Examining the effects of diabetic kidney disease on neuropathy severity and nerve excitability: a comparative study — ASN Events
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Examining the effects of diabetic kidney disease on neuropathy severity and nerve excitability: a comparative study (#94)

Ria Arnold 1 , Natalie Kwai 2 , Bruce A Pussell 2 , Ann Poynten 3 , Arun V Krishnan 2
  1. School of Medical Sciences, UNSW Australia, Sydney, NSW, Australia
  2. Prince of Wales Clinical School, UNSW Australia, Sydney, NSW, Australia
  3. Department of Endocrinology, Prince of Wales Hospital, Randwick, NSW, Australia

Diabetes Mellitus (DM) is the most common cause of chronic kidney disease (CKD) worldwide.  Peripheral neuropathy is a highly prevalent and burdensome complication of both DM and CKD. However, the concomitant effect of these disorders on neurological outcomes is not well defined. This study aimed to examine neuropathy and nerve function in patients with DM+CKD compared to cohorts of DM and CKD alone. 

Sixty patients with type 2 diabetes were recruited and stratified according to the presence or absence of clinically diagnosed stage 3-4 CKD (DM+CKD n=30; DM n=30). Groups were compared to an age matched disease control cohort of CKD patients (n=15) and a healthy control cohort (n=20).  Neuropathy was graded using the total neuropathy score (TNS). Nerve function was assessed using nerve excitability testing on the median motor nerve.

Neuropathy was most severe in the DM+CKD group (TNS 11.4±7.5; p<0.05) and was similar between the DM (6.9±6.3) and CKD (4.9±5.0) groups. Neuropathy was prevalent in all groups with reduced sural amplitudes in 53% of CKD, 53% of DM and 80% of DM+CKD patients. Compared to age-matched controls, the DM and CKD groups demonstrated significant and distinct nerve excitability abnormalities. The CKD group demonstrated changes specifically related to membrane depolarisation (resting current threshold slope and depolarising threshold electrotonus p<0.05). In contrast, the DM group demonstrated abnormal stimulus response behaviour and accommodative properties (S2-accommodation and overshoot p<0.05). Importantly, the DM+CKD showed evidence of stimulus response changes and enhanced features of depolarisation which reflect the combined effect of dual pathological processes, hyperglycaemia and uraemia.

This study clearly demonstrates the detrimental effect of co-existing DM+CKD on neuropathy and nerve function. In isolation DM or CKD demonstrated similar neuropathy levels and specific nerve excitability abnormalities, while DM+CKD had more severe neuropathy and compound nerve function abnormalities. These findings highlight the importance of early detection and management of neuropathy in both DM and CKD