<unk>  <unk>  is within the broad spectrum of Chronic Kidney Disease (CKD)- Mineral Bone Disease (MBD). The disease occurs as a natural complication of the CKD and is characterized by abnormal levels and metabolism of calcium (Ca), phosphorus (Ph), parathyroid Hormone (PTH), and vitamin D, as well as calcification of soft tissues and bone turn over and mineralization abnormalities. Secondary hyperparathyroidism and 1,25-dihydroxycholecalciferol (vitamin D3) deficiency play a major role in<unk> . Any factor leading to CKD is potentially a risk factor for<unk> . Hypocalcemia, hyperphosphatemia, vitamin D deficiency, parathyroid gland hyperplasia and acidosis are the other contributors of<unk> . Aluminum related<unk>  is mostly seen in patients who undergo dialysis.<unk>  is an important cause of morbidity, decreased quality of life, and extravascular calcifications that have been associated with increased cardiovascular mortality.  Primary investigation of<unk>  includes measurement of blood levels of parathyroid hormone (PTH), calcium, phosphorus, alkaline phosphatase and bicarbonate. Imaging studies should focus on finding calcification in soft tissues. A bone biopsy is indicated if the results of biochemical markers are not consistent or when there is unexplained bone pain, or in case of presence of unexplained bone fractures. However, bone biopsies are infrequently used in clinical practice due to invasiveness and low cost-effectiveness. Common complications of<unk>  include bone fractures and vascular calcifications leading to atherosclerosis, coronary artery calcification, hypertension, left ventricular hypertrophy, and congestive heart failure (CHD). Extra-skeletal calcification can also affect the heart valves and the cardiac conduction system. Calcification of skin arterioles may lead to a condition of ischemia and necrosis of the skin known as calciphylaxis. Patients with<unk>  usually present with bone pain, arthralgia, chest pain, dyspnea, and palpitation. Physical examination of patients with<unk>  may include bone deformity, bone fracture, hypertension, ongestive heart failure, heart murmur, increased pulse pressure (due to aortic calcification) and skin ischemia and necrosis. In laboratory findings, serum calcium levels are typically low. Serum phosphorous is elevated depending on the stage of chronic kidney disease, dietary phosphorous, and use of phosphate binders. Alkaline phosphatase levels (total or bone-specific) are elevated and show increased osteoblastic activity. High levels of alkaline phosphatase are seen in severe osteitis fibrosa. Elecrocardiographic findings in patients with<unk>  include heart block and non-ST-elevation myocardial infarction. Radiographic findings are less sensitive for diagnosis compared to parathyroid hormone levels. Imaging is usually performed for patients with unexplained bone pain or fractures. Radiographic findings of osteitis fibrosa cystica include subperiosteal resorption. Resorptive loss of bone may be seen at the terminal phalanges, distal ends of the clavicles, and in the skull. Radiographs will show soft tissue calcification that involves the vasculature. Phosphate binders and supplemental calcium are mainly used for prevention and treatment of<unk> . The major objective in the prevention and management of<unk>  is either prevention of hyperparathyroidism or its treatment if present.
Renal osteodystrophy
Pseudohyperparathyroidism
Renal amyloidosis
Secondary amyloidosis
Secondary hyperparathyroidism
Phosphate nephropathy
Tumor induced osteomalacia
Hyperparathyroidism