Russian Call Girls in Pune Riya 9907093804 Short 1500 Night 6000 Best call gi...
Calcium & Phosphorus in CKD: A Guide to Management
1. Calcium & Phosphorus
In CKD
By
Dr. Magdy El- Sharkawy
Prof of Int. Medicine & Nephrology
Ain Shams University
2. Distribution of Calcium in 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 Ph Metabolism
• There are three
main hormones:
– PTH
– Active Vit D
– Calcitonin
• There are three
target organ:
– Intestine
– Bone
– Kidneys
6. Calcium Homeostasis in Renal
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 in Renal
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 Different Types 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 .
10. Akmal M et al. 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
11.
12. Biochemical Markers of Renal
Osteodystrophy
• Routine bone markers.
–Calcium, ionized calcium, and
phosphorus.
–PTH assays.
–Alkaline phosphatase.
– Osteocalcin.
–Aluminum.
13. Therapeutic Modalities
• I-Control of 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 of hyperparathyroidism:
– 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 in the
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.
17. NKF. Am J Kidney 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 containing Po 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. EVALUATION OF
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. 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)
21. GUIDELINE 5. USE OF
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. USE OF
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. 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)
24. 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)
25. GUIDELINE 5. USE OF
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)
