Polyneuropathy in the diabetic patient--update on pathogenesis and management

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Abstract
Distal symmetrical sensory or sensorimotor polyneuropathy (DSP) affects ∼30% of the hospital-based population and 20% of community-based samples of diabetic patients. The incidence of DSP is ∼2% per year. The most important aetiological factors that have been associated with DSP are poor glycaemic control, diabetes duration and height, with possible roles for hypertension, age, smoking, hypoinsulinaemia and dyslipidaemia [1]. Moreover, DSP is related to both lower extremity impairments such as diminished position sense and functional limitations such as walking ability. There is accumulating evidence suggesting that not only surrogate markers of microangiopathy such as albuminuria, but also those indicating the presence of polyneuropathy such as impaired nerve conduction velocity (NCV) and vibration perception threshold (VPT) predict mortality in diabetic patients [2,3]. Elevated VPT also predicts the development of neuropathic foot ulceration, one of the most common causes for hospital admission and lower limb amputations among diabetic patients [4]. Pain associated with diabetic neuropathy has a substantial impact on the quality of life, particularly interfering with sleep and enjoyment of life [5]. Chronic painful diabetic neuropathy is a long-term complication of diabetes and, hence, not infrequent in the diabetic patient with renal complications. An update on the current state of the art in this field is therefore of interest to the nephrologist.