Abstract
Background
Chronic kidney disease (CKD), or chronic renal failure (CRF) as it was historically termed, includes all degrees of decreased renal function, starting from mild, and moderate, to severe chronic kidney failure. Skeletal muscle atrophy frequently complicates the course of CKD and is associated with excess morbidity and mortality. Cardiovascular diseases have been reported to be the leading causes of death in CKD patients. Chronic Kidney Disease was also reported to be associated with an increased incidence of acid-related gastrointestinal disorders.
Aim of the work
The aim of this study was to investigate the effect of chronic kidney disease experimentally induced by gentamicin intramuscular injection on the histological structure of gastrocnemius skeletal muscle, left ventricular cardiac muscle and smooth muscle fibers of lower esophagus.
Materials and methods
Twenty male adult Wistar albino rats were randomly and equally divided into two groups. Group I (control group) received physiological saline intramuscular injection, once daily for 28 consecutive days, in a dose equivalent to that taken in group II. Group II (Gentamicin-treated group) were given Gentamicin intramuscular injection for induction of CKD. Gentamicin was given as Gentamycin sulfate, 40 mg/ml (Sandoz, Switzerland), once daily, in a dose of 80 mg/kg/day for 28 days to induce CKD. After 28 days of the first injection of gentamicin, rats were anaesthetized and blood samples were collected to measure the level of serum urea and creatinine. The left kidneys, the middle third of left gastrocnemius muscle, the lateral wall of left ventricle (LV) and the gastroesophageal junction of all rats of both groups (I and II) were processed for light microscopic study. The middle third of left gastrocnemius muscle, the lateral wall of left ventricle (LV) were further processed for transmission electron microscopic study. Histomorphometrical and statistical analysis were also done.
Results
The LM examination revealed moderate obliteration of glomeruli, dilatation in some renal tubules and collapse in others, mainly in distal convoluted tubules, with significant fibrosis of renal parenchyma. Serum urea and creatinine levels were increased significantly. The skeletal muscle fibers of the rats in group II (CKD) showed focal areas of myofibers degeneration with siginificant fibrosis. The cardiac muscle fibers of the rats in the group II (CKD) showed focal areas of cardiomyocytes degeneration and other areas of significantly hypertrophied fibers. The smooth muscle fibers of the lower esophageal sphincter of the rats in group II
(CKD) showed no significant structural changes compared with the control group, however, the myenetric plexus showed multiple pyknotic and karyolitic nuclei with vacuolated cytoplasm. In addition, insignificant increase in the amount of collagen fibers was observed in almost all layers.
Conclusion
CKD produced moderate atrophy of skeletal muscle fibers, significant increase in the cardiomyocyte size and no significant structural effect of smooth muscle fibers of the lower esophageal sphincter.
Reductions in skeletal muscle mitochondrial mass are not restored following exercise training in patients with chronic kidney disease