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    Add as Friendmetabolic bone disease in chronic kidney disease

    by: salwa

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    1 : CKD-mineral and bone disorder Salwa Ibrahim, MD MRCP (UK) Cairo University
    2 : Agenda Definition Spectrum of CKD- MBD Prevention and treatment
    3 : Definition Systemic disorder of mineral and bone metabolism as a result of CKD It can manifest by one or more of the followings Abnormalities in calcium, phosphorus, parathyroid hormone, vitamin D Abnormalities of bone turnover, mineralization, volume, linear growth and strength Vascular and soft tissue calcification
    4 : Pathogenesis of MBD in CKD
    5 : High turnover MBD
    6 : High turnover MBD in CKD It results from the development of secondary hyperparathyroidism Retention of phosphorus, decreased calcitriol level and hypocalcaemia causes increased PTH levels Skeletal resistance to the action of PTH
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    8 : Phosphate retention Reduction in GFR results in phosphate retention and parathyroid hyperplasia The effect of hyperphosphatemia on PTH secretion is posttranscriptional (mRNA)
    9 : Hypocalcaemia Hypocalcaemia is a powerful stimulus of PTH secretion and growth Its effect is mediated by the calcium sensing receptors Decrease in expression of calcium sensing receptors lead to increased PTH and gland growth
    10 : Decreased synthesis of calcitriol Decrease kidney mass leads to decrease calcitriol production by the kidney FGF 23 decreases the activity of 1-alpha hydroxylase Calcitriol is a major regulator of PTH secretion, calcitriol suppress PTH secretion at the level of transcription of PTH gene Calcitriol increases intestinal calcium absorption Calcitriol increases parathyroid vitamin D receptor expression
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    12 : Skeletal resistance to PTH actions Phosphorus retention Decreased calcitriol level Downregulation of PTH receptors Potential action of PTH fragments All have been shown to blunt the calcemic effects of PTH
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    14 : Low turnover MBD in CKD
    15 : Low turnover MBD in CKD Slow rate of bone formation Osteomalacia with defective bone mineralization Causes include High calcium loads Age Vitamin D therapy
    16 : Decrease BFR Increase in PTH fragments, uremic toxins, acidosis, decrease expression of PTH receptors, previous steroid therapy, malnutrition Aluminum accumulation
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    20 : Extraskeletal calcification
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    29 : Biochemical assessment of MBD
    30 : Biomarkers
    31 : Bone ALP is the most sensitive marker
    32 : PTH Assay PTH(1-84) has a plasma half-life of two to four minutes. In comparison, the C-terminal fragments, which are cleared principally by the kidney, have a half-life that is 5 to 10 times longer. As a result, circulating immunoreactive PTH in normocalcemic subjects comprises: PTH(1-84) – 5 to 30 percent C-terminal fragments – 70 to 95 percent N-terminal fragments – a small percentage 3rd generation assay is more specific
    33 : Sensitivity of PTH assay Serum PTH levels alone are frequently not able to distinguish adynamic bone disease from hyperparathyroidism iPTH levels between 65-450 pg/ml could not predict bone turnover in dialysis patients iPTH levels 3.5 times above the upper normal values had 97% positive predictive value for the diagnosis of HTBD
    34 : Bone biopsy The gold standard for diagnosis of ROD is bone biopsy with mineralized bone histology after double tetracycline labeling, iron staining and aluminum staining
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    38 : Prevention of MBD in CKD
    39 : Prevention of MBD OBJECTIVES Maintain the blood levels of calcium and phosphorus as close to normal Prevent the development of secondary hyperparathyroidism Prevention of extraskeletal calcification Prevention of adynamic bone disease
    40 : Stepped care CKD 3 Monitor PTH Evaluate Vitamin D status 25 hydroxy vitamin D were found to be extremely low in a large majority of CKD and need to be corrected to a level above 30 ng/ml Dietary restriction of phosphorus Treat metabolic acidosis Calcium supplements/ phosphate binders
    41 : CKD 4 Active vitamin D (calcitriol, paricalcitriol) Calcium containing phosphate binders Non calcium containing phosphate binders
    42 : CKD 5 Dialysate calcium Limit calcium intake Calcimimetic parathyriodectomy
    43 : Paricalcitriol 19-nor-1,25-(OH)2-vitamin D2.
    44 : Paricalcitriol
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    49 : Sevelamer Hydrochloride Sevelamer hydrochloride a polymeric amine that binds phosphate and is meant for oral administration
    50 : Lanthanum carbonate (Fosrenol) Usual Adult Dose for Hyperphosphatemia of Renal Failure: Initial dose: 1500 mg daily with meals in divided doses. Adjust dose every 2 to 3 weeks until desired serum phosphate level is achieved. Maintenance dose: 1500 to 3000 mg daily with meals in divided doses Maximum dose: Doses up to 4500 mg daily were evaluated in clinical trials.
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    52 : Calcimemtic Cinacalcet is a calcimimetic agent that increases the sensitivity of the calcium-sensing receptor to activation by extracellular calcium The recommended starting dose of cinacalcet is 30 mg once daily. Serum calcium and serum phosphorus should be measured within 1 week and (iPTH) should be measured 1 to 4 weeks after initiation. Cinacalcet should be titrated every 2 to 4 weeks through sequential doses of 30, 60, 90, 120, and 180 mg once daily to target iPTH levels of 150 to 300 pg/mL
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