Hyperparathyroidism hyperphosphatemia

Renal osteodystrophy Altered bone turnover that results from sustained metabolic conditions that occur in chronic kidney disease, including secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, and vitamin D deficiency. 

Renal osteodystrophy (ROD)—The condition resulting from sustained metabolic changes that occur with chronic kidney disease including secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, and vitamin D deficiency. The skeletal complications associated with ROD include osteitis fibrosa cystica (high bone turnover disease), osteomalacia (low bone turnover disease), adynamic bone disease, and mixed bone disorders. 

Secondary hyperparathyroidism Increased secretion of parathyroid hormone from the parathyroid glands caused by hyperphosphatemia, hypocalcemia, and vitamin D deficiency that result from decreased kidney function. It can lead to bone disease (renal osteodystrophy). 

Patients with advanced renal insufficiency (Ccr less than 30 mL/min) exhibit phosphate retention and some degree of hyperphosphatemia. The retention of phosphate plays a role in causing secondary hyperparathyroidism associated with osteodystrophy and soft-tissue calcification. Calcium acetate, when taken with meals, combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in the feces. 

Patients with chronic renal failure develop hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism, and severe metabolic bone disease. The secondary hyperparathyroidism is thought to be due to hyperphosphatemia and decreased 1, 25-(OH)2 formation. Oral or intravenous l,25-(OH)2D3 (calcitriol) therapy along with oral phosphate-binding agents and calcium supplementation is effective in reducing the effects of renal osteodystrophy. 

The metabolism of phosphorus (P) is largely related to that of calcium (Ca). The Ca P ratio in the diet affects the absorption and excretion of these elements (Harper 1969). Any increase in serum phosphorus results in a decrease of serum calcium by mechanisms which are still unknown. For example, increased serum phosphorus levels and decreased serum calcium levels are seen in uremia (renal retention of phosphorus), hypoparathyroidism, hypocalcemia (decreased serum calcium levels), and hyperphosphatemia (increased serum phosphorus levels), and the reverse is seen in hypercalcemia (increased serum calcium levels) and hyperparathyroidism. Hypophosphatemia (low serum phosphorus levels) is seen in ricketts (vitamin D deficiency) (Harper 1969 Tietz 1970). 

Of 19 chronic hemodialysis patients taking a combination of alfacalcidol and calcitriol for 12 months, six had increased bone resorption, six had reduced bone resorption, and seven had no change. Histologically documented aggravation of hyperparathyroidism was associated with a statistically significant increase in plasma concentrations of phosphate and parathyroid hormone. The administration of vitamin D analogues may therefore be either beneficial or noxious depending on whether or not induced hyperphosphatemia is adequately prevented (55). 

Decreased 1,25 0H)2D Renal failure Hyperphosphatemia Hypomagnesemia Hypoparathyroidism Pseudohypoparathyroidism Vitamin D-dependent rickets, type I Hypercalcemia of malignancy Increased l,25(OH)2D Granulomatous diseases Primary hyperparathyroidism Lymphoma... 

Osteitis fibrosa (hyperparathyroid bone disease) is the most common high-turnover bone disease. This disorder is caused by the high concentrations of serum PTH in secondary hyperparathyroidism. Secondary hyperparathyroidism is a consequence of the hypocalcemia associated with hyperphosphatemia and l,25(OH)2D deficiency. Hyperphosphatemia is a result of the kidneys inability to excrete phosphate. l,25(OH)2D deficiency results from the inability of the kidneys to synthesize l,25(OH)2 because of decreased renal mass and suppression of 25(OH)D-la-hydroxylase activity by high concentrations of phosphate. Deficiency of l,25(OH)2D leads to reduced intestinal absorption of calcium and reduced inhibition of PTH secretion by l,25(OH)2D. Skeletal resistance to PTH also contributes to the hypocalcemia and secondary hyperparathyroidism. 

Parathyroid hormone (PTH) Primary hyperparathyroidism causes hypercalcemia, hypophosphatemia, and increased urinary cAMP hypoparathyroidism causes hypocalcemia and hyperphosphatemia, often with soft-tissue calcification and tetany and convulsions. Binds to cell-surface receptors and activates adenylate cyclase increases bone mineralization and activity of renal lot-hydroxylase in kidney, reabsorption of Ca " " increases and reabsorption of phosphate decreases. 

Common complications of Stages 3 to 5 CKD include anemia, hyperphosphatemia, secondary hyperparathyroidism, fluid and electrolyte abnormalities, metabolic acidosis, and malnutrition. 

Hyperphosphatemia, changes in calcium homeostasis, and secondary hyperparathyroidism are common in patients with CKD and contribute to extravascular calcifications and an increased risk of cardiovascular mortality. 

Management of hyperphosphatemia, calcium balance, and secondary hyperparathyroidism includes dietary phosphorus restriction, use of phosphate binding agents, and vitamin D therapy. 

Block GA, Port FK. Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients Recommendations for a change in management. Am J Kidney Dis 2000 35 1226-1237. 

FI 1. Fournier, A., Moriniere, P., Sebert, J. L., et al., Calcium carbonate, an aluminum-free agent for control of hyperphosphatemia, hypocalcemia, and hyperparathyroidism in uremia. Kidney Int. 29, Suppl. 18, 114-119 (1986). 

The most common cause of hypercalcemia in outpatients is primary hyperparathyroidism, due either to a single adenoma or diffuse hyperplasia. Primary hyperparathyroidism is often associated with significant hypophosphatemia due to PTH effects on renal phosphate reabsorption. The diagnosis is generally apparent from the elevated serum CcP associated with an inappropriately high PTH level. In contrast, secondary hyperparathyroidism is a disorder in which PTH levels are elevated in response to persistent threats to norrruil calcium homeostasis such as hyperphosphatemia from chronic renal disease. 

Hyperphosphatemia occurs commonly in chronic renal failure. The increased phosphate level direcdy stimulates PTH secretion and also has secondary effects due to the reduction in serum Cd . Because renal function is impaired, the increased PTH is unable to increase phosphate excretion sufficiently to avoid ongoing phosphate retention. The chronic secondary hyperparathyroidism may result in a bone disease called renal osteodystrophy. 

Calciphylaxis is a rare life-threatening disorder characterized hy progressive vascular calcification and ischemic tissue loss in patients with end-stage renal disease (Wood et al. 1997 Hafner et al. 1998 Karpman et al. 2003 Guvel et al. 2004). The pathogenesis is poorly understood it is likely the result of a multiplicity of co-morbid factors or events. Disorders that are most often implicated include chronic renal failure, hypercalcemia, hyperphosphatemia, an elevated calcium-phosphate product and secondary hyperparathyroidism. Very rare cases of calciphylaxis not associated with chronic renal failure have been reported with breast cancer, hyperparathyroidism and alcoholic cirrhosis. 

Disorders of the calcium-phosphate metabolism are additional risk factors for renal disease progression. Several factors related to disturbed calcium-phosphorus metabolism, such as hyperphosphatemia, hyperparathyroidism, lack of... 

Hyperphosphatemia is common in patients with end-stage renal disease (ESRD), since a large fraction (60-70%) of dietary phosphorus is absorbed and normally excreted by the kidneys, and as kidney function deteriorates, less phosphorus is exereted by the kidneys (Emmett 2004). Dietary restrictions have insuffieient effect. The condition may have serious consequences. Hyperphosphatemia stimulates parathyroid hormone and suppresses vitamin D3 production, and thus induces hyperparathyroid bone disease. In addition, it leads to myocardial and vascular calcification and cardiac microcirculatory abnormalities, which results in cardiac causes of death. Phosphate levels henee should be eontrolled early in the... 

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