P0267CLINICAL MANIFESTATIONS, PREVALENCE AND PREDICTORS OF PERIPHERAL NEUROPATHY IN NON DIABETIC CHRONIC KIDNEY DISEASE PATIENTS. A CROSS SECTIONAL STUDY FROM TERTIARY CARE CENTRE

Abstract

Abstract Background and Aims There is a progressive increase in the prevalence of chronic kidney disease (CKD). The impairment of functions of kidney secondary to CKD leads to uraemia. Peripheral neuropathy is one of the common manifestations of uraemia. The present study focuses on the prevalence, clinical manifestations and predictors of peripheral neuropathy in patients with non-diabetic CKD. Method This was a cross sectional study conducted in the Department of General Medicine, Maharaja Krishna Chandra Gajapathi Medical College and Hospital, Berhampur, Odisha, India from October 2015 to October 2017. Patients with serum creatinine >2 mg/dl, estimated glomerular filtration rate <60 ml/min (calculated by using Modification of Diet in Renal Disease equation), kidney size < 8.5cm on ultrasound abdomen were included in the study and patients with age less than 18 years, patients with diabetes mellitus and other recognizable risk factors for peripheral neuropathy (Alcoholism, Drugs, Connective tissue disorders, Sarcoidosis, Vasculitis, Thyroid dysfunction, HIV, Hansen’s disease, Paraneoplastic disease etc.) and patients on dialysis were excluded. Peripheral neuropathy was assessed by both clinical methods and nerve conduction studies (NCS). Reduced motor nerve conduction velocity, delayed distal latency, fall in the amplitude of compound muscle action potential on Motor Nerve Conduction Study (MNCS) and delay in the peak latencies, reduced sensory nerve action potential on Sensory Nerve Conduction study (SNCS) were considered as evidence for peripheral neuropathy. From upper limb, median nerve and ulnar nerve were selected for MNCS and SNCS. From lower limb, common peroneal and posterior tibial nerves were selected for MNCS and sural nerve was selected for SNCS. Results Total 109 patients were included in the study and 75(68.8%) were proved to have peripheral neuropathy. Majority of the affected patients were in 40 to 50 years age group (n=24;32%). Forty four of 75 (58.6%) were males and 31(41.33%) were females. Patients with both sensory and motor neuropathy were 35(32.1%), 26(23.9%) were affected with only sensory neuropathy, while 14(12.8%) were affected with only motor neuropathy. Patients with clinical neuropathy (patients who have clinical symptoms and signs of neuropathy and also evidence on NCS) were 35(46.6%) and with subclinical neuropathy (only evident on NCS) were 40(53.3%).On univariate analysis, age (p-0.015), hypertension (p-0.031), duration of disease (p<0.0001), serum creatinine (p<0.0001), eGFR (p<0.0001), serum uric acid (p<0.0001), serum parathyroid (p<0.0001), serum phosphorus (p<0.0001), serum calcium (p-0.0003), serum magnesium (p-0.0002) and serum potassium (p-0.0028) were significantly correlated with peripheral neuropathy however on logistic regression analysis, sex [OR-0.058;95%CI(0.004-0.831)], serum parathyroid hormone [OR-1.032;95%CI(2.708-6043.5)], serum phosphorus[OR3.881;95%CI(1.114-13.524)], serum magnesium [OR-127.28;95%CI(0.901-1.113)] and duration of CKD[OR1.109;95%CI(1.005-1.224)] were shown to be independent predictors. Conclusion Peripheral neuropathy is one of the frequent complications of uremia. Subclinical presentation is most common. Serum parathyroid, serum phosphorus, serum magnesium and duration of disease are independent predictors of uremia induced peripheral neuropathy