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Skeletal disorders that primarily occur in patients with renal failure Osteitis fibrosa Osteomalacia Adynamic bone lesions Mixed lesions Dialysis related amyloidosis
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Osteitis fibrosa and secondary hyperparathyrodism High level of PTH, increase number and activity of osteoblasts and osteoclasts High bone turnover Increased quantity of unmineralized bone matrix( osteoid)
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Pathogenesis of secondary hyperparathyrodism(1) Phosphate retention and Calcitriol deficiency GFR less than 20% of normal ,hyperphosphatemia develops Limited amount of residual renal mass available for Calcitriol synthesis Calcium malabsorption Calcitriol deficiency leads to impaired GI absorption of calcium, as GFR falls below 50 ml /min
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Pathogenesis of secondary hyperparathyrodism(2) Skeletal resistance to Calcemic action of PTH Decreased number of Calcitriol receptors in the uremic parathyroid gland Calcitriol reduces prepro-PTH messenger RNA levels by decreasing the rate of gene transcription Parathyroid hyperplasia Little is known about the factors that lead to cellular proliferation Once established ,not reversed by short term calcitriol treatment
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Diagnosis of uremic hyperparathyrodism High level of I-PTH. Without liver disease, serum Alk-P level often correlate with PTH Radiographic changes of osteitis fibrosa Subperiosteal erosions of phalanges Erosions at proximal end of the tibia ,neck of femur or humerus and inferior surface of distal end of clavicle In the skull, salt and pepper appearance Bone biopsy necessary when diagnosis uncertain
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Prevention and treatment of uremic hyperparathyrodism Phosphorus control In early renal failure, phosphorus accumulation may be avoided by restriction of dietary phosphorus intake to 600-800mg/d Limiting meats and dairy products More strict dietary phosphorus restriction is usually impractical
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Phosphorus control Phosphorus binder Containing aluminum Calcium carbonate Calcium acetate not containing calcium or aluminum , sevelamer hydrochloride As patients begin dialysis therapy, increase dietary phosphorus to 800-1200 mg/d Hemodialysis removes approximately 1000mg /treatment CAPD removes 300 mg/d
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Prevention and treatment of uremic hyperparathyrodism Control of calcium Use of vitamin D sterols Metabolite of vitamin D directly suppressing PTH secretion, marked suppression of PTH administering 1-2 ug of calcitriol intravenously after each hemodialysis three times a week Pulse oral calcitriol 2-4 ug twice a week If PTH levels do not fall into an acceptable range after 1 year of treatment ,surgical parathyroidectomy or parathyroid gland ablation by ethanol should be considered
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Use of vitamin D sterols Calcitriol should not be used when hyperphosphatemia is present Calcium-phosphorus product of greater than 75 may lead to soft tissue calcifications Paricalcitol and doxercalciferol , analogs of calcitriol ,less active in raising calcium and phosphorus level were approved in United States If PTH less than 250 pg/ml( or less than four times the upper limits of normal) Inducing adynamic bone lesions
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Use of vitamin D sterols Vitamin D induced hypercalcemia is particularly prolonged and may require weeks for resolution
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Osteomalacia Pathogenesis Metabolic acidosis Aluminum intoxication ,directly suppresses PTH secretion Contamination of dialysate phosphorus binders containing aluminum Citrate increases absorption of aluminum from the gut
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Osteomalacia Diagnosis Low PTH level Exposure to aluminum Bone and muscle pain ,spontaneous fractures occur in approximately 15% Radiographic findings are not distinctive DFO test Gold standard is bone biopsy
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Diagnosis DFO test 5-20 mg/kg administered intravenously at the end of dialysis Serum aluminum measured 24 to 48 hrs later Basal serum aluminum level of >100 ug/L and an increment in aluminum level of >150 ug/L following chelation with DFO
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Prevention and treatment of osteomalacia caused by aluminum Dialysate purified Avoidance of phosphorus binders containing aluminum Chronic chelation therapy with DFO Risk of mucormycosis infections occurs in up to 5% of treated patients Acute encephalopathy has been described with DFO Binds iron DFO should be restricted to those who have severe symptoms of aluminum intoxication and histological evidence of aluminum accumulation in the bone
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Adynamic bone lesions Decreased bone mineralization ,with normal amounts of osteoid 50% of cases ,cause if aluminum deposition .Little is known about the etiology in the remaining Common in patients treated with PD ,in the elderly and patients with DM Fewer symptoms of bone pain, myopathy and fractures than osteomalacia and osteitis fibrosa
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Mixed lesions Histological evidence of both osteitis fibrosa and osteomalacia High PTH level Previously established osteodystrophy who developing a aluminum-related bone disease Treatment is withdrawal of aluminum exposure and aggressive treatment of the hyperparathyrodism
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Dialysis-related Amyloidosis Bone cysts ,pathological fracture ,arthritis ,and carpal tunnel syndrome treated with long term dialysis Deposition of ß 2-microglobulin No proven treatment for the amyloidosis arthropathy Use of high flux hemodialysis or hemodiafiltration removes some ß 2-microglobulin Early renal transplantation completely prevents the disease
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Acute Renal Failure
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acute renal failure
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Osteitis fibrosa; Osteomalacia; Adynamic bone lesions; Mixed lesions; Dialysis related amyloidosis.
Osteitis fibrosa; Osteomalacia; Adynamic bone lesions; Mixed lesions; Dialysis related amyloidosis. Osteitis fibrosa and secondary hyperparathyrodism ...