Ropper A H
Neurology Service, St Elizabeth's Hospital, Boston, Mass 02135.
Arch Neurol. 1993 May;50(5):536-9. doi: 10.1001/archneur.1993.00540050078020.
To describe a syndrome of rapidly evolving polyneuropathy in patients with severe renal failure.
Retrospective case series of four patients.
In-hospital evaluations and personal examinations of patients.
Four patients with severe or end-stage renal failure who were receiving peritoneal dialysis.
These patients had an acute or subacute syndrome characterized by generalized limb weakness over days or weeks, severe imbalance, diminished reflexes, and numbness. Spinal fluid protein levels were elevated and some demyelinating features were noted on electrophysiological testing. Improvement occurred with more frequent peritoneal dialysis in one patient and transplantation in another, but the neuropathy progressed in the other two in whom diabetes may have played a role.
This partly reversible acute uremic neuropathy, which is probably caused by the metabolic disturbances of end-stage renal failure, simulates Guillain-Barré syndrome or chronic inflammatory demyelinating polyneuropathy and may be complicated by diabetic neuropathy.
描述严重肾衰竭患者中快速进展的多发性神经病综合征。
4例患者的回顾性病例系列。
患者的住院评估和个人检查。
4例接受腹膜透析的严重或终末期肾衰竭患者。
这些患者出现急性或亚急性综合征,其特征为在数天或数周内出现全身性肢体无力、严重失衡、反射减弱和麻木。脑脊液蛋白水平升高,电生理测试发现一些脱髓鞘特征。1例患者通过更频繁的腹膜透析病情改善,另1例通过移植病情改善,但另外2例患者的神经病变进展,糖尿病可能在其中起了作用。
这种部分可逆的急性尿毒症性神经病可能由终末期肾衰竭的代谢紊乱引起,类似格林-巴利综合征或慢性炎症性脱髓鞘性多发性神经病,可能并发糖尿病性神经病。