Neuromuscular complications of kidney diseases

affected than females [2,6 ]. Bolton pointed out that The uraemic syndrome is characterized by overall 60% of patients receiving haemodialysis for uraemia deterioration of biochemical and physiological funchave neuropathy by electrodiagnostic criteria [2]. The tions in parallel with the progression of renal failure. main symptoms are restless legs, spontaneous cramps, Uraemia results in variable symptoms pointing to distal paresthesias, numbness and burning feet, which, damage of multiple organs, due to retention of comhowever, are not necessarily related to the neuropathy, pounds normally cleared by the healthy kidneys [1]. but due possibly to transient disturbances of peripheral The identified mechanisms currently are attributed to sensory receptors, induced by fluctuation in water and increased protein catabolism, reduced excretory electrolytes [2]. Symptoms may occur either prior to capacity and altered water–electrolyte homeostasis [2]. or during a regular haemodialysis programme; the Major neurotoxins accumulating in uraemia are latter could indicate that the achieved control is not urea, creatinine, guanidine compounds, a number of optimal [2,3]. Clinical signs of uraemic polyneuropathy aromatic acids, uric and ossalic acids, myo-inositol, include symmetric muscle weakness, areflexia and ‘middle molecules’, b2-microglobulin, amines and parasensory loss for all modalities, especially pin-prick and thyroid hormone (PTH) [2]. The nervous system, both vibration. An early finding is elevation of the vibratory central and peripheral, may show changes, mimicking threshold [2,3,6 ] (Table 2). exogenous poisoning or drug overdose [1]. Here we review the clinical, electrophysiological and morpholoPathology of uraemic polyneuropathy gical aspects of peripheral nervous system syndromes