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Management of hyperphosphataemia of chronic kidny disease. Presented by Pharmacist/ Eman Youssif. Role of calcium balance and phosphorus retention. Hypocalcaemia and phosphorus retention has a role in secondary hyperparathyroidism and renal osteodystrophy .
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Management of hyperphosphataemia of chronic kidny disease Presented by Pharmacist/ EmanYoussif
Role of calcium balance and phosphorus retention • Hypocalcaemia and phosphorus retention has a role in secondary hyperparathyroidism and renal osteodystrophy. 1- Aluminum based phosphate binders. 2- Calcium based phosphate binders. 3- Non-aluminum, non-calcium based phosphate binders. 4- magnesium based phosphate binders(experimentally).
Calcium based phosphate binding agents • Relatively benign. • Requires large daily calcium dose. • Ingestion of large amount causes positive calcium balance(hyper-calcaemia, progressive metastatic calcification, and a dynamic bone disorder) • Ca x p increases the risk of cardiac calcification in the dialysis patients.
The phosphate binding capacity of CCP binders is not as efficient as aluminum containing phosphate binders. • To avoid metastatic calcification recommendations to limit calcium intake to less than 2000mg/day(of this amount 1500 may be from phosohate binder and 500 from dietary source). • CCP should be re-evaluated if serum calcium increases above 10.2 mg/dl or if Ca x p is greater than 55 mg2/dl2
Different calcium salts differ in the amount of elemental calcium as well as side effects. • Calcium citrate is avoided in KD as it increases acidity(enhances aluminum absorption). • Calcium actate : • (phos-lo 667)one tablet contain 169mg elemental calcium. • Dose: 2-3 tablets with meals.
It contain lower amount of elemental calcium than calcium carbonate(25% VS 40% respectively). • Calcium acetat is more efficient phosphorus binder. • Increasing binding of calcium to phosphorus with acetate salt is due to *Decreased GIT absorption of calcium. *Increased solubility and dissociation of acetate moiety.
Calcium acetate and calcium carbonate are given in doses that are equivalent regard to elemental calcium content. • The acetate salt not only lowers the phosphorus concentration more effectively , but also associated with lower incidence of hypercalcemia than the carbonate salt. • The problem is calcium acetate formulation is unpalatable and cause uncomfortable GIT effect, this problem has led to poor compliance among patients.
Any of the calcium salts react with anti-microbial agents(fluroquinolones and tetracyclins) so, it should be administered 1 hr before or 3 hr after calcium products. • Spacing between calcium salts and iron is recommended for better iron absorption. • H2 blockers and PPI affects the calcium binding to phosphorus, so spacing is advisable. • Calcium carbonate dose:0.8-2g elemental calcium with meals.
Aluminum based phosphate binding agents • Efficient binding to phosphate. • Chemically able to form tight, insoluble complex with phosphate. • Reserved for situations in which phosphorus concenteration is very high(7.0 mg/dl)and Ca x p is greater than(55mg2/dl2 • Kidney is the primary route of aluminum excretion.
Ingestion of large doses over extended period of time was found to show absorption. • Uremic stat enhance absorption and retention of aluminum to toxic level(encephalopathy, osteomalacia, decreased responsiveness to erythropoietic agents, constipation). • Aluminum concentration should be assessed and should be below 20µg/dl. • Aluminum containing binders used for a maximum 30 days.
Aluminum hydroxide dose: 300-600mg with meals.
Non-aluminum,non-calcium based phosphate binders • Lanthanum salts(lanthanum carbonate). • SevelamerHCl.
Lanthanum salts • Lanthanum is a rare earth metal, found in trace amount in the body • Lanthanum cations bind phosphate anions to form an insoluble salt that is poorly absorbed by GIT. • Lanthanum chloride shows some solubility and absorption, while lanthanum carbonate shows less solubility.
After long term use in rates, accumulation in body organs occurred (liver, lung, and kidny tissues). • Long term safety studies have not been reported. • Not evaluated for drug-drug interactions. • Dose:500-1000mg.
sevelamerHCl • Bind to phosphorus in exchange to chloride ion. • Controls serum phosphorus and Ca x P in dialysis patients. • Minimum impact on serum calcium level and low incidence of side effects. • Positive changes in blood lipids occurred during treatment(lowers LDL, raises HDL).
Lowers risk of hospitalization. • Adverse effects ay include: *Nausea. *Vomiting. *Bloating. *Constipation. *Increased risk of colonic obstruction and perforation. *Increased incidence metabolic acidosis associated with exchange of chloride ion for short chain fatty acid ions.
*Insoluble in water, expands upon contact with water, tablets or capsules should not be crushed, so it is in-approprite for alternative routes of administration(naso-gastric, oral-gastric or per-cutaneousentero-gastric feeding tubes). • *significantly decrease the bio-availability of ciprofloxacin. • *no sufficient study on drug-drug interaction.
sevelamerHCl dose: 800-1600mg with meals.
These medications: - given with food(meals/snaks) to bind the intestinal phosphorus from dietary intake before it's absorption. - given routinely and multiple times a day. - phosphate binders from different classes may be combined to achieve target concentration of phosphorus and calcium.
Salivary phosphate binding chewing gum reduces hyperphosphatemia in dialysis patients • A hyper phosphoric salivary content, which correlates linearly with serum phosphate, has been reported in HD patients. • Adding salivary phosphate binding to traditional phosphate binders could be a useful approach for improving treatment of hyper-phosphatemia in HD patients.
