الفهرس | Only 14 pages are availabe for public view |
Abstract Chronic kidney disease is a worldwide public health problem. The outcomes of CKD include not only progression to renal failure but also increased risk of cardiovascular morbidity and mortality. The increased risks are evident at even moderate reductions in kidney function. End-stage renal disease has reached epidemic proportion with more than 400,000 affected individuals in the United States and well over one million worldwide. This staggering number represents only the tip of the iceberg, as the incidence of CKD is at least 30-fold higher than that of ESRD. Metabolic bone disease is a common complication of CKD and is part of a broad spectrum of disorders of mineral metabolism that occur in this clinical setting. Alterations in the control mechanisms for Ca and P homeostasis occur early in the course of CKD and progress as kidney function decreases; if left untreated, then alterations can result in significant consequences. The disorders of bone have to be considered not only with regard to the bone itself but also with regard to the consequences of disturbed mineral metabolism at extra- skeletal sites, including the vasculature. Cardiovascular mortality is 3.5 times higher in renal patients than in the general population. Heart failure represents 15%, myocardial infarction 10%, uremic pericarditis 3% of dialysis associated mortality. Sudden cardiac death accounts for 60% of cardiovascular mortality. |