The Burden of Peripheral Neuropathy in Nondiabetic Chronic Kidney Disease and the Role of Ghrelin Isoforms in its Development

Madumathy Ramachandran; Velkumary Subramanian; Saranya Kuppusamy; Sreejith Parameswaran; Palanivel Chinnakali; Balasubramaniyan Vairappan

doi:10.4103/ijn.IJN_557_20

The Burden of Peripheral Neuropathy in Nondiabetic Chronic Kidney Disease and the Role of Ghrelin Isoforms in its Development

Indian J Nephrol. 2022 Nov-Dec;32(6):567-573. doi: 10.4103/ijn.IJN_557_20. Epub 2022 Nov 21.

Authors

Madumathy Ramachandran¹, Velkumary Subramanian², Saranya Kuppusamy², Sreejith Parameswaran³, Palanivel Chinnakali⁴, Balasubramaniyan Vairappan⁵

Affiliations

¹ Department of Physiology, All India Institutes of Medical Sciences (AIIMS), Bhubaneswar, Odisha, India.
² Department of Physiology, Jawaharlal Institute of Post-Graduate Medical Education and Research (JIPMER), Pondicherry, India.
³ Department of Nephrology, Jawaharlal Institute of Post-Graduate Medical Education and Research (JIPMER), Pondicherry, India.
⁴ Department of Preventive and Social Medicine, Jawaharlal Institute of Post-Graduate Medical Education and Research (JIPMER), Pondicherry, India.
⁵ Department of Biochemistry, Jawaharlal Institute of Post-Graduate Medical Education and Research (JIPMER), Pondicherry, India.

Abstract

Introduction: Peripheral neuropathy is one of the most common complications in chronic kidney disease (CKD). The neuroprotective role of ghrelin is being explored recently. Here we aim to determine the burden of neuropathy in nondiabetic CKD and to find the association of peripheral nerve function with plasma ghrelin levels in these patients.

Methods: This was a cross-sectional study conducted in nondiabetic CKD patients on conservative management to determine the magnitude of neuropathy. The association of ghrelin isoforms with nerve functions was assessed between three groups, namely CKD with neuropathy, CKD without neuropathy, and healthy volunteers, with 20 participants in each group.

Results: The proportion of neuropathy in nondiabetic CKD was 78% (n = 78), of which 51% (n = 40) were asymptomatic. Des acyl ghrelin (DAG) and total ghrelin (TG) levels were 1545.5 ± 487.4 and 1567.4 ± 485.3 pg/mL, respectively, in CKD patients with neuropathy and were found to be elevated compared to those without neuropathy, who had 1000.4 ± 264.2 and 1019.7 ± 264.3 pg/mL of DAG and TG, respectively (P < 0.001). Assessment of correlation between nerve conduction parameters and DAG levels showed positive correlation between DAG levels and common peroneal latency (r = 0.69; P < 0.01), median sensory latency (r = 0.45; P < 0.05), and sural latency (r = 0.51; P < 0.05). We found negative correlation between median velocity (r =-0.56; P < 0.05), common peroneal velocity (r = -0.64; P < 0.01), median sensory velocity (r =-0.49; P < 0.05), and sural velocity (r = -0.54; P < 0.05). There was no statistically significant difference in acyl ghrelin levels among the groups.

Conclusion: The prevalence of peripheral neuropathy in CKD is significantly higher with almost half of them being asymptomatic. Impaired renal clearance in CKD leads to the accumulation of DAG, which subsequently inhibits the neuroprotective functions of AG leading to neuropathy in CKD.

Keywords: Acyl ghrelin; chronic kidney disease; des acyl ghrelin; nerve conduction study; peripheral neuropathy.