RESUMO
Patients with chronic kidney disease (CKD) are generally affected by secondary hyperparathyroidism (SHPT). 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.
Assuntos
Quelantes/uso terapêutico , Hiperparatireoidismo Secundário , Naftalenos/uso terapêutico , Insuficiência Renal Crônica , Idoso , Cinacalcete , Humanos , Hiperparatireoidismo Secundário/etiologia , Hiperparatireoidismo Secundário/cirurgia , Hiperparatireoidismo Secundário/terapia , Hormônio Paratireóideo/sangue , Paratireoidectomia , Fosfatos/metabolismo , Guias de Prática Clínica como Assunto , Receptores de Calcitriol/agonistas , Insuficiência Renal Crônica/complicações , Insuficiência Renal Crônica/terapiaRESUMO
Secondary hyperparathyroidism (SHPT) is a classical feature of chronic kidney disease (CKD). Commonly, hypocalcemia, hyperphosphatemia, and vitamin D deficiency are involved into the pathogenesis of SHPT. Parathyroid (PT) glands are characterized by a low turnover and rarely undergo mitoses. However, in the presence of low calcium, high phosphorus, vitamin D deficiency, and uremia, PT cells leave quiescence. In the last decade, both new molecular and cellular mechanisms have been investigated in the pathophysiology of SHPT, between them the emerging role of the PT vitamin D receptor and calcium-sensing receptor. Furthermore, recent studies indicate that the fibroblast growth factor-23 may play a central role in the regulation of phosphate-vitamin D metabolism in CKD. Certainly, in the next future, these new insights into the pathogenesis of SHPT will give the possibility to improve the treatment of this condition in the CKD population.
