Sclerostin: Just One More Player in Renal Bone Disease?

[摘要] Renal osteodystrophy (ROD) is one of the three components of chronic kidney disease–mineral and bone disorder (CKD-MBD) (1). Patients with CKD may develop various types of bone disease, spanning the spectrum of extreme situations such as severe osteitis fibrosa, osteomalacia, mixed osteopathy, and adynamic bone disease. In addition, patients may have osteoporosis, which increases the risk for fractures, both in advanced and in less severe CKD stages (2–4), which, in turn, result in excess mortality (5,6). In many instances, the pathogenesis of the precise type of ROD in a given patient seems to be obvious, for instance secondary hyperparathyroidism for osteitis fibrosa, vitamin D deficiency or aluminum overload for osteomalacia, hypoparathyroidism for adynamic bone disease, and advanced age and female gender for osteoporosis. However, other factors may also play a role, including abnormal levels or functions of hormones involved in mineral metabolism (other than parathyroid hormone [PTH] and calcitriol), in gonadal function, or in energy metabolism (in particular diabetes) (7); abnormal growth factors or cytokine levels and dysfunction of their receptors (8,9); acidosis (10); oxidative stress and advanced glycation end products (11); uremic toxins (12,13); metal overload (14,15); insufficient mechanical loading (8); and inappropriate diets and malnutrition (16,17). A better understanding, at the patient level and the molecular level, of the underlying pathogenesis and the risk factors involved in ROD including osteoporosis might help to prevent this important health problem in the patient population with CKD (6).

[学科分类] 泌尿医学

[关键词] Bone marrow necrosis;Sickle cell disease;Hyperhemolysis syndrome