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![GUIDELINE 4. RESTRICTION OF DIETARY
PHOSPHORUS IN PATIENTS WITH CKD
• 4.1 Dietary phosphorus should be restricted to 800 to
1,000 mg/day (adjusted for dietary protein needs) when
the serum phosphorus levels are elevated (>4.6 mg/dL
[1.49 mmol/L]) at Stages 3 and 4 of CKD, (OPINION)
and >5.5 mg/dL (1.78 mmol/L) in those with kidney
failure (Stage 5). (EVIDENCE)
• 4.2 Dietary phosphorus should be restricted to 800 to
1,000 mg/day (adjusted to dietary protein needs) when
the plasma levels of intact PTH are elevated above
target range of the CKD stage. (EVIDENCE)
• 4.3 The serum phosphorus levels should be monitored
every month following the initiation of dietary phosphorus
restriction. (OPINION)](https://image.slidesharecdn.com/calciumphosphorusinckd2-200106073643/75/Calcium-amp-phosphorus-in-ckd-2-20-2048.jpg)
![GUIDELINE 5. USE OF
PHOSPHATE BINDERS IN CKD
• 5.4 In dialysis patients who remain
hyperphosphatemic (serum phosphorus >5.5
mg/dL [1.78 mmol/L]) despite the use of either of
calcium-based phosphate binders or other
noncalcium-, nonaluminum-, nonmagnesium-
containing phosphate-binding agents, a
combination of both should be used. (OPINION)
• 5.5 The total dose of elemental calcium provided
by the calcium-based phosphate binders should
not exceed 1,500 mg/day (OPINION), and the
total intake of elemental calcium (including
dietary calcium) should not exceed 2,000 mg/day.
(OPINION)](https://image.slidesharecdn.com/calciumphosphorusinckd2-200106073643/75/Calcium-amp-phosphorus-in-ckd-2-23-2048.jpg)
![GUIDELINE 5. USE OF
PHOSPHATE BINDERS IN CKD
• 5.6 Calcium-based phosphate binders should
not be used in dialysis patients who are
hypercalcemic (corrected serum calcium of
>10.2 mg/dL [2.54 mmol/L]), or whose plasma
PTH levels are <150 pg/mL (16.5 pmol/L) on 2
consecutive measurements. (EVIDENCE)
• 5.7 Noncalcium-containing phosphate binders
are preferred in dialysis patients with severe
vascular and/or other soft tissue calcifications.
(OPINION)](https://image.slidesharecdn.com/calciumphosphorusinckd2-200106073643/75/Calcium-amp-phosphorus-in-ckd-2-24-2048.jpg)
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Calcium & phosphorus in ckd (2)
- 1. Calcium & Phosphorus InCKD By Dr. Magdy El- Sharkawy Prof of Int. Medicine & Nephrology Ain Shams University
- 2. Distribution of Calciumin the Body Bone 99% (990 g) Intracellular Ca 0.9% (9 g) Interstitial Ca 0.075% (0.75 g) Plasma Ca 0.025% (0.25 g) Total Body Calcium = 1000 g
- 3. Calcium and PhMetabolism • There are three main hormones: – PTH – Active Vit D – Calcitonin • There are three target organ: – Intestine – Bone – Kidneys
- 5. Consequences of Hyperphosphatemia P Mortality Risk of Calcification Parathyroid CellGrowth PTH Secretion PTH Resistance Ca++ Calcitriol Resistance Calcitriol PTH=parathyroid hormone
- 6. Calcium Homeostasis inRenal Insufficiency • In renal failure the regulation of serum calcium is considerably different than in normal individuals due to: • 1- Defective renal regulation of excretion of calcium and phosphorus. • 2- Defective absorption of calcium from intestine. • 3-Defective production of active vitamin D from the kidney. • 4-Abnormal handling of PTH.
- 7. Calcium Homeostasis inRenal Insufficiency • 1-phosphate retention with rise in serum phosphate concentration. • 2-altered vitamin D metabolism with malabsorption of calcium. • 3-skeletal resistance to calcium action of PTH. • 4-abnormal set point for calcium in parathyroid glands. • 5-impaired degradation of PTH secondary to reduced renal functions. • 6-other factors with limited roles includes: acidosis, aluminum toxicity, and, b2-microglobulin toxicity.
- 8. Pathogenesis of DifferentTypes of ROD There are five components in the pathogenesis of renal osteodystrophy: 1- Secondary hyperparathyroidism due to: -Phosphate retention. - An abnormal set point for calcium. - Altered metabolism of vit.D. - Skeletal resistance to PTH. - Impaired degradation of PTH. - Altered feed back regulation of PTH by calcium. 2- Defective meniralization of bone (osteomalacia): - Altered vitamin D metabolism. - Acidosis. - Altered synthesis and maturation of collagen. - Retention of aluminum. - Retention of iron. - Skeletal accumulation of magnesium, fluoride,pyrophosphate, and oxalately stranchium.. 3- Adynamic bone disease. 4 - Osteosclerosis. 5- -Osteoporosis .
- 9. These manifestations include: -Bone pains - Fractures. - Muscle pain and weakness - Tendon rupture - Skeletal deformities - Pruritis - Pseudogout - Calciphelaxis - Calcefic periartheritis - Vascular calcification
- 10. Akmal M etal. Kidney Int. 1995;47:158-163. Drüeke TB. Nephrol Dial Transplant. 1996;11(suppl 3):37-42. Hsu CH. Am J Kidney Dis. 1997;29:641-649. Janigan DT et al. Am J Kidney Dis. 2000;35:588-597. Rostand SG et al. Am J Med. 1988;85:651-657. Soft-Tissue Calcification Type of Calcification Morbid Effects Myocardial and valvular Atrioventricular block, cardiac failure, pulmonary hypertension, arrhythmia, left and right ventricular hypertrophy Peripheral arteries Bone and soft tissue necrosis, amputation Skin arterioles Calcific uremic arteriolopathy (calciphylaxis) Pulmonary Cough, dyspnea, restrictive defects, decreased diffusion, hypoxia
- 12. Biochemical Markers ofRenal Osteodystrophy • Routine bone markers. –Calcium, ionized calcium, and phosphorus. –PTH assays. –Alkaline phosphatase. – Osteocalcin. –Aluminum.
- 13. Therapeutic Modalities • I-Controlof phosphorus: • Dietary phosphate restriction. • Phosphate-binding. • Removal of phosphorus by dialysis. • II-Control of calcium: • Calcium supplementation. • Vitamin D analogues. • Choice of dialysate calcium concentration.
- 14. • III-control ofhyperparathyroidism: – By using active vitamin D analogues mainly. – 1 alpha (OH)D3. – 1,25(OH)2D3 (Calcitriol). – Combination of 1,25(OH)2D3 and 24,25(OH)2D3. – Other new vitamin D analogues (ZEMPLAR). – Parathyroidectomy. • V-removal of aluminum: e.G. disferrioxamine.
- 15. Clinical Challenges inthe Management of Hyperphosphatemia • Treatment is complicated by complex interrelationships between calcium, PTH, vitamin D, and diet • Dietary restriction of phosphorus often conflicts with traditional nutritional requirements for protein • Hemodialysis does not adequately clear phosphorus • Negative health consequences have been associated with calcium- and aluminium-based phosphorus binders PTH = parathyroid hormone. Emmet M et al. Am J Kidney Dis. 1991;17:544-550. Mucsi I et al. Kidney Int. 1998;53:1399-1404. Rufino M et al. Nephrol Dial Transplant. 1998;13(suppl 3):65-67.
- 16.
- 17. NKF. Am JKidney Dis. 2000;35(suppl 2):S1-S140. Limitations of Diet to Control Hyperphosphatemia in Stage 5 CKD • Nonadherence with dietary phosphorus recommendations – Difficulty with long-term compliance • Phosphorus restrictions may compromise protein intake and nutritional status – Recommended protein intake (1.2 g/kg body weight per day for adults)
- 18. Phosphate Binders 1-Metal containingPo Binders Aluminum gels. Lanthanum 2-Calcium containing Po Binders Calcium Carbonate Calcium Acetate 3-Non-Calcium Non-Aluminum Containing Po Binders Renagel
- 19. GUIDELINE 3. EVALUATIONOF SERUM PHOSPHORUS LEVELS • 3.1 In CKD patients (Stages 3 and 4), the serum level of phosphorus should be maintained at or above 2.7 mg/dL (0.87 mmol/L) (EVIDENCE) and no higher than 4.6 mg/dL (1.49 mmol/L). (OPINION) • 3.2 In CKD patients with kidney failure (Stage 5) and those treated with hemodialysis or peritoneal dialysis, the serum levels of phosphorus should be maintained between 3.5 and 5.5 mg/dL (1.13 and 1.78 mmol/L). (EVIDENCE)
- 20. GUIDELINE 4. RESTRICTIONOF DIETARY PHOSPHORUS IN PATIENTS WITH CKD • 4.1 Dietary phosphorus should be restricted to 800 to 1,000 mg/day (adjusted for dietary protein needs) when the serum phosphorus levels are elevated (>4.6 mg/dL [1.49 mmol/L]) at Stages 3 and 4 of CKD, (OPINION) and >5.5 mg/dL (1.78 mmol/L) in those with kidney failure (Stage 5). (EVIDENCE) • 4.2 Dietary phosphorus should be restricted to 800 to 1,000 mg/day (adjusted to dietary protein needs) when the plasma levels of intact PTH are elevated above target range of the CKD stage. (EVIDENCE) • 4.3 The serum phosphorus levels should be monitored every month following the initiation of dietary phosphorus restriction. (OPINION)
- 21. GUIDELINE 5. USEOF PHOSPHATE BINDERS IN CKD • In CKD Patients (Stages 3 and 4): • 5.1 If phosphorus or intact PTH levels cannot be controlled within the target range , despite dietary phosphorus restriction phosphate binders should be prescribed. (OPINION) • 5.2 Calcium-based phosphate binders are effective in lowering serum phosphorus levels (EVIDENCE) and may be used as the initial binder therapy. (OPINION)
- 22. GUIDELINE 5. USEOF PHOSPHATE BINDERS IN CKD • In CKD Patients With Kidney Failure (Stage 5): • 5.3 Both calcium-based phosphate binders and other noncalcium-, nonaluminum-, nonmagnesium-containing phosphate-binding agents (such as sevelamer HCl) are effective in lowering serum phosphorus levels (EVIDENCE) and either may be used as the primary therapy. (OPINION)
- 23. GUIDELINE 5. USEOF PHOSPHATE BINDERS IN CKD • 5.4 In dialysis patients who remain hyperphosphatemic (serum phosphorus >5.5 mg/dL [1.78 mmol/L]) despite the use of either of calcium-based phosphate binders or other noncalcium-, nonaluminum-, nonmagnesium- containing phosphate-binding agents, a combination of both should be used. (OPINION) • 5.5 The total dose of elemental calcium provided by the calcium-based phosphate binders should not exceed 1,500 mg/day (OPINION), and the total intake of elemental calcium (including dietary calcium) should not exceed 2,000 mg/day. (OPINION)
- 24. GUIDELINE 5. USEOF PHOSPHATE BINDERS IN CKD • 5.6 Calcium-based phosphate binders should not be used in dialysis patients who are hypercalcemic (corrected serum calcium of >10.2 mg/dL [2.54 mmol/L]), or whose plasma PTH levels are <150 pg/mL (16.5 pmol/L) on 2 consecutive measurements. (EVIDENCE) • 5.7 Noncalcium-containing phosphate binders are preferred in dialysis patients with severe vascular and/or other soft tissue calcifications. (OPINION)
- 25. GUIDELINE 5. USEOF PHOSPHATE BINDERS IN CKD • 5.8 In patients with serum phosphorus levels >7.0 mg/dL (2.26 mmol/L), aluminum-based phosphate binders may be used as a short-term therapy (4 weeks), and for one course only, to be replaced thereafter by other phosphate binders. (OPINION) In such patients, more frequent dialysis should also be considered. (EVIDENCE)