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Cozzolino M et al. – High phosphate, low calcium and vitamin D deficiency represent the classical 'triad' involved into the pathogenesis of SHPT in renal insufficiency, in which downregulation of the parathyroid vitamin D receptor and calcium–sensing receptor represents a critical step. Recently, new studies indicate that fibroblast growth factor 23 may play a central role in the regulation of phosphate–vitamin D metabolism in patients with CKD. These new insights into the pathogenesis of SHPT will possibly improve the treatment of this condition in patients with CKD. The 'modern' treatment of SHPT in CKD patients consists of free–calcium and aluminium phosphate binders, vitamin D receptor activators and calcimimetics. However, calcium– and aluminium–based phosphate binders and calcitriol are therapeutic tools that are not without complications, including increasing the risk of cardiovascular calcification in patients with CKD. This review summarizes the current understanding and evidence supporting strategies for SHPT treatment in CKD patients, with particular focus on the elderly, although specific guidelines for control of this disorder in this age group are lacking.

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