Neuropathy, axonal Na+/K+ pump function and activity-dependent excitability changes in end-stage kidney disease

Area of Science:

• Nephrology
• Neurology
• Physiology

Background:

• Peripheral neuropathy is a common complication in end-stage kidney disease (ESKD).
• The role of axonal sodium-potassium (Na(+)/K(+)) pump function in ESKD-related neuropathy is not fully understood.
• Investigating neurotoxic mechanisms and pump function is crucial for managing ESKD complications.

Purpose of the Study:

• To investigate the mechanisms of peripheral neuropathy in ESKD patients.
• To assess axonal Na(+)/K(+) pump function in ESKD.
• To explore the relationship between nerve excitability, dialysis, and neurotoxin levels.

Main Methods:

• Nerve excitability tests were performed on 10 ESKD patients before and after hemodialysis, and on 29 controls.
• Changes in excitability were measured at rest and after maximal voluntary contraction (MVC) of the abductor pollicis brevis (APB) muscle.
• Serum levels of potassium, urea, parathyroid hormone, and beta-2-microglobulin were analyzed.

Main Results:

• Baseline nerve excitability in ESKD patients indicated axonal depolarization before dialysis.
• Activity-dependent changes in excitability post-MVC were similar in ESKD patients and controls, suggesting normal Na(+)/K(+) pump function.
• Post-dialysis changes indicated increased Na(+)/K(+) pump activity in ESKD patients, contrary to expectations for impaired function.

Conclusions:

• Axonal Na(+)/K(+) pump function is not impaired in ESKD patients.
• Pre-dialysis excitability changes in ESKD are likely attributable to hyperkalemia.
• Na(+)/K(+) pump dysfunction is not a significant factor in the development of neuropathy in ESKD.