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Chronic kidney disease (CKD) is characterised by an increasing prevalence, with the current prevalence of approximately 10 % in adults > 20 years in Western industrialized countries. In patients with CKD, frequently both the central nervous system (CNS) and the peripheral nervous system (PNS) are affected. Uremia, accumulation of AGE and oxidative stress, hyperkalemia, insulin resistance, adipocytokines, and erythropoietin deficiency and resistance have been identified as potential triggering factors. An impaired cerebral cognitive function in uremic patients is demonstrable even in clinically asymptomatic stages. Typical neurological sequelae include, among others, uremic encephalopathy, dialysis disequilibrium syndrome, and uremic polyneuropathy. In general, initiation of renal replacement treatment is suggested as the most promising therapeutic approach. Additionally, symptomatic treatment of neuropathic pain with first line drugs, such as gabapentin, pregabalin, tricyclic antidepressants or duloxetine, remains a reasonable approach. With respect to the important role of inflammation and oxidative stress in the further deterioration of renal function and nervous damage, additional treatment with benfotiamine may be considered as a pathogenesis-oriented approach.

Wittmann, I., Stirban, A., Tesfaye, S., Gurieva, I., Czupryniak, L., Mankovsky, B.N., et al. (2015). Neuropathy in chronic kidney disease. DIABETES, STOFFWECHSEL UND HERZ, 24(4), 251-255.

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