الفهرس | Only 14 pages are availabe for public view |
Abstract Chronic kidney disease (CKD) is currently a public health problem. More than 60 million worldwide people lose their lives annually due to the risk of kidney failure (1), CKD defined as decreased kidney function shown by glomerular filtration rate (GFR) of less than 60 mL/min per 1.73 m2 or markers of kidney damage or both of at least 3 months duration (2). Irrespective of the type of kidney disease diagnosis, diabetes and hypertension are the main causes of CKD. Many patients are asymptomatic or have nonspecific symptoms such as lethargy, itching, vomiting or loss of appetite (2). When the kidney fails to perform most of its function, the clinical state is labeled end-stage renal disease (ESRD) and dialysis or transplantation is required to sustain life. Hemodialysis (HD) is the most common renal treatment today (1). Complications include anemia due to reduced production of erythropoietin by the kidney, reduced red blood cell survival, iron deficiency and mineral bone disease caused by disturbed vitamin D, calcium, and phosphate metabolism (2). Metabolic bone disease is a common complication of CKD and is part of abroad spectrum disorders of mineral metabolism that occur in this clinical setting during dialysis (3). In the course of chronic renal failure most of the metabolic bone diseases are characterized by alteration in the bone resorption / formation balance as secondary hyperparathyroidism, osteoporosis, mixed bone diseases, osteomalacia, a dynamic osteopathy, and extra skeletal calcifications (4). |