Uremic neuropathy

Yi Pan MD PhD (Dr. Pan of St. Louis University has no relevant financial relationships to disclose.)
Florian P Thomas MD MA PhD MS (Dr. Thomas, Chair, Department of Neurology, Seton Hall-Hackensack Meridian School of Medicine, has no relevant financial relationships to disclose.)
Louis H Weimer MD, editor. (Dr. Weimer of Columbia University has received consulting fees from Roche.)
Originally released November 15, 1997; last updated April 27, 2017; expires April 27, 2020

This article includes discussion of uremic neuropathy and uremic peripheral neuropathy. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Chronic renal failure is one of the common causes for peripheral neuropathy. In this article, the authors summarize the clinical, electrophysiological, and pathological features of uremic neuropathy. Prevention and treatment of uremic neuropathy focus on dialysis and renal transplantation.

Key points

 

• Uremic neuropathy is a distal sensorimotor polyneuropathy caused by uremic toxins.

 

• Symptoms are insidious in onset. Paresthesias are usually the earliest symptoms; weakness and atrophy will follow the sensory symptoms.

 

• The pathologic features are severe axonal degeneration in the most distal nerve trunks with secondary segmental demyelination.

 

• Chronic dialysis may prevent neuropathy in some patients, especially if begun early. Renal transplantation is generally the most successful method to prevent neuropathy.

Historical note and terminology

Uremic neuropathy is a distal sensorimotor polyneuropathy caused by uremic toxins. It is considered a dying-back neuropathy, or central-peripheral axonopathy, associated with secondary demyelination. Its existence was suspected by Charcot in 1880 (Charcot 1880) and Osler in 1892 (Osler 1892). Since the introduction of hemodialysis and renal transplantation in early 1960s, uremic neuropathy has been thoroughly investigated. Before then there were only scant reports of an association between chronic renal failure and polyneuropathy, and its nature was unclear. In 1961, the cases of 2 young men with hereditary interstitial nephritis, nerve deafness, and polyneuropathy were reported (Marin and Tyler 1961). Asbury, Victor, and Adams described the clinical and pathological features in detail (Asbury et al 1962; Asbury et al 1963). Dyck and colleagues established the current concept of uremic neuropathy based on nerve conduction studies and light and electron microscopy studies (Dyck et al 1971). Using quantitative histology, they demonstrated axonal shrinkage. Myelin sheaths appeared to be affected out of proportion to axons. Neuronal rather than axonal dysfunction appeared to result in reduced axonal diameter, myelin rearrangement, and finally, complete degeneration of the axon (Dyck et al 1971). Nielsen published numerous papers in clinical and electrophysiologic studies in the 1970s (Nielsen 1974a; Nielsen 1974b). These descriptions have not changed significantly over time. The greatest strides have been in the documentation of the therapeutic effects of dialysis and renal transplantation on the peripheral neuropathy (Taylor et al 1972; Nielsen 1974b; Hupperts et al 1990; Yildiz et al 1998).

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