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Nephrol Dial Transplant (2003) 18: 2074-2081
© 2003 European Renal Association-European Dialysis and Transplant Association


Original Article

Atrophy of non-locomotor muscle in patients with end-stage renal failure

Giorgos K. Sakkas1,*, Derek Ball1,{dagger}, Thomas H. Mercer2, Anthony J. Sargeant1,3, Keith Tolfrey2 and Patrick F. Naish4

1Centre for Biophysical and Clinical Research into Human Movement and 2Exercise Physiology Group, Manchester Metropolitan University, Alsager, Stoke-on-Trent, UK, 3Institute for Fundamental and Clinical Human Movement Sciences, Vrije University, Amsterdam, The Netherlands and 4Directorate of Renal Medicine, North Staffordshire Hospital Trust, Stoke-on-Trent, UK

Correspondence and offprint requests to: P. F. Naish, MB FRCP, Renal Medicine, North Staffordshire Hospital Trust, Princes Road, Stoke-on-Trent ST4 7LN, UK. Email: patrick.naish{at}nstaffsh.wmids.nhs.uk

Background. All previous histological studies of skeletal muscles of patients with renal failure have used locomotor muscle biopsies. It is thus unclear to what degree the observed abnormalities are due to the uraemic state and how much is due to disuse. The present study was undertaken to attempt to investigate this question by examining a non-locomotor muscle (rectus abdominis) in patients with end-stage renal failure.

Methods. Biopsies from rectus abdominis were obtained from 22 renal failure patients (RFPs) undergoing surgical Tenchkoff catheter implantation for peritoneal dialysis and 20 control subjects undergoing elective abdominal surgery. Histochemical staining of frozen sections and morphometric analysis was used to estimate the proportion of each fibre type, muscle fibre area and capillary density. Myosin heavy chain composition was examined by SDS–PAGE.

Results. There were no differences in fibre type distribution between RFPs and controls. All RFPs showed fibre atrophy [mean cross-sectional area (CSA) 3300 ± 1100 µm2, compared to 4100 ± 1100 µm2 in controls (P < 0.05)]. All fibre types were smaller in mean CSA in RFPs than in controls (15, 26 and 28% for types I, IIa and IIx, respectively). These differences could not be accounted for by differences in age, gender or cardiovascular or diabetic comorbidity. Muscle fibre capillarization, expressed as capillaries per fibre or capillary contacts per fibre, was significantly less in RFPs.

Conclusions. Since a non-locomotor muscle was examined, the effects of disuse as a cause of atrophy have been minimized. It is likely, therefore, that the decreased muscle fibre CSA and capillary density of RFPs compared to controls were due predominantly to uraemia itself.

Keywords: atrophy; non-locomotor muscle; renal failure

*Present address: University of California, San Francisco, San Francisco General Hospital, Department of Medicine, San Francisco, CA, USA.

{dagger}Present address: Department of Biomedical Sciences, University Medical School, Forsterhill, Aberdeen, UK.


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