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Saudi Journal of Kidney Diseases and Transplantation
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RENAL DATA FROM ASIA–AFRICA  
Year : 2018  |  Volume : 29  |  Issue : 5  |  Page : 1139-1149
A clinical and electrophysiological study of peripheral neuropathies in peritoneal dialysis patients: Our experience from rural South India


1 Department of Neurology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India
2 Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India

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Date of Submission05-May-2017
Date of Acceptance01-Jul-2017
Date of Web Publication26-Oct-2018
 

   Abstract 

The objective was to study the prevalence, clinical features, electrophysiological features, and severity of peripheral neuropathy in chronic kidney disease (CKD) patients on peritoneal dialysis (PD) and effect of the presence of diabetes mellitus (DM). Between May 2015 and December 2016, 100 CKD patients on PD were assessed. The prevalence of peripheral neuropathy was 65% based on clinical symptoms and 92% based on electrophysiological parameters. The mean age was 55.7 ± 10.9 years. About 64% were male. Twelve patients (12%) had motor weakness, 64 patients (64%) had positive symptoms and 60 patients (60%) had negative symptoms. Autonomic symptoms were seen in 14 patients (14%). Definite damage was seen in 68 patients (68%), early damage was seen in 16 patients (16%). In PD patients with DM (n = 50), 50 patients (100%) had definite damage. In PD patients without DM (n = 50), 18 patients (36%) had definite damage, 16 patients (32%) had early damage. In CKD patients on PD, patients aged >50 years (definite damage in 75.7%) showed more severe peripheral neuropathy when compared to patients aged ≤50 years (definite damage in 53%). Most common nerves involved in the present study were median motor nerve, sural nerve, ulnar sensory nerve, common peroneal nerve, posterior tibial nerve followed by the median sensory nerve. Peripheral neuropathy is common in CKD patients on PD, with higher prevalence and severity in elderly females and diabetics. Rationale management of diabetes in CKD patients on PD probably lowers the prevalence and severity of peripheral neuropathy.

How to cite this article:
Mallipeddi S, Jasti DB, Apparao A, Vengamma B, Sivakumar V, Kolli S. A clinical and electrophysiological study of peripheral neuropathies in peritoneal dialysis patients: Our experience from rural South India. Saudi J Kidney Dis Transpl 2018;29:1139-49

How to cite this URL:
Mallipeddi S, Jasti DB, Apparao A, Vengamma B, Sivakumar V, Kolli S. A clinical and electrophysiological study of peripheral neuropathies in peritoneal dialysis patients: Our experience from rural South India. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2018 Nov 15];29:1139-49. Available from: http://www.sjkdt.org/text.asp?2018/29/5/1139/243942

   Introduction Top


Chronic kidney disease (CKD) is a progressive decline in renal function, which is responsible for significant morbidity and mortality. Due to decline in renal function, there will be accumulation of toxins resulting in multiple systemic complications. Uremia leads to several neurological complications which include uremic encephalopathy, atherosclerosis, neuropathy, and myopathy. Electrophysiological studies in adults revealed that almost 80% of CKD patients had electrophysiological evidence of impaired nerve function, although only one-half of these patients were symptomatic.[1],[2],[3] Kussmaul was the first to report this neurological complication.[4] The uremic neuropathy was suspected by Charcot in 1880.[5] and then by Osler in 1892. In 1962, the detailed explanation regarding the pathologic and clinical features was given by Asbury et al.[6] Males have more predilection to develop uremic neuropathy than females. The female-to-male ratio is 49:60 in 109 patients as observed by Nielsen.[7] The present concept of uremic neuropathy was established by Dyck et al, in 1971.[8]

Neuropathy in CKD patients is often multifactorial. Uremic toxins,[9] middle molecules,[10] and vitamin deficiency[11] are various factors which were proposed in the pathogenesis of uremic neuropathy. Studies revealed that patients treated with peritoneal dialysis (PD) had lower rates of uremic neuropathy which may suggest that the neuropathy-caused toxin more efficiently cleared by the peritoneum than by the membranes used in hemodialysis (HD).

The data about electrophysiological features and patterns of uremic neuropathy in PD patients is very sparse in Indian literature.

The present study was carried out to assess prevalence of peripheral neuropathy in CKD patients on PD patients with special emphasis on electrophysiological parameters and severity of peripheral neuropathy and its relation with diabetes mellitus.


   Materials and Methods Top


During the period from May 2015 to December 2016, 100 consecutive patients from rural areas diagnosed to have CKD and are on PD at Sri Venkateswara Institute of Medical Sciences, Tirupati were included in the present study. Patients with pre-existing peripheral neuropathy prior to the diagnosis of CKD, patients from urban and semi urban areas were excluded from the present study. The study was approved by the Institutional Ethics Committee and written informed consent was obtained from the patients for their participation in the study.

One hundred consecutive CKD patients, who were on PD and had given consent to participate in the study were included in the present study. These 100 patients were divided into two groups. Group 1 included 50 diabetic patients Group 2 included 50 nondiabetic patients. Each group was further subdivided into subgroups based on age, sex, duration of CKD, and duration of dialysis for further analysis.

Detailed history was elicited pertaining to symptoms of peripheral neuropathy and diabetes mellitus (DM). Detailed general physical examination and neurological examination were done and documented. Duration of PD was noted in all the patients. Biochemical investigations including blood urea, serum creatinine, and blood sugars were measured in all the patients as per the standard methods used in the Department of Biochemistry.

All cases were subjected to nerve conduction studies (NCS) using Medelec synergy and Natus machines. NCS procedure was done for both motor conductions and sensory conductions. Median nerve, ulnar nerve, common peroneal nerve, and posterior tibial nerve were assessed for motor conductions. Median nerve, ulnar nerve, and sural nerve were assessed for sensory conductions. In motor conductions, distal latency, conduction velocity, amplitude, and F wave were assessed. In sensory conductions, distal latency, conduction velocity, and amplitude were assessed.

Only right upper limb parameters were used as many dialysis patients who participated in the study had an arteriovenous fistula on their left upper limb. In lower limbs, sensory and motor conductions were done in both the lower limbs.

The gain was normally set at 2–5 mV per division for the motor conduction studies. The recording electrodes were placed on the muscle being studied. The belly-tendon montage was used commonly. The center of the muscle belly (over the motor endplate) was used for placing the active recording electrode (also known as G1) and the reference electrode (also known as G2) was placed distally, over the tendon of the muscle. The nerve that supplies the muscle was used for placing the stimulator, where the cathode was placed close to the recording electrode. The duration of the electrical pulse was generally set to 200 ms for the motor NCS. To achieve supramaximal stimulation, current in the range of 20 to 50 mA was used. The underlying nerve fibers were brought to action potential as the current was steadily increased from a baseline, usually by 5-10 mA. The summation of all the underlying individual muscle fiber action potentials was represented by the compound muscle action potential (CMAP). When all the nerve fibers have been excited and the supra-maximal stimulation has been achieved then the CMAP shall no longer increase in size.

For median nerve motor conduction studies, the recording electrode was placed over the motor point of the abductor pollicis brevis muscle, at the midpoint of a line drawn from the first metacarpophalangeal joint to the insertion of the tendon of the flexor carpi radialis muscle, and the reference electrode was placed over the distal interphalangeal joint. Mid arm, antecubital fossa, and wrist were sites of stimulation for median nerve motor conduction studies. For ulnar nerve motor conduction studies, the recording electrode was placed over the motor point of the abductor digiti minimi muscle, at the midpoint of a line between the 5th metacarpopha-langeal joint and the pisiform bone, with the reference electrode over the middle phalanx of digit V. Axilla, above elbow, ulnar groove, and medial wrist were sites of stimulation for ulnar nerve motor conduction studies. For the posterior tibial nerve, the CMAP was recorded by placing the active electrode over the middle of the adductor hallucis muscle, and the reference electrode over the proximal phalanx of digit I. The posterior tibial nerve was stimulated below the medial malleolus and in the popliteal fossa. For common peroneal nerve motor conduction studies, the recording electrode was placed in the middle of the extensor digitorum brevis muscle. The common peroneal nerve was stimulated at the ankle, 80 mm proximal to the recording electrode, lateral to the tendon of tibialis anterior muscle, and below the knee 20–50 mm distal to the proximal part of the caput fibula.

Latency was described as the time from the stimulus to the initial CMAP deflection from the baseline. The CMAP amplitude was measured from the baseline to the negative peak. Conduction velocity was calculated using the formula - Distance between the proximal and distal stimulation sites/proximal latency- distal latency. The standardized normal adult values of motor NCS in both upper and lower extremities as per our electrophysiology laboratory are shown in [Table 1].[12]
Table 1: Motor nerve conduction studies: standardized normal adult values in both upper and lower extremities.

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The F response also known as the late motor response occurs after the CMAP.[13] Normal minimal F latency was 25–30 ms in median and ulnar nerves, whereas it was 45–59 ms in common peroneal and posterior tibial nerves.

Median and ulnar sensory nerve action potentials (SNAPs) were obtained orthodromically, stimulating from the index finger (median nerve) or the little finger (ulnar nerve) and recording at the wrist. Sural SNAPs were obtained antidromically, recording behind the lateral malleolus and stimulating on the dorsal aspect of the calf, 140 mm proximal to the recording site. The responses were averaged at least 10 times. The standardized normal adult values of sensory NCS in both upper and lower extremities as per our electrophysiology laboratory are shown in [Table 2].[14]
Table 2: Sensory nerve conduction studies: standardized normal adult values in both upper and lower extremities.

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Based on electrophysiological parameters, peripheral neuropathy patterns were sub classified into axonal neuropathy, demyelinating neuropathy, and mixed neuropathy. In axonal neuropathy, CMAP’s decrease, conduction velocities are normal or slightly decreased but never <75% of the lower limit of normal, distal latencies are normal or slightly prolonged but never >130% of the upper limit of normal. In demyelinating neuropathy, CMAP’s are usually normal with marked slowing of conduction velocity (slower than 75% of the lower limit of normal) and/or marked prolongation of distal latency (longer than 130% of the upper limit of normal). It was classified as mixed neuropathy if it has features of both axonal neuropathy and demyelinating neuropathy. Degree of severity of peripheral neuropathy was divided into three groups as follows: normal, early damage and definite damage, according to the number of peripheral nerves involved. Normal or no peripheral damage was defined if NCS were normal or only one peripheral nerve was involved. Early damage, if two or three peripheral nerves were involved and definite damage, if more than three peripheral nerves were involved.


   Statistical Analysis Top


The data were collected and tabulated using Microsoft Excel 2010 version. Data were analyzed using Statistical Package for Social Sciences (SPSS) version 20.0 (SPSS Inc. Chicago, IL, USA). All the continuous variables were expressed as mean ± standard deviation or median with interquartile range as appropriate. All categorical variables were expressed as frequencies (percentage). Independent t-test and ANOVA test were applied to compare nominal data between the groups and P <0.05 was considered statistically significant.


   Results Top


Between May 2015 and December 2016, 100 consecutive patients with CKD on PD who consented to participate were included in the study. These 100 patients were divided into two groups – Group 1 included 50 diabetic patients and Group 2 included 50 nondiabetic patients.

The prevalence of peripheral neuropathy in 100 CKD patients on PD was 65% based on clinical symptoms and 84% based on electrophysiological parameters. Based on electrophysiological data, prevalence of peripheral neuropathy in CKD patients on PD with DM and without DM was 100% and 68%, respectively.

The mean age of 100 CKD patients on PD who participated in the study was 55.7 ± 10.9 years. In this study, males were 64 (64%) and females were 36 (36%). The mean age of 50 patients in Group 1 (PD patients with DM) who participated in the study was 58.9 ± 9.5 years. In Group 1, males were 30 (60%) and females were 20 (40%). The mean age of 50 patients in Group 2 (PD patients without DM) who participated in the study was 52.5 ± 11.5 years. In Group 2, males (n = 34, 68%) outnumbered females (n = 16, 32%).

Comparison of symptoms and signs of 100 CKD patients on PD who participated in the study is shown in [Table 3].
Table 3: Comparison of symptoms and signs of 100 chronic kidney disease patients on peritoneal dialysis who participated in the study.

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On comparing symptoms and signs of peripheral neuropathy in CKD patients on PD, patients with DM showed statistical significance in the presence of negative symptoms (P = 0.009).

The mean serum creatinine of CKD patients on PD, with and without DM was 8.2 ± 2.8 mg/dL and 6.9 ± 2.5 mg/dL, respectively. The mean blood urea of CKD patients on PD, with and without DM was 99.8 ± 30.7 mg/dL and 94.6 ± 37.0 mg/dL, respectively. The mean duration of DM in 50 diabetic patients on PD was 10.7 ± 3.2 years. The mean duration of patients on PD was 4.2 ± 3.2 years.

Nerve conduction abnormalities in CKD patients on PD are shown in [Table 4].
Table 4: Nerve conduction abnormalities in 100 CKD patients on PD.

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Comparison of electrophysiological parameters of 100 CKD patients on PD who participated in the study is shown in [Table 5].
Table 5: Comparison of electrophysiological parameters of 100 CKD patients on PD who participated in the study.

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On comparing electrophysiological data of CKD patients on PD; patients with DM showed statistically significant prolonged median nerve motor distal latency (P <0.001), low median nerve motor amplitude (P = 0.001), prolonged median nerve F wave (P = 0.003), prolonged ulnar nerve motor distal latency (P = 0.012) , low ulnar nerve motor conduction velocity (P <0.001), prolonged ulnar nerve F wave (P = 0.004), low common peroneal nerve motor conduction velocity (P <0.001), low common peroneal nerve motor amplitude (P <0.001), absent common peroneal F wave (P <0.001), low posterior tibial nerve motor conduction velocity (P = 0.001), low posterior tibial nerve motor amplitude (P <0.001), absent posterior tibial nerve F wave P <0.001), low median nerve sensory conduction velocity (P = 0.029), low median nerve (sensory amplitude (P <0.001), low ulnar nerve sensory conduction velocity (P 0.001), low ulnar nerve sensory amplitude (P < 0.001), low sural nerve sensory conduction velocity (P <0.001), and low sural nerve sensory amplitude (P <0.001).

CKD patients on PD and without DM showed statistical significance in the presence of prolonged common peroneal nerve motor distal latency (P = 0.014), prolonged ulnar nerve sensory distal latency (P = 0.002) and prolonged sural nerve sensory distal latency (P <0.001).

Definite damage was seen in 68 patients (68%), early damage was seen in 16 patients (16%) whereas 16 patients (16%) had no significant peripheral neuropathy. In PD patients with DM (n = 50), 50 patients (100%) had definite damage. In PD patients without DM (n = 50), 18 patients (36%) had definite damage, 16 patients (32%) had early damage, whereas 16 patients (32%) had no evidence of significant peripheral neuropathy.

Patients in each group were further subdivided into two subgroups, based on age, sex, duration of CKD, duration of dialysis. Based on age, each group was subdivided into two subgroups; subgroup 1 with age ≤50 years and subgroup 2 with age >50 years. Based on sex, each group was subdivided into two subgroups; males and females. Based on the duration of CKD, each group was subdivided into two subgroups; subgroup 1 with duration ≤5 years and subgroup 2 with duration >5 years. Based on duration of dialysis, each group was subdivided into two subgroups; subgroup 1 with duration ̤5 years and subgroup 2 with duration >5 years.

Comparison of severity of peripheral neuropathy in subgroups of CKD patients on PD is shown in [Table 6].
Table 6: Comparison of severity of peripheral neuropathy in subgroups of CKD patients on PD.

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   Discussion Top


Peripheral neuropathy is a common neurological complication seen in CKD patients, prevalence of which increases in end-stage renal disease patients. Patients who are on maintenance dialysis have more prevalence of peripheral neuropathy when compared to predialysis patients. Patients on PD have relatively less severe peripheral neuropathy when compared to patients on maintenance HD. NCS are the most commonly used diagnostic procedure used for establishing the presence and type of peripheral neuropathy. Indian literature regarding prevalence, electrophysiological parameters, and severity of peripheral neuropathy in CKD patients on PD is sparse. Hence, the present study was undertaken to study the prevalence, clinical features, electrophysiological features, and severity of peripheral neuropathy in CKD patients on PD in the South Indian population and to study the effect of the presence of DM on peripheral neuropathy. The present study showed a high prevalence of uremic neuropathy; About 65% based on clinical symptoms and 84% according to electrophysiological studies. In this study, 19% had asymptomatic peripheral neuropathy. About 77.4% of CKD patients on PD showed evidence of peripheral neuropathy according to Janda et al.[15] Comparable prevalence rates of peripheral neuropathy were documented in other published international studies.[17],[18]

The mean age of 100 CKD patients on PD who participated in the study was 55.7 ± 10.9 years which was almost similar to other published studies.[16],[17],[18] Kim et al, studied 29 CKD on PD, while Kayalar et al, and Tilki et al, studied 16 patients and 12 patients, respectively. Our sample size (n = 100) is larger when compared to other studies. Hence, our study might probably reflect the patterns of peripheral neuropathy and abnormalities in electrophysiological parameters better than other smaller studies.

Sixty-five percent patients on PD were symptomatic for peripheral neuropathy in the present study in the form of both positive and negative symptoms. Fourteen percent patients had features of associated autonomic neuropathy. However, around 90% of patients had absent ankle jerk, all of whom had electrophysiological evidence of peripheral neuropathy. Hence, good clinical examination and meticulous history elicitation regarding peripheral neuropathy will help in judicious use of NCS. The mean serum creatinine and urea of 100 CKD patients who participated in the study were almost similar to study by Kayalar et al,[17] on 16 CKD patients on PD, in which mean serum creatinine and blood urea were 9.1 ± 1.8 mg/dL and 100.0 ± 43.8 mg/dL, respectively.

Comparison of an electrophysiological profile in 100 CKD patients on PD with other published international studies[16],[18] is shown in [Table 7]. Indian data regarding electrophysiological parameters in PD patients is sparse.
Table 7: Comparison of electrophysiological parameters in chronic kidney disease patients on peritoneal dialysis as reported in published studies.

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On comparing electrophysiological parameters of CKD patients on PD with other published studies, motor amplitude and motor conduction velocity were higher in our study. In PD patients (n = 100); eight patients had carpal tunnel syndrome. Eighty-four percent patients had significant peripheral neuropathy. No significant neuropathy was seen in 16 patients (16%).

Most common nerves involved in the present study were median motor nerve, sural nerve, ulnar sensory nerve, common peroneal nerve, posterior tibial nerve followed by median the sensory nerve in the present study. Lower limbs were most commonly affected than upper limbs, which indicate a length dependent pattern. Sensory nerves were commonly affected than motor nerves in the present study.

Diabetic patients (100%) on PD showed higher prevalence and severity of peripheral neuropathy when compared to nondiabetic CKD patients (68%). In addition to factors responsible for uremic neuropathy, probably the presence of DM might contribute to higher prevalence and severity of peripheral neuropathy in diabetic CKD patients.

Statistically most significant electrophysiological parameters differentiating diabetic CKD patients on PD and nondiabetic CKD patients on PD were median nerve motor distal latency, ulnar nerve motor conduction velocity, common peroneal nerve motor conduction velocity, common peroneal nerve motor amplitude, common peroneal F wave, posterior tibial nerve motor amplitude, posterior tibial nerve F wave, median nerve sensory amplitude, ulnar nerve sensory conduction velocity, ulnar nerve sensory amplitude, sural nerve sensory conduction velocity and sural nerve sensory amplitude.

The patients aged >50 years (definite damage in 75.7%) showed more severe peripheral neuropathy when compared to patients aged ≤50 years (definite damage in 53%). Females (definite damage in 72.2%) showed more severe peripheral neuropathy when compared to males (definite damage in 65.6%). In the present study, dialysis duration and disease duration did not have statistically significant difference in severity and prevalence of peripheral neuropathy. There are no major Indian studies comparing prevalence and severity of peripheral neuropathy in diabetic and nondiabetic CKD patients PD.

The most common patterns of peripheral neuropathy in our patients were pure axonal sensorimotor neuropathy pattern (34%) and mixed sensorimotor neuropathy pattern (34%). The most common patterns of peripheral neuropathy in the patients of with DM were pure axonal sensorimotor neuropathy pattern (56%) followed by mixed sensorimotor neuropathy pattern (44%). The most common patterns of peripheral neuropathy in the patients without DM were mixed sensorimotor neuropathy pattern (24%) followed by pure axonal sensory neuropathy pattern (20%).

In developing countries like India, financial constraints become a major issue for periodic NCS. However to diagnose peripheral neuropathy early to minimize discomfort to the patient, meticulous history, and neurological examination with judicious use of NCS is required. Moreover most of our population belong to rural areas, who consult medical care very late, which might be responsible for higher prevalence and severity of uremic neuropathy. However, newer treatment modalities are required to manage uremic neuropathy better.


   Limitations of the Present Study Top


Electrophysiologic parameters might be slightly altered due to the presence of edema in CKD patients.


   Conclusion Top


Peripheral neuropathy is common in CKD patients on PD, with higher prevalence and severity in elderly females. CKD patients with DM on PD showed higher prevalence and more severe peripheral neuropathy when compared to nondiabetic patients. Rationale management of diabetes in CKD patients on PD probably lowers the prevalence and severity of peripheral neuropathy.

Conflict of interest: None declared.

 
   References Top

1.
Bazzi C, Pagani C, Sorgato G, Albonico G, Fellin G, D’Amico G. Uremic polyneuropathy: A clinical and electrophysiological study in 135 short- and long-term hemodialyzed patients. Clin Nephrol 1991;35:176-81.  Back to cited text no. 1
    
2.
Van den Neucker K, Vanderstraeten G, Vanholder R. Peripheral motor and sensory nerve conduction studies in haemodialysis patients. A study of 54 patients. Electromyogr Clin Neurophysiol 1998;38:467-74.  Back to cited text no. 2
    
3.
Laaksonen S, Metsäarinne K, Voipio-Pulkki LM, Falck B. Neurophysiologic parameters and symptoms in chronic renal failure. Muscle Nerve 2002;25:884-90.  Back to cited text no. 3
    
4.
Jennekens FG. Peripheral neuropathy in renal and hepatic insufficiency. In: Matthews WB, editor. Handbook of Clinical Neurology. Vol. 51. Neuropathies Amsterdam: Elsevier; 1987. p. 355-64.  Back to cited text no. 4
    
5.
Charcot JM. Lecons Sur les Maladies du Systeme Nerveux. XVI Des Paraplegies Urinares. 3rd ed. Paris; 1880. p. 295.  Back to cited text no. 5
    
6.
Asbury AK, Victor M, Adams RD. Uremic polyneuropathy. Arch Neurol 1963;8:413-28.  Back to cited text no. 6
    
7.
Nielsen VK. Recovery from peripheral neuropathy after renal transplantation. Acta Neurol Scand 1970;46:207-8.  Back to cited text no. 7
    
8.
Dyck PJ, Johnson WJ, Lambert EH, O’Brien PC. Segmental demyelination secondary to axonal degeneration in uremic neuropathy. Mayo Clin Proc 1971;46:400-31.  Back to cited text no. 8
    
9.
Halar EM, Brozovich FV, Milutinovic J, Inouye VL, Becker VM. H-reflex latency in uremic neuropathy: Correlation with NCV and clinical findings. Arch Phys Med Rehabil 1979;60:174-7.  Back to cited text no. 9
    
10.
Krishnan AV, Phoon RK, Pussell BA, Charlesworth JA, Bostock H, Kiernan MC. Altered motor nerve excitability in end-stage kidney disease. Brain 2005;128:2164-74.  Back to cited text no. 10
    
11.
Bolton CF, Young GB. Neurological complications of renal disease. Ann Neurol 1993;33: 94-100.  Back to cited text no. 11
    
12.
Chen S, Andary M, Buschbacher R, et al. Electrodiagnostic reference values for upper and lower limb nerve conduction studies in adult populations. Muscle Nerve 2016;54:371-7.  Back to cited text no. 12
    
13.
Nobrega JA, Pinheiro DS, Manzano GM, Kimura J. Various aspects of F-wave values in a healthy population. Clin Neurophysiol 2004; 115:2336-42.  Back to cited text no. 13
    
14.
Bolton CF, Carter KM. Human sensory nerve compound action potential amplitude: Variation with sex and finger circumference. J Neurol Neurosurg Psychiatry 1980;43:925-8.  Back to cited text no. 14
    
15.
Janda K, Stompór T, Gryz E, et al. Evaluation of polyneuropathy severity in chronic renal failure patients on continuous ambulatory peritoneal dialysis or on maintenance hemo-dialysis. Przegl Lek 2007;64:423-30.  Back to cited text no. 15
    
16.
Kim D, Blair G, Wu G, Ayiomamitis A, Oreopoulos DG. Electrophysiological studies of nerve function in patients on CAPD over long periods. Perit Dial Int 1985;5:45-8.  Back to cited text no. 16
    
17.
Kayalar AO, Basturk T, Koc Y, et al. Comparison of long-term complications in patients on haemodialysis and peritoneal dialysis longer than 10 years. J Clin Diagn Res 2016;10:OC05-8.  Back to cited text no. 17
    
18.
Tilki HE, Akpolat T, Coşkun M, Stålberg E. Clinical and electrophysiologic findings in dialysis patients. J Electromyogr Kinesiol 2009;19:500-8.  Back to cited text no. 18
    

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Correspondence Address:
Dr. Sarat Mallipeddi
Department of Neurology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh
India
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DOI: 10.4103/1319-2442.243942

PMID: 30381511

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