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. 2011 Aug 10;63(3):355–376. doi: 10.3138/ptc.2010-18

Table 1.

Muscle Biopsy Studies in People with End-Stage Kidney Disease on Haemodialysis

Author (Date) Study Design Muscle; Biopsy Type Measure of Muscle Strength Sample (n) Results
 Comments
Type I Fibres Type II Fibres Other Microscopic Changes
Adeniyi (2004)55 Single case report Quadriceps; type of biopsy not indicated Clinical assessment of muscle strength (measures not reported); report of difficulty rising from the chair HD=1 Scattered atrophic fibres Scattered atrophic fibres Type I and II fibres equally involved, consistent with neuropathic myopathy Reports do not support myopathy as a primary cause of weakness.
Ahonen (1980)36 Case-control Gastrocnemius (medial head); open muscle biopsy Implicit suggestions of muscle weakness based on prior published reports of myopathy in people with ESRD/HD HD=11
Con=9		 Diameter of type I fibres slightly larger than reference group (type I hypertrophy) (p>0.01)

  • Type II fibre diameter smaller

  • Type II fibre distribution more frequent (p>0.01)

  • Myopathic changes of fibre size variation (18%), central nuclei (9%), necrotic and phagocytic fibres (36%), and moth-eaten and whorled fibres (73%) in 3/11 biopsies

  • Typical neurogenic changes were angulated atrophic fibres

  • Neurogenic changes in 7/11 biopsies

  • Mixed neuropathic and myopathic changes in 1/11 biopsies

  • Results suggest presence of myopathic changes in distal muscles.

  • Mixed results indicating effect of uremia on the different components of motor-unit complex
Bautista (1983)56 Case series Deltoid; method of biopsy not indicated Clinical evaluation demonstrated proximal muscle weakness (measures not reported) HD=10

  • Occasional atrophy of type I fibres

  • Negative hypertrophy factor

  • Type II atrophic fibres

  • Infrequent angulated, rounded, or polygonal atrophic fibres

  • Negative hypertrophy factor

  • No predominance of either type of fibres

  • Electron microscopy (n=9)—all biopsies showed abnormal amount of subcutaneous lipofuscin located beneath cell membrane

  • One case showed loss and derangement of myofilaments

  • One case showed sub-sarcolemmal aggregates of normal mitochondria

 Myofibrillar changes suggestive of myopathic factors contributing to muscular weakness
Crowe (2007)26 Case-control Quadriceps femoris (lateral); percutaneous needle biopsy Implicit suggestions of muscle weakness based on prior published reports of limited exercise capacity contributing to poor quality of life HD=10
Con=10		 Fibre diameter reduced by 15% (p=0.04) Fibre diameter reduced by 20% (p=0.03) No difference in proportion of type I and II fibres compared to Con (p=0.9)

  • Change in fibre size was unrelated to oxidative stress.

  • Relative atrophy (change in fibre size) of type 1 fibres suggestive of myopathies

  • Type II fibre atrophy— non-specific

  • Results support changes in the muscle causing muscular weakness.
Diesel (1993)27 Case-control Vastus lateralis; open muscle biopsy

  • Isokinetic muscle strength using Cybex II

  • HD=Isokinetic strength (p<0.05)

 HD=8
Athl=7
Con=5		 Hypertrophy of type I fibres (n=2)

  • Atrophied type II fibres (n=8) from 6%—62%, n=2 significant type II fibre atrophy

  • Predominance of type II fibres (n=2)

  • Electron microscopy revealed mitochondrial changes, Z-band degeneration, and loss of myofilaments (n=8)

  • Changes suggestive of progressive muscle involvement, with some cells more affected than others

  • Selective hypertrophy of type I fibres and type II predominance in n=2 supports neuropathic factors affecting muscular strength.

  • Myofibrilar changes and atrophy of type I fibres supports myopathic causes of weakness.

  • Results suggest neuro/myopathy causing muscular weakness.
Fahal (1997)37 Case-control Quadriceps femoris (lateral); percutaneous conchotome biopsy

  • 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=12
Con=10

  • Low prevalence of type I fibres (n=5)

  • High prevalence of type I fibres (n=1)

  • Mean prevalence of type I fibres similar in both groups (p=0.1)

  • High prevalence of type II fibres (n=1)

  • Difference of prevalence of type II fibres in the two groups not significant (p=0.5)

  • Fibre areas slightly smaller in participants on HD

  • Mean difference of fibre areas similar in both groups

  • Atrophy and high prevalence of type I fibres suggestive of myopathic changes

  • High prevalence of type II fibres in n=1 suggestive of neuropathic changes

  • Results reflect heterogeneity of neuro/myopathic changes in muscles of HD group causing muscular weakness.
Floyd (1974)15 Case-control Quadriceps or biceps; open muscle biopsy Clinical assessment of strength (measures not reported) HD=10
Non-
dialyzed=4		 Variation in muscle fibre size was outside normal limits in the majority of the cases Type II fibre atrophy in each case

  • Some fibres were rounded, and a few contained internal nuclei

  • Type I fibres contained excessive amounts of glycogen in the region of subsarcolemmal aggregates

 Results support myopathic changes associated with renal failure as possible cause of muscular weakness.
Giovenali (1994)53 Case series Vastus lateralis; open muscle biopsy

  • MVC—using objective methodology described by Edwards et al. (1977)

  • HD—all results below normal values

 HD=26 Atrophy of type I fibres Atrophy of type II fibres N/A The main objective of the study was to assess the effect of L-carnitine on muscle strength. The baseline data were included.
Kouidi (1998)9 Case series Vastus lateralis; open muscle biopsy MVC using dynamometer HD=7 Changes in HD:

  • Reduced mean fibre area

  • Atrophy of type I fibres

  • Random variation in fibre size

  • Predominance of type I fibres

  • Type II fibre size almost equal to type I fibre size

  • Atrophy of type II>type I fibres

  • Glycogen deposition in most muscle fibres

  • Non-specific degenerative changes in muscle fibres, mitochondria, and capillaries

  • External lamina of fibres' sarcolemma and basal lamina of capillaries remained after their necrosis

  • Central nuclei with invaginations

  • Disorganization of sarcomeres with Z-disk streaming and loss of A & I bands in many fibres

  • Atrophy and high prevalence of type I fibres, changes in the myofibrils, mitochondrial changes, and central nuclei suggestive of myopathic changes

  • Glycogen deposition associated with carnitine deficiency

  • Supports neuro/myopathy causing muscular weakness, as suggested by fibre atrophy grouping and small-group atrophy in most patients.
Lazaro (1980)16 Case series Quadriceps femoris; open muscle biopsy Clinical assessment of strength (measures not reported), participant reports of gait abnormalities such as waddling gait or difficulty walking, difficulty rising from chair HD=4 No comment on changes in type I fibres

  • 90% atrophic fibres (n=1)

  • Comprised 80% and 85% of the small fibres (n=2)

  • No evidence of phagocytosis, necrosis, or regeneration

  • Few moth-eaten fibres were seen (n=4)

  • Type II fibre atrophy— non-specific

  • Results indicate possible myopathic changes associated with muscular weakness in people with renal disease.
Moore (1993)57 Case series Rectus femoris; percutaneous needle biopsy Implicit suggestions of muscle weakness based on prior published reports of uremic myopathy HD=11 Numerous atrophic type I fibres Numerous atrophic type II fibres Variability in type I and type II fibres was large Peripheral factors contributing to skeletal muscle weakness
Molsted (2007)31 Case-control Vastus lateralis; open muscle biopsy

  • Implicit suggestions of muscle weakness based on prior published reports of uremic myopathy

  • Researchers tested aerobic capacity, but results not reported in context to Con population

 HD=14
Con=12		 Several patients on HD had <15% type I fibres p<0.001 More of type IIx fibres N/A

  • Uremia affected composition rather than size of muscle fibres; increase of type IIx fibres was considered compensatory for loss of type I fibres.

  • Atrophy of type I fibres usually associated with myopathic changes

  • Results support myopathy causing muscular weakness.
Sakkas (2003)58 Case series Medial head of gastrocnemius; percutaneous muscle biopsy using conchotome technique Implicit suggestions of muscle weakness based on prior published reports of reduced exercise capacity in people on HD HD=12 Dominance of type I fibres Type IIa fibres dominant in the distribution of type II fibres Proportion of fibres with central nuclei within the normal range

  • Atrophy of type IIb fibres has been associated with painless myopathies associated with chronic alcohol- or steroid-related neuro/myopathy.

  • Results support myopathy as a possible cause of skeletal muscle weakness.
Sakkas (2004)4 Case series Medial head of gastrocnemius; percutaneous muscle biopsy using conchotome technique Implicit suggestions of muscle weakness based on prior published reports of uremic myopathy HD=12 No data No significant difference between mean CSA of type IIa and IIx fibres No data

  • Suggestive of type II fibre atrophy

  • Primary objective was to examine differences in morphology of muscles of patients on CAPD and HD. Data on participants on HD were included in this review.
Shah (1983)49 Case-control Quadriceps; method of biopsy not indicated Complaints of proximal muscle weakness in all participants HD=10
Con=8		 Atrophy of type I fibres Preferential atrophy of type II fibres Abundant lipid droplets in type I and II fibres

  • Findings attributed to myopathic changes

  • Possible relation to effects of HD on muscle metabolism
van den Ham (2007)34 Case-control Vastus lateralis; needle biopsy techniques MVC using dynamometry
HD=Reduced MVC		 HD=14
Con=18		 Similar to that of Con group Similar to Con group N/A Physical inactivity in people on HD contributes to muscle weakness.

Athl=athletes; CAPD=continuous ambulatory peritoneal dialysis; Con=control group; CSA=cross-sectional area; HD=haemodialysis; MVC=maximim voluntary contraction; N/A=not applicable