multivariate analysis, duration of hospitalization after transplantation was significantly associated with this increased weakness; (3) increased weakness is probably due to development of myopathy, which m ay be related to graft rejection, immunosuppression, sepsis, and intercurre nt infections; (4) in future transplantation trials, weakness should be eva luated separately from neuropathic status, and the lowest efficacious dosag es of immunotherapy should be used; and (5) essentially all diabetic patien ts reported that SPK or PAK transplantation was worthwhile because it freed them from diabetic lifestyle concerns.