The main source of vitamin D in a man is its synthesis in human skin. 7-dehydrocholesterol converts into cholecalciferol – vitamin D3 - as a result u UV radiation. Cholecalciferol hydroxylates in liver into 25-hydroxyvitamin D3 [25(OH)D, calcidiol], which concentration in blood is a relevant indicator of the total of vitamin D in a human body. 25(OH)D hydroxylates in kidneys into 1.25-dihydroxyvitamin D3 [1.25(OH)2D, calcitriol], which is considered an active metabolite of vitamin D. Epidemiological studies showed high prevalence of low concentrations of 25(OH)D especially in older population and people with chronic diseases. 25(OH)D concentrations were defined at which rise parathormone levels, increases bone conversion, impairs bone mineralization and develops osteomalacia. Based on these results a deficiency of vitamin D was defined. Patients with chronic renal disease experience development of serious bone impairments described as renal osteodystrophy. These disorders are caused by secondary hyperparathyreoidism which develops as a result of mineral metabolism impairment, especially of hypocalemia, 25(OH)D deficiency, and insufficient synthesis of 1,25(OH)2D. Presently published guidelines K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification and Stratification define processes of vitamin D supplementation, particularly 1.25(OH)2D according to a degree of renal disease. Early prevention and treatment of hypovitaminosis D is a treatment goal in order to reduce or stop development of secondary hyperparathyreoidism with its consequences for bone metabolism.

        Key words: Vitamin D - Deficiency - Chronic renal disease - Prevention - Therapy