Relative contributions of diabetes and chronic kidney disease to neuropathy development in diabetic nephropathy patients

被引：21

作者：

Issar, Tushar ^{[1
]}

Arnold, Ria ^{[2
]}

Kwai, Natalie C. G. ^{[1
,3
]}

Walker, Susan ^{[1
]}

Yan, Aimy ^{[1
]}

Borire, Adeniyi A. ^{[1
]}

Poynten, Ann M. ^{[4
]}

Pussell, Bruce A. ^{[5
]}

Endre, Zoltan H. ^{[5
]}

Kiernan, Matthew C. ^{[6
,7
]}

Krishnan, Arun, V ^{[1
]}

机构：

[1] UNSW Sydney, Prince Wales Clin Sch, Sydney, NSW 2031, Australia

[2] UNSW Sydney, Sch Med Sci, Sydney, NSW 2052, Australia

[3] UNSW Sydney, Dept Exercise Physiol, Sydney, NSW 2052, Australia

[4] Prince Wales Hosp, Dept Endocrinol, Sydney, NSW 2031, Australia

[5] Prince Wales Hosp, Dept Nephrol, Sydney, NSW 2031, Australia

[6] Univ Sydney, Brain & Mind Ctr, Sydney, NSW 2050, Australia

[7] Royal Prince Alfred Hosp, Sydney, NSW 2050, Australia

来源：

CLINICAL NEUROPHYSIOLOGY | 2019年 / 130卷 / 11期

基金：

英国医学研究理事会; 澳大利亚国家健康与医学研究理事会;

关键词：

Diabetic neuropathy; Diabetic kidney disease; Diabetic nephropathy; Chronic kidney disease; Uremic neuropathy; Nerve excitability; EXCITABILITY PROPERTIES; NERVE EXCITABILITY; INSULIN-RESISTANCE; DYSFUNCTION; CONDUCTANCES; TEMPERATURE; VALIDATION; DEPENDENCE; SCORE;

D O I：

10.1016/j.clinph.2019.08.005

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Objective: Chronic kidney disease (CKD) caused by diabetes is known as diabetic kidney disease (DKD). The present study aimed to examine the underlying mechanisms of axonal dysfunction and features of neuropathy in DKD compared to CKD and type 2 diabetes (T2DM) alone. Methods: Patients with DKD (n = 30), CKD (n = 28) or T2DM (n = 40) and healthy controls (n = 41) underwent nerve excitability assessments to examine axonal function. Neuropathy was assessed using the Total Neuropathy Score. A validated mathematical model of human axons was utilised to provide an indication of the underlying causes of nerve pathophysiology. Results: Total neuropathy score was significantly higher in patients with DKD compared to those with either CKD or T2DM (p < 0.05). In DKD, nerve excitability measures (S2 accommodation and superexcitability, p < 0.05) were more severely affected compared to both CKD and T2DM and worsened with increasing serum K+ (p < 0.01). Mathematical modelling indicated the basis for nerve dysfunction in DKD was an elevation of extracellular K+ and reductions in Na+ permeability and the hyperpolarisation-activated cation current, which was similar to CKD. Conclusions: Patients with DKD manifested a more severe neuropathy phenotype and shared features of nerve dysfunction to that of CKD. Significance: The CKD, and not diabetes component, appears to underlie axonal pathophysiology in DKD. (C) 2019 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.

引用

页码：2088 / 2095

页数：8