Calcium Carbonate
NOTE: Referenced from Lexi-Comp - View References below**
Dosing:
500 mg elemental calcium at each meal and titrated according to serum calcium and phosphorus levels.
According to KDIGO guidelines, max calcium 2 g/day. Administer with food to decrease absorption of phosphate.
Dosing: Renal Impairment
Clcr <25 mL/minute: Dosage adjustments may be necessary depending on the serum calcium levels.
Dietary Considerations
May decrease iron absorption, so should be administered 1-2 hours before or after iron supplementation.
Contraindications
Hypercalcemia, renal calculi, hypophosphatemia; patients with suspected digoxin toxicity
Warnings/Precautions
Concerns related to adverse effects:
• Gastrointestinal effects: Constipation, bloating, and gas are common with calcium supplements (especially carbonate salt).
• Hypercalcemia: Mild-to-severe hypercalcemia may occur; decrease calcium acetate dose or temporarily discontinue, depending on severity of hypercalcemia; in addition, decrease or discontinue any concomitant vitamin D therapy. Chronic hypercalcemia may result in vascular calcification and other soft-tissue calcification.
Disease-related concerns:
• Arrhythmias: Use with caution in patients who may be at risk of cardiac arrhythmias.
• Kidney stones (calcium-containing): Use caution when administering calcium supplements to patients with a history of kidney stones.
Concurrent drug therapy issues:
• Digitalis: Use with caution in digitalized patients; hypercalcemia may precipitate cardiac arrhythmias.
• Minerals/other oral drugs: Calcium administration interferes with absorption of some minerals and drugs; use with caution..
• Vitamin D: It is recommended to concomitantly administer vitamin D for optimal calcium absorption.
Adverse Reactions
Well tolerated
1% to 10%
Central nervous system: Headache
Endocrine & metabolic: Hypophosphatemia, hypercalcemia
Gastrointestinal: Constipation, laxative effect, acid rebound, nausea, vomiting, anorexia, abdominal pain, xerostomia, flatulence
Miscellaneous: Milk-alkali syndrome with very high, chronic dosing and/or renal failure (headache, nausea, irritability, and weakness or alkalosis, hypercalcemia, renal impairment)
Drug Interactions ***
ACE Inhibitors: Antacids may decrease the serum concentration of ACE Inhibitors. Management: Separate fosinopril administration from antacids by at least 2 hours. US and Canadian recommendations for use of other ACE- inhibitors with antacids may vary. Consult appropriate labeling. Monitor for decreased therapeutic effects of ACE-inhibitors. Exceptions: Enalaprilat; Ramipril. Risk D: Consider therapy modification
Allopurinol: Antacids may decrease the absorption of Allopurinol. Risk D: Consider therapy modification
Bisacodyl: Antacids may diminish the therapeutic effect of Bisacodyl. Antacids may cause the delayed-release bisacodyl tablets to release drug prior to reaching the large intestine. Gastric irritation and/or cramps may occur. Risk D: Consider therapy modification
Bisphosphonate Derivatives: Calcium Salts may decrease the serum concentration of Bisphosphonate Derivatives. Management: Avoid administration of oral calcium supplements within: 2 hours before or after tiludronate/clodronate/etidronate; 60 minutes after oral ibandronate; or 30 minutes after alendronate/risedronate. Exceptions:Pamidronate; Zoledronic Acid. Risk D: Consider therapy modification
Calcium Acetate: Calcium Salts may enhance the adverse/toxic effect of Calcium Acetate. Risk X: Avoid combination
Calcium Polystyrene Sulfonate: Antacids may enhance the adverse/toxic effect of Calcium Polystyrene Sulfonate. The combined use of these two agents may result in metabolic alkalosis and/or loss of efficacy of the cation exchange resin. Management: To minimize this interaction, consider: a)separating doses by 2 or more hours; b)rectal administration of the exchange resin; or c)alternatives to antacids. Monitor for metabolic alkalosis and attenuation of CPS effects. Avoid magnesium hydroxide.Risk D: Consider therapy modification
Cefuroxime: Antacids may decrease the serum concentration of Cefuroxime. Management: Consider administering antacids and cefuroxime at least 2 hours apart. Risk D: Consider therapy modification
Chloroquine: Antacids may decrease the serum concentration of Chloroquine. Management: Separate administration of antacids and chloroquine by at least 4 hours to minimize any potential negative impact of antacids on chloroquine bioavailability. Risk D: Consider therapy modification
Corticosteroids (Oral): Antacids may decrease the bioavailability of Corticosteroids (Oral). Risk D: Consider therapy modification
Dabigatran Etexilate: Antacids may decrease the serum concentration of Dabigatran Etexilate. Management: Dabigatran etexilate Canadian product labeling recommends avoiding concomitant use with antacids for 24 hours after surgery. In other situations, administer dabigatran etexilate 2 hours prior to antacids. Monitor clinical response to dabigatran therapy. Risk D: Consider therapy modification
Erlotinib: Antacids may decrease the serum concentration of Erlotinib. Management: Separate the administration of erlotinib and any antacid by several hours in order to minimize the risk of a significant interaction. Risk D: Consider therapy modification
Gabapentin: Antacids may decrease the serum concentration of Gabapentin. Management: Administer gabapentin at least 2 hours after antacid administration. Monitor patients closely for evidence of reduced response to gabapentin therapy when both of these drugs are being used. Risk D: Consider therapy modification
Iron Salts: Antacids may decrease the absorption of Iron Salts. Exceptions: Ferric Gluconate; Ferumoxytol; Iron Dextran Complex; Iron Sucrose. Risk D: Consider therapy modification
Itraconazole: Antacids may decrease the serum concentration of Itraconazole. Management: Administer itraconazole at least 1 hour after and 2 hours before administration of any antacids. Itraconazole oral suspension may be less sensitive to the effects of decreased gastric acidity. Risk D: Consider therapy modification
Ketoconazole (Systemic): Antacids may decrease the serum concentration of Ketoconazole (Systemic). Management: Administer oral ketoconazole at least 2 hours prior to use of any antacid product. Monitor patients closely for signs of inadequate clinical response to ketoconazole. Risk D: Consider therapy modification
Multivitamins/Minerals (with ADEK, Folate, Iron): Antacids may decrease the serum concentration of Multivitamins/Minerals (with ADEK, Folate, Iron). Specifically, antacids may decrease the absorption of orally administered iron. Management: Separate dosing of oral iron-containing multivitamin preparations and antacids by as much time as possible in order to minimize impact on therapeutic efficacy of the iron preparation. Risk D: Consider therapy modification
Phosphate Supplements: Antacids may decrease the absorption of Phosphate Supplements. Exceptions: Potassium Phosphate. Risk D: Consider therapy modification
Quinolone Antibiotics: Calcium Salts may decrease the absorption of Quinolone Antibiotics. Of concern only with oral administration of both agents. Exceptions: Moxifloxacin (Systemic). Risk D: Consider therapy modification
Sodium Polystyrene Sulfonate: Antacids may enhance the adverse/toxic effect of Sodium Polystyrene Sulfonate. The combined use of these two agents may result in metabolic alkalosis and/or loss of efficacy of the exchange resin. Management: To minimize this interaction, consider: a)separating doses by 2 or more hours; b)rectal administration of the exchange resin; or c)alternatives to antacids. Monitor for metabolic alkalosis and attenuation of SPS effects. Avoid magnesium hydroxide. Risk D: Consider therapy modification
Tetracycline Derivatives: Calcium Salts may decrease the serum concentration of Tetracycline Derivatives. Management: If coadministration of oral calcium with oral tetracyclines can not be avoided, consider separating administration of each agent by several hours. Risk D: Consider therapy modification
Thyroid Products: Calcium Salts may diminish the therapeutic effect of Thyroid Products. Management: Separate the doses of the thyroid product and the oral calcium supplement by at least 4 hours. Risk D: Consider therapy modification
*** List is not comprehensive, please seek further interaction software where concerned. Risk D or X only included***
Ethanol/Nutrition/Herb Interactions
Ethanol: Avoid ethanol (may increase risk of osteoporosis).
Monitoring Parameters
Serum calcium (twice weekly during initial dose adjustments), serum phosphorus; serum calcium-phosphorus product; intact parathyroid hormone (iPTH)
Reference Range
Corrected total serum calcium (K/DOQI, 2003): CKD stages 3 and 4: 2.1-2.6 mmol/L; CKD stage 5: 2.1-2.37 mmol/L; KDIGO guidelines recommend maintaining normal ranges for all stages of CKD (3-5D) (KDIGO, 2009)
Phosphorus (K/DOQI, 2003):
CKD stages 3 and 4: 0.87-1.48mmol/L (adults)
CKD stage 5 (including those treated with dialysis): 1.13-1.78 mmol/L (children >12 years and adults); 1.29-1.94 mmol/L (children 1-12 years)
KDIGO guidelines recommend maintaining normal ranges for CKD stages 3-5 and lowering elevated phosphorus levels toward the normal range for CKD stage 5D (KDIGO, 2009)
Due to a poor correlation between the serum ionized calcium (free) and total serum calcium, particularly in states of low albumin or acid/base imbalances, direct measurement of ionized calcium is recommended
In low albumin states, the corrected total serum calcium may be estimated by:
Corrected total calcium = total serum calcium + 0.8 (4.0 - measured serum albumin)
Mechanism of Action
Used to treat hyperphosphatemia in patients with advanced renal insufficiency by combining with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces.
Patient Education
Take with meals. Avoid alcohol. May cause constipation or dry mouth. Report severe, unresolved GI disturbances.
Pharmacodynamics/Kinetics
Excretion: Primarily feces (as unabsorbed calcium); urine (20%)
Pharmacotherapy Pearls
20 mEq calcium/g; 400 mg elemental calcium/g calcium carbonate (40% elemental calcium)
Cardiovascular Considerations
Hypercalcemia is evident on ECG by shortening of the QT interval and possibly lengthening of the PR interval. Hypocalcemia causes prolongation of the QT interval. This prolongation is due to lengthening of the ST segment; the T waves remain unchanged. However, in severe hypocalcemia, T waves may be inverted. Note that only hypocalcemia and hypothermia lengthen the ST segment without altering T-wave duration. Hypocalcemia may also present clinically with skeletal muscle spasm.
Calcium salts may enhance the arrhythmogenic effects of digoxin. Part of the inotropic action of digoxin appears to be associated with increased intracellular calcium availability. Chronotropic effects are also calcium mediated. The administration of exogenous calcium (especially by parenteral routes) can lead to cardiac arrhythmias.
Dosing:
500 mg elemental calcium at each meal and titrated according to serum calcium and phosphorus levels.
According to KDIGO guidelines, max calcium 2 g/day. Administer with food to decrease absorption of phosphate.
Dosing: Renal Impairment
Clcr <25 mL/minute: Dosage adjustments may be necessary depending on the serum calcium levels.
Dietary Considerations
May decrease iron absorption, so should be administered 1-2 hours before or after iron supplementation.
Contraindications
Hypercalcemia, renal calculi, hypophosphatemia; patients with suspected digoxin toxicity
Warnings/Precautions
Concerns related to adverse effects:
• Gastrointestinal effects: Constipation, bloating, and gas are common with calcium supplements (especially carbonate salt).
• Hypercalcemia: Mild-to-severe hypercalcemia may occur; decrease calcium acetate dose or temporarily discontinue, depending on severity of hypercalcemia; in addition, decrease or discontinue any concomitant vitamin D therapy. Chronic hypercalcemia may result in vascular calcification and other soft-tissue calcification.
Disease-related concerns:
• Arrhythmias: Use with caution in patients who may be at risk of cardiac arrhythmias.
• Kidney stones (calcium-containing): Use caution when administering calcium supplements to patients with a history of kidney stones.
Concurrent drug therapy issues:
• Digitalis: Use with caution in digitalized patients; hypercalcemia may precipitate cardiac arrhythmias.
• Minerals/other oral drugs: Calcium administration interferes with absorption of some minerals and drugs; use with caution..
• Vitamin D: It is recommended to concomitantly administer vitamin D for optimal calcium absorption.
Adverse Reactions
Well tolerated
1% to 10%
Central nervous system: Headache
Endocrine & metabolic: Hypophosphatemia, hypercalcemia
Gastrointestinal: Constipation, laxative effect, acid rebound, nausea, vomiting, anorexia, abdominal pain, xerostomia, flatulence
Miscellaneous: Milk-alkali syndrome with very high, chronic dosing and/or renal failure (headache, nausea, irritability, and weakness or alkalosis, hypercalcemia, renal impairment)
Drug Interactions ***
ACE Inhibitors: Antacids may decrease the serum concentration of ACE Inhibitors. Management: Separate fosinopril administration from antacids by at least 2 hours. US and Canadian recommendations for use of other ACE- inhibitors with antacids may vary. Consult appropriate labeling. Monitor for decreased therapeutic effects of ACE-inhibitors. Exceptions: Enalaprilat; Ramipril. Risk D: Consider therapy modification
Allopurinol: Antacids may decrease the absorption of Allopurinol. Risk D: Consider therapy modification
Bisacodyl: Antacids may diminish the therapeutic effect of Bisacodyl. Antacids may cause the delayed-release bisacodyl tablets to release drug prior to reaching the large intestine. Gastric irritation and/or cramps may occur. Risk D: Consider therapy modification
Bisphosphonate Derivatives: Calcium Salts may decrease the serum concentration of Bisphosphonate Derivatives. Management: Avoid administration of oral calcium supplements within: 2 hours before or after tiludronate/clodronate/etidronate; 60 minutes after oral ibandronate; or 30 minutes after alendronate/risedronate. Exceptions:Pamidronate; Zoledronic Acid. Risk D: Consider therapy modification
Calcium Acetate: Calcium Salts may enhance the adverse/toxic effect of Calcium Acetate. Risk X: Avoid combination
Calcium Polystyrene Sulfonate: Antacids may enhance the adverse/toxic effect of Calcium Polystyrene Sulfonate. The combined use of these two agents may result in metabolic alkalosis and/or loss of efficacy of the cation exchange resin. Management: To minimize this interaction, consider: a)separating doses by 2 or more hours; b)rectal administration of the exchange resin; or c)alternatives to antacids. Monitor for metabolic alkalosis and attenuation of CPS effects. Avoid magnesium hydroxide.Risk D: Consider therapy modification
Cefuroxime: Antacids may decrease the serum concentration of Cefuroxime. Management: Consider administering antacids and cefuroxime at least 2 hours apart. Risk D: Consider therapy modification
Chloroquine: Antacids may decrease the serum concentration of Chloroquine. Management: Separate administration of antacids and chloroquine by at least 4 hours to minimize any potential negative impact of antacids on chloroquine bioavailability. Risk D: Consider therapy modification
Corticosteroids (Oral): Antacids may decrease the bioavailability of Corticosteroids (Oral). Risk D: Consider therapy modification
Dabigatran Etexilate: Antacids may decrease the serum concentration of Dabigatran Etexilate. Management: Dabigatran etexilate Canadian product labeling recommends avoiding concomitant use with antacids for 24 hours after surgery. In other situations, administer dabigatran etexilate 2 hours prior to antacids. Monitor clinical response to dabigatran therapy. Risk D: Consider therapy modification
Erlotinib: Antacids may decrease the serum concentration of Erlotinib. Management: Separate the administration of erlotinib and any antacid by several hours in order to minimize the risk of a significant interaction. Risk D: Consider therapy modification
Gabapentin: Antacids may decrease the serum concentration of Gabapentin. Management: Administer gabapentin at least 2 hours after antacid administration. Monitor patients closely for evidence of reduced response to gabapentin therapy when both of these drugs are being used. Risk D: Consider therapy modification
Iron Salts: Antacids may decrease the absorption of Iron Salts. Exceptions: Ferric Gluconate; Ferumoxytol; Iron Dextran Complex; Iron Sucrose. Risk D: Consider therapy modification
Itraconazole: Antacids may decrease the serum concentration of Itraconazole. Management: Administer itraconazole at least 1 hour after and 2 hours before administration of any antacids. Itraconazole oral suspension may be less sensitive to the effects of decreased gastric acidity. Risk D: Consider therapy modification
Ketoconazole (Systemic): Antacids may decrease the serum concentration of Ketoconazole (Systemic). Management: Administer oral ketoconazole at least 2 hours prior to use of any antacid product. Monitor patients closely for signs of inadequate clinical response to ketoconazole. Risk D: Consider therapy modification
Multivitamins/Minerals (with ADEK, Folate, Iron): Antacids may decrease the serum concentration of Multivitamins/Minerals (with ADEK, Folate, Iron). Specifically, antacids may decrease the absorption of orally administered iron. Management: Separate dosing of oral iron-containing multivitamin preparations and antacids by as much time as possible in order to minimize impact on therapeutic efficacy of the iron preparation. Risk D: Consider therapy modification
Phosphate Supplements: Antacids may decrease the absorption of Phosphate Supplements. Exceptions: Potassium Phosphate. Risk D: Consider therapy modification
Quinolone Antibiotics: Calcium Salts may decrease the absorption of Quinolone Antibiotics. Of concern only with oral administration of both agents. Exceptions: Moxifloxacin (Systemic). Risk D: Consider therapy modification
Sodium Polystyrene Sulfonate: Antacids may enhance the adverse/toxic effect of Sodium Polystyrene Sulfonate. The combined use of these two agents may result in metabolic alkalosis and/or loss of efficacy of the exchange resin. Management: To minimize this interaction, consider: a)separating doses by 2 or more hours; b)rectal administration of the exchange resin; or c)alternatives to antacids. Monitor for metabolic alkalosis and attenuation of SPS effects. Avoid magnesium hydroxide. Risk D: Consider therapy modification
Tetracycline Derivatives: Calcium Salts may decrease the serum concentration of Tetracycline Derivatives. Management: If coadministration of oral calcium with oral tetracyclines can not be avoided, consider separating administration of each agent by several hours. Risk D: Consider therapy modification
Thyroid Products: Calcium Salts may diminish the therapeutic effect of Thyroid Products. Management: Separate the doses of the thyroid product and the oral calcium supplement by at least 4 hours. Risk D: Consider therapy modification
*** List is not comprehensive, please seek further interaction software where concerned. Risk D or X only included***
Ethanol/Nutrition/Herb Interactions
Ethanol: Avoid ethanol (may increase risk of osteoporosis).
Monitoring Parameters
Serum calcium (twice weekly during initial dose adjustments), serum phosphorus; serum calcium-phosphorus product; intact parathyroid hormone (iPTH)
Reference Range
Corrected total serum calcium (K/DOQI, 2003): CKD stages 3 and 4: 2.1-2.6 mmol/L; CKD stage 5: 2.1-2.37 mmol/L; KDIGO guidelines recommend maintaining normal ranges for all stages of CKD (3-5D) (KDIGO, 2009)
Phosphorus (K/DOQI, 2003):
CKD stages 3 and 4: 0.87-1.48mmol/L (adults)
CKD stage 5 (including those treated with dialysis): 1.13-1.78 mmol/L (children >12 years and adults); 1.29-1.94 mmol/L (children 1-12 years)
KDIGO guidelines recommend maintaining normal ranges for CKD stages 3-5 and lowering elevated phosphorus levels toward the normal range for CKD stage 5D (KDIGO, 2009)
Due to a poor correlation between the serum ionized calcium (free) and total serum calcium, particularly in states of low albumin or acid/base imbalances, direct measurement of ionized calcium is recommended
In low albumin states, the corrected total serum calcium may be estimated by:
Corrected total calcium = total serum calcium + 0.8 (4.0 - measured serum albumin)
Mechanism of Action
Used to treat hyperphosphatemia in patients with advanced renal insufficiency by combining with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces.
Patient Education
Take with meals. Avoid alcohol. May cause constipation or dry mouth. Report severe, unresolved GI disturbances.
Pharmacodynamics/Kinetics
Excretion: Primarily feces (as unabsorbed calcium); urine (20%)
Pharmacotherapy Pearls
20 mEq calcium/g; 400 mg elemental calcium/g calcium carbonate (40% elemental calcium)
Cardiovascular Considerations
Hypercalcemia is evident on ECG by shortening of the QT interval and possibly lengthening of the PR interval. Hypocalcemia causes prolongation of the QT interval. This prolongation is due to lengthening of the ST segment; the T waves remain unchanged. However, in severe hypocalcemia, T waves may be inverted. Note that only hypocalcemia and hypothermia lengthen the ST segment without altering T-wave duration. Hypocalcemia may also present clinically with skeletal muscle spasm.
Calcium salts may enhance the arrhythmogenic effects of digoxin. Part of the inotropic action of digoxin appears to be associated with increased intracellular calcium availability. Chronotropic effects are also calcium mediated. The administration of exogenous calcium (especially by parenteral routes) can lead to cardiac arrhythmias.
References
Bauwens SF, Drinka PJ, and Boh LE, “Pathogenesis and Management of Primary Osteoporosis,” Clin Pharm, 1986, 5:639-59. [PubMed 3527528]
Heaney RP, Recker RR, and Saville PD, “Menopausal Changes in Calcium Balance Performance,” J Lab Clin Med, 1978, 92(6):953-63. [PubMed 739173]
IOM (Institute of Medicine), Dietary Reference Intakes for Calcium and Vitamin D, Washington, DC: The National Academies Press, 2011.
Mahadevan U and Kane S, "American Gastroenterological Association Institute Medical Position Statement on the Use of Gastrointestinal Medications in Pregnancy,"Gastroenterology, 2006, 131(1):278-82.[PubMed 16831610]
Mokhlesi B, Leikin JB, Murray P, et al, “Adult Toxicology in Critical Care: Part II: Specific Poisonings,” Chest, 2003, 123(3):897-922. [PubMed 12628894]
NIH Consensus Conference, “Optimal Calcium Intake,” JAMA, 1994, 272(24):1942-8. [PubMed 7990248]
Recker RR, “Calcium Absorption and Achlorhydria,” N Engl J Med, 1985, 313(2):70-3.[PubMed 4000241]
Bauwens SF, Drinka PJ, and Boh LE, “Pathogenesis and Management of Primary Osteoporosis,” Clin Pharm, 1986, 5:639-59. [PubMed 3527528]
Heaney RP, Recker RR, and Saville PD, “Menopausal Changes in Calcium Balance Performance,” J Lab Clin Med, 1978, 92(6):953-63. [PubMed 739173]
IOM (Institute of Medicine), Dietary Reference Intakes for Calcium and Vitamin D, Washington, DC: The National Academies Press, 2011.
Mahadevan U and Kane S, "American Gastroenterological Association Institute Medical Position Statement on the Use of Gastrointestinal Medications in Pregnancy,"Gastroenterology, 2006, 131(1):278-82.[PubMed 16831610]
Mokhlesi B, Leikin JB, Murray P, et al, “Adult Toxicology in Critical Care: Part II: Specific Poisonings,” Chest, 2003, 123(3):897-922. [PubMed 12628894]
NIH Consensus Conference, “Optimal Calcium Intake,” JAMA, 1994, 272(24):1942-8. [PubMed 7990248]
Recker RR, “Calcium Absorption and Achlorhydria,” N Engl J Med, 1985, 313(2):70-3.[PubMed 4000241]
Calcium Acetate
** Listed below are differences from above**
*** Calcium Acetate is not commonly used in Canada as a phosphate binder***
Dosing:
Control of hyperphosphatemia (ESRD, on dialysis): Oral: Initial: 1334 mg with each meal, can be increased gradually (ie, every 2-3 weeks) to bring the serum phosphate value < 1.8 mmol/L as long as hypercalcemia does not develop (usual dose: 2001-2668 mg calcium acetate with each meal); do not give additional calcium supplements
*** Calcium Acetate is not commonly used in Canada as a phosphate binder***
Dosing:
Control of hyperphosphatemia (ESRD, on dialysis): Oral: Initial: 1334 mg with each meal, can be increased gradually (ie, every 2-3 weeks) to bring the serum phosphate value < 1.8 mmol/L as long as hypercalcemia does not develop (usual dose: 2001-2668 mg calcium acetate with each meal); do not give additional calcium supplements
References
IOM (Institute of Medicine), Dietary Reference Intakes for Calcium and Vitamin D, Washington, DC: The National Academies Press, 2011.
Kaiser W, Biesenbach G, Kramar R, et al, “Calcium Free Hemodialysis: An Effective Therapy in Hypercalcemic Crisis - Report of Four Cases,” Intensive Care Med, 1989, 15(7):471-4. [PubMed 2600293]
“K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. Guideline 1. Evaluation of Calcium and Phosphorus Metabolism.” Available at http://www.kidney.org/professionals/KDOQI/guidelines_pedbone/guide1.htm
"K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease, Guideline 13. Treatment of Bone Disease in Chronic Kidney Disease." Available at http://www.kidney.org/professionals/KDOQI/guidelines_bone/index.htm
"K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease," 2002. Available at http://www.kidney.org/professionals/KDOQI/guidelines_ckd/toc.htm
Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group, "KDIGO Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)," Kidney Int Suppl, 2009, 76(S113):1-130.[PubMed 19644521]
Mokhlesi B, Leikin JB, Murray P, et al, “Adult Toxicology in Critical Care: Part II: Specific Poisonings,” Chest, 2003, 123(3):897-922. [PubMed 12628894]
Texier D, Chevallier P, Perrotin D, et al, “Hypercalcemia Associated With Resorbable Haemostatic Compresses,” Lancet, 1982, 1(8273):688-9.
IOM (Institute of Medicine), Dietary Reference Intakes for Calcium and Vitamin D, Washington, DC: The National Academies Press, 2011.
Kaiser W, Biesenbach G, Kramar R, et al, “Calcium Free Hemodialysis: An Effective Therapy in Hypercalcemic Crisis - Report of Four Cases,” Intensive Care Med, 1989, 15(7):471-4. [PubMed 2600293]
“K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease. Guideline 1. Evaluation of Calcium and Phosphorus Metabolism.” Available at http://www.kidney.org/professionals/KDOQI/guidelines_pedbone/guide1.htm
"K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease, Guideline 13. Treatment of Bone Disease in Chronic Kidney Disease." Available at http://www.kidney.org/professionals/KDOQI/guidelines_bone/index.htm
"K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease," 2002. Available at http://www.kidney.org/professionals/KDOQI/guidelines_ckd/toc.htm
Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group, "KDIGO Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)," Kidney Int Suppl, 2009, 76(S113):1-130.[PubMed 19644521]
Mokhlesi B, Leikin JB, Murray P, et al, “Adult Toxicology in Critical Care: Part II: Specific Poisonings,” Chest, 2003, 123(3):897-922. [PubMed 12628894]
Texier D, Chevallier P, Perrotin D, et al, “Hypercalcemia Associated With Resorbable Haemostatic Compresses,” Lancet, 1982, 1(8273):688-9.