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Kidney Week

Abstract: FR-PO139

Relationship of Serum Parathyroid Hormone (PTH) Levels with Objective Measures of Nerve Function in ESRD

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Doshi, Simit, Indiana University, Indianapolis, Indiana, United States
  • Cranor, Alissa Ann, Indiana University School of Medicine, Indianapolis, Indiana, United States
  • Swinney, Kimberly, Indiana University, Indianapolis, Indiana, United States
  • Avin, Keith G., Indiana University-Indianapolis, Indianapolis, Indiana, United States
  • Moe, Sharon M., Indiana University School of Medicine, Indianapolis, Indiana, United States
  • Moorthi, Ranjani N., Indiana University School of Medicine, Indianapolis, Indiana, United States
Background

Advanced kidney disease is a risk factor for motor and sensory nerve deficits, independent of diabetes. The pathophysiology for nerve deficits in renal failure remains unclear. We tested the hypothesis that secondary hyperparathyroidism is associated with a distinct nerve function profile in ESRD patients.

Methods

Seventeen patients with ESRD underwent testing after their routine dialysis session. We measured action potentials (amplitude) and nerve conduction velocity (NCV) in motor (ulnar, peroneal) and sensory (ulnar, sural) nerves in the upper and lower extremities. Symptoms were assessed using the neuropathic pain questionnaire (NPQ). Muscle function was measured as handgrip strength and knee extension strength using a dynamometer. Physical performance was measured as gait speed during a 4 meter walk test. Labs drawn closest to date of testing were used for all analyses. Predefined and validated cut-offs were used to define a deficit. Statistical analyses were done using SPSS 24.

Results

Seventeen pts were enrolled: aged 23-66, 9 male, 15 black, 10 diabetic, median dialysis vintage 5.4 yrs. Ten patients had high PTH ie > 500 pg/ml (median 522 pg/ml; range 25-2364). Neuropathic pain was noted in ~60% patients overall. NCV deficits were prevalent but mean motor NCV (ulnar: 46 vs 46, peroneal 39 vs 40 m/s) or sensory NCV (ulnar 26 vs 26, sural 26 vs 28 m/s) measures were not different between high vs low PTH groups. Vibration detection threshold (48 vs 52 microns) was also similar. A deficit in ulnar motor amplitude was seen in 2 patients with high PTH levels (566 and 528) (1/2 diabetic). Both patients had neuropathic pain (function score >0), low grip strength (<20 kg) and low gait speed (<0.8 m/s).

Conclusion

Deficits in NCV, a marker of myelination, were noted in most patients on dialysis and did not differ between groups. Deficits in amplitude, a marker of axonal damage, were noted exclusively in patients with elevated PTH levels. Whether elevated PTH levels predispose to axonal neuropathy will be evaluated by ongoing enrollment of subjects and follow up testing after decreases PTH in this study.