Altered motor nerve excitability in end-stage kidney disease

Abstract

Although multiple toxins have been implicated in the development of uraemic neuropathy, no causative agent has been identified. In the present study, the excitability properties of lower limb motor nerves in patients with end-stage kidney disease treated with haemodialysis were measured before, during and after a standard 5 h haemodialysis session, in an attempt to explore the pathophysiology of uraemic neuropathy. Compound muscle action potentials were recorded from tibialis anterior and extensor digitorum brevis, following stimulation of the common peroneal nerve in 14 patients. Measures of excitability were assessed in relation to changes in serum levels of potential neurotoxins, including potassium, calcium, urea, uric acid, parathyroid hormone and beta-2-microglobulin. Before dialysis, measures of nerve excitability were significantly abnormal in the patient group for axons innervating tibialis anterior and extensor digitorum brevis, consistent with axonal depolarization: refractoriness was increased and superexcitability and depolarizing threshold electrotonus were reduced. Pre-dialysis excitability abnormalities were strongly correlated with serum K+. Correlation was also noted between the severity of symptoms and excitability abnormalities. Haemodialysis normalized the majority of nerve excitability parameters. In conclusion, lower limb motor axons in uraemic patients are depolarized before dialysis. The correlation between serum K+ and excitability measures indicates that hyperkalaemia is primarily responsible for uraemic depolarization, and a likely contributing factor to the development of neuropathy.

Association Between Calcineurin Inhibitor Treatment and Peripheral Nerve Dysfunction in Renal Transplant Recipients

“…Multiple excitability parameters were recorded using previously published protocols (10,14,15). These parameters included threshold electrotonus and current threshold recordings which utilize subthreshold electrical stimuli to provide information on nerve membrane potential and internodal conductances (16).…”

“…These insights were provided through the use of novel nerve excitability techniques, a clinical method that enables indirect assessment of ion channels, pumps and exchangers that are involved in the process of nerve impulse conduction (8). These techniques have proven particularly useful in detecting changes in peripheral nerve function in patients with chronic kidney disease (CKD), with previous studies demonstrating prominent changes in CKD patients receiving renal replacement therapies (9,10), changes that are undetectable using routine nerve conduction studies (11). The present study was undertaken to investigate the mechanisms underlying neurotoxicity in patients receiving immunosuppressive treatment following renal transplantation.…”

Neurological Assessment of Hemodialysis Patients a Single Center Study

“…Peripheral Neuropathy -is diagnosed (10) • When the patient complained of at least one of the followings in his extremities: Numbness, pain or burning sensation…”

“…(10) Mononeuropathy: is diagnosed when the patient complained of pain and/or numbness and there is impaired pinprick, light touch and/or reflexes in dermatomal distribution of a single nerve. (10) Cranial Neuropathy: is considered (10) when one of the following is present:…”

Neuropathy in Chronic Renal Failure

“…Studies of neuropathy in ESKD have demonstrated prevalence rates which vary from 60 to 100%, depending on the choice of nerve segments, the indices measured and the number of nerves studied [10][11][12][13][14][15][16][17][18][19][20][21] .…”