It is well-known that as<unk>  function declines, there is a progressive deterioration in<unk>  homeostasis, with a disruption of normal serum and tissue concentrations of phosphorus and calcium, and changes in circulating levels of hormones. These include parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH) vitamin D; calcidiol), 1,25-dihydroxyvitamin D (1,25(OH)2 vitamin D; calcitriol), and other vitamin D metabolites, fibroblast growth factor 23 (FGF-23), and growth hormone. Beginning in CKD stage 3, the ability of the<unk> s to appropriately excrete a phosphate load is diminished, leading to hyperphosphatemia, elevated PTH (secondary hyperparathyroidism), and decreased 1,25(OH)2 vitamin D with associated elevations in the levels of FGF-23. The conversion of 25(OH) vitamin D to 1,25(OH)2 vitamin D is impaired, reducing intestinal calcium absorption and increasing PTH. The<unk>  fails to respond adequately to PTH, which normally promotes phosphaturia and calcium reabsorption, or to FGF-23, which also enhances phosphate excretion. In addition, there is evidence at the tissue level of a downregulation of vitamin D receptor and of resistance to the actions of PTH. Therapy is generally focused on correcting biochemical and hormonal abnormalities in an effort to limit their consequences. The<unk>  and endocrine functions disrupted in CKD are critically important in the regulation of both initial<unk>  formation during growth <unk>  modeling) and<unk>  structure and function during adulthood <unk>  remodeling). As a result,<unk>  abnormalities are found almost universally in patients with CKD requiring dialysis (stage 5D), and in the majority of patients with CKD stages 3–5. More recently, there has been an increasing concern of extraskeletal calcification that may result from the deranged<unk>  and<unk>  metabolism of CKD and from the therapies used to correct these abnormalities. Numerous cohort studies have shown associations between<unk> s of<unk>  metabolism and fractures, cardiovascular<unk> , and mortality. These observational studies have broadened the focus of CKD-related<unk>  and<unk><unk> s (MBDs) to include cardiovascular<unk>  (which is the leading cause of death in patients at all stages of CKD). All three of these processes (abnormal<unk>  metabolism, abnormal<unk> , and extraskeletal calcification) are closely interrelated and together make a major contribution to the morbidity and mortality of patients with CKD. The traditional definition of renal osteodystrophy did not accurately encompass this more diverse clinical spectrum, based on serum biomarkers, noninvasive imaging, and<unk>  abnormalities. The absence of a generally accepted definition and diagnosis of renal osteodystrophy prompted<unk><unk> : Improving Global Outcomes (KDIGO) to sponsor a controversies conference, entitled Definition, Evaluation, and Classification of Renal Osteodystrophy, in 2005. The principal conclusion was that the term CKD–Mineral and<unk><unk>  <unk>  should now be used to describe the broader clinical syndrome encompassing<unk> ,<unk> , and calcific cardiovascular abnormalities that develop as a complication of CKD.
Chronic kidney disease-mineral and bone disorder
complications of Kidney disease
complications of Osteoporosis
complications of Hyperparathyroidism
complications of Osteomyelitis
Senile osteoporosis
complications of Hypercalcaemia
Intervertebral disc damage and spaceflight