Table 2.

Electrophysiological Studies of People with End-Stage Renal Disease on Haemodialysis

Author (Date)	Study Design	Muscle; Type of Investigation	Measure of Muscle Strength	Sample (n)	Results	Comments
Adeniyi (2004)55	Single case report	Iliopsoas, quadriceps, and TA; EMG recordings (type of electrode used not clearly indicated)	Clinical assessment of muscle strength (measures not reported); participant report of difficulty rising from chair	HD=1	Brief, small, abundant polyphasic potentials characteristic of myopathy	EMG studies suggestive of neuropathic and myopathic changes
Albertazzi (1980)46	Case-control	TA and EDB; EMG using co-axial needle electrode amplitude, duration, and phases of MUAPs, EMG of MVC, were recorded and analyzed using FFT	Unclear	HD=20 Con=20	4 patients showed myopathic EMG pattern with low voltage peaks Low muscle contraction to reach a full interference pattern	Results support myopathy as a possible cause of muscular weakness.
Bautista (1983)56	Case series	Deltoid; type of electrodes used not indicated	Clinical evaluation demonstrated proximal muscle weakness (measures not reported)	HD=8	Normal interference pattern	Normal EMG changes
Blank (1986)61	Case series	BB; EMG using needle electrode	Implicit suggestions of muscle weakness based on prior published reports of common complaints of muscle weakness in people on haemodialysis	HD=9	Increased frequency of spikes was seen in 6/9 participants with peripheral neuropathy during progressive muscle contraction Average maximal amplitude and average duration increased in the same 4 participants and decreased in 5 participants Total voltage area increased in 5 participants and decreased in 4 participants; 4 participants exhibited pattern similar to myopathic or healthy muscles, and 5 participants demonstrated neuropathic pattern	Observations suggest neuropathic origin in 4 participants and myopathic origin in 5 participants.
Fahal (1997)37	Case-control	Quadriceps; tetanic electrical stimulation at 100 Hz contraction up to 60% MVC Stimulations were applied at frequency range of 1, 10, 20, 50, and 100 Hz, each for 1s, except 10 Hz was applied for 2s E-C coupling—20:50 Hz stimulation	MVC using strain-gauge measurements recorded using rapid-response oscillograph: HD=Reduced MVC (p<0.01) Objective functional measures: HD=most-to-all results abnormal	HD=19 Con=27	Muscle strength—male and female HD patients were significantly weaker than the Con group (p<0.001) E-C coupling—the force/frequency curve was similar in the HD and Con groups	Observations of this study support the hypothesis that muscle weakness contributes to fatigue and that these changes are perhaps intrinsic to the muscle. Altered Ca+ release
Floyd (1974)15	Case-control	Quadriceps and deltoid; EMG recordings using needle electrode	Clinical assessment of strength (measures not reported)	HD=10 Con=7	Average MAPD in the quadriceps and deltoid significantly shorter than Con group (p<0.01) MAPA differed significantly between groups (p<0.05) Increased polyphasic potentials in participants on HD (p<0.002)	Results suggest skeletal muscle weakness of neuropathic and myopathic origin.
Gambaro (1987)29	Case-control	ABD and EDB (authors have not clearly indicated the muscles explored); EMG using needle electrode to study motor unit action potential following stimulation of ulnar and CPN	Symptoms of peripheral nervous system involvement, including muscle weakness, present in 55% of participants on HD (measures not reported)	HD=31 Con=30	Values of MUAP on stimulation of CPN were significantly lower in HD group than in Con group Values of MUAP on stimulation of ulnar nerve were similar to Con values	EMG findings suggestive of neuropathic (“dying-back degeneration”) changes affecting LEs>UEs Results support neuropathy as leading to muscle weakness.
Harrison (2006)59	Case series	1st dorsal interrosseous and vastus lateralis; EMG recordings using surface electrode	30-second chair-stand test (12±0.8); no comparison with Con	HD=25	EMG frequency recorded prior to HD was generally low and abnormal.	Results support possible disorder of the muscle causing muscle weakness. Primary objective of the study was to compare pre- vs. post-HD changes using EMG.
Isaacs (1969)63	Case series	APB and deltoid; EMG using needle electrode Deltoid muscle was explored for presence of polyphasic potentials. Fatigue test—isometric contraction against 2 lb weight maintained until 7 min or inability to hold the muscle contraction	Participant complaints of muscle weakness by the participants on HD associated with functional limitations (measures not reported)	HD=15	Focal areas of denervation in all participants; recruitment of the motor unit activity was abnormal and in most severe cases only isolated functioning motor units were present. Polyphasic counts were on the high side and ranged between 6% and 15% of total activity. Fatigue test—12 cases with clinical evidence of neuropathy showed considerable fallout of motor-unit activity, and the motor-unit amplitude fell when the tension could no longer be maintained.	Demonstrates involvement of the distal muscle Results indicative of neuropathic involvement affecting muscular strength
Johansen (2005)38	Case-control	TA; CMAP before and after exercise protocol; start @ 10% MVC and ↑ 10% every 2 min. End-of-exercise MVC and CMAP obtained	MVC using dynamometry (p=0.04)	HD=33 Con=12	CMAP was lower at baseline and did not change significantly after the exercise (p=0.003).	Fatigue was neural in nature, with reduced central activation ratio and poor metabolic response. Findings support neural causes of fatigue.
Konishi (1981)30	Case-control	EDC; SFEMG using needle electrode to obtain fibre-density and jitter values	Implicit suggestions of muscle weakness based on presence of peripheral neuropathy in people on HD as per prior published reports	HD=19 Con=20	8 participants showed abnormal jitter recordings. Mean fibre-density value was similar to Con group.	Abnormal jitter values indicate either impaired neuromuscular junction or variability of conduction time in each nerve twig. Results support possible neuropathic involvement affecting muscle function.
Lazaro (1980)16	Case series	Variable proximal muscles	Clinical assessment of strength (measures not reported), participant reports of gait abnormalities such as waddling gait or difficulty walking, difficulty rising from the chair	HD=4	Bizarre high-frequency discharges in one participant; all participants demonstrated short-amplitude and short-duration polyphasic potentials in all muscles examined.	Changes attributed to uremic myopathy
Rochhi (1986)48	Case-control	TA; EMG recordings using surface and needle electrode Total power obtained using FFT analysis	Possible presence of weakness based on presence of myopathy and neuropathy as per prior published reports	HD=20 Comparison with normal values for the laboratory	8 HD participants showed significant shift of the peak frequency of the spectral array toward values higher than Con group.	The shift in the spectral power frequency to higher values has been reported in people with myopathic disorders and is related to presence of polyphasic potentials. Results support myopathy as cause of muscle weakness.
Sobh (1992)62	Case series	BB representative of proximal muscle, and APB representative of distal muscle; EMG study including duration of MUAP amplitude, and interference pattern	Possible presence of weakness based on presence of neuropathy as per prior published reports	HD=6	Clinical neuropathy (n=2) Incomplete interference pattern on EMG of the APB (n=3)	Results indicate distal involvement and neuropathic pattern.
Tilki (2009)25	Case-control	BB and TA; QEMG NCS median, ulnar, and sural nerves	Possible presence of weakness based on presence of neuropathy as per prior published reports	HD=30 Comparison with normal values for the laboratory	Clinical neuropathy present in most the participants Evidence of axonal and/or demylinating polyneuropathy in all patients on HD	The primary objective of the study was to determine the most common abnormality of electrophysiologic changes among participants on HD and CAPD. Clinical evidence of polyneuropathy was presented for the whole group. Differences in clinical presentations of participants on HD and CAPD cannot be determined from the data.

APB=abductor pollicis brevis; ABD=abductor digiti minimi; BB=biceps brachii; Con=control group; CPN=common peroneal nerve; CMAP=compound muscle action potential; CRF=chronic renal failure; EDB=extensor digitorum brevis; EDC=extensor digitorum communis; EMG=electromyography; E-C coupling=excitation–contraction coupling; FFT=fast Fourier transform; HD=haemodialysis group; Hz=hertz; MAPD=mean action-potential duration; MAPA=mean action-potential amplitude; MUAP=motor-unit action potential; MVC=maximum voluntary contraction; NCS=nerve-conduction studies; QEMG=quantitative electromyography; SFEMG=single-fibre electromyography; TA=tibialis anterior; UE=upper extremity