Version May 2024
Hypocalcemia associated with hypoparathyroidism/pseudohypoparathyroidism:
Oral: Initial: 0.25 to 0.5 mcg twice daily (Ref). May adjust dose in 0.25 mcg/day increments every 1 to 4 weeks if needed to achieve target albumin-corrected serum calcium levels; usual dosage range: 0.5 to 2 mcg/day (Ref).
Patients discontinuing recombinant parathyroid hormone (rPTH) therapy: Increased doses of calcitriol and supplemental calcium may be required to prevent severe acute hypocalcemia, especially if rPTH therapy is discontinued abruptly. Resume pre-rPTH treatment doses of calcitriol and calcium supplementation within 12 hours of discontinuation, with close monitoring of serum calcium (eg, every 3 days); some patients may require calcium and calcitriol doses up to 2 to 3 times the pre-rPTH treatment doses (Ref).
Hypophosphatemia, X-linked (ie, vitamin D-resistant rickets) (off-label use): Oral: Initial: 0.5 to 0.75 mcg/day in 2 divided doses; after 4 to 6 weeks, assess biochemical response; dose may be adjusted upward or downward in increments of 0.25 mcg/day every 3 to 4 weeks to maintain normal serum parathyroid hormone (PTH) and calcium while avoiding hypercalciuria. Consider discontinuing therapy if clinical improvement is not observed within 9 to 12 months. Note: Calcitriol may be initiated ~1 week prior to initiating phosphate therapy to reduce the risk of exacerbating preexisting secondary hyperparathyroidism or causing it to develop (Ref).
Secondary hyperparathyroidism in chronic kidney disease: Note: Kidney Disease: Improving Global Outcomes (KDIGO) guidelines do not recommend routine use of calcitriol or other vitamin D analogs in patients with chronic kidney disease (CKD) stages G3 to G5; it may be reasonable to reserve use for patients with CKD stages G4 or G5 and with severe and progressive hyperparathyroidism. Caution is advised to avoid hypercalcemia or elevated phosphate levels (Ref).
Patients on dialysis:
Oral: Initial: 0.25 mcg once daily (Ref); some experts recommend more conservative initial doses (eg, 0.25 mcg 3 times weekly) (Ref); may increase dose by 0.25 mcg/day at 4- to 8-week intervals, up to 0.5 to 1 mcg/day. Patients with normal or mildly decreased serum calcium levels may respond to 0.25 mcg every other day.
IV: Initiate carefully; 0.5 mcg 3 times weekly is the lowest recommended dose in the manufacturer’s labeling; some experts recommend more conservative initial doses (eg, 0.25 mcg 3 times weekly) (Ref). Adjust dose by 0.5 to 1 mcg at 2- to 4-week intervals; dosing range: 0.5 to 4 mcg 3 times weekly. Gradual dose reduction and discontinuation of therapy may be necessary as PTH levels decrease in response to therapy.
Patients with moderate to severe chronic kidney disease not yet on dialysis: Note: The magnitude of PTH response is highly variable (Ref). KDIGO guidelines recommend initiating with low doses independent of initial PTH concentration and then titrating based on PTH response while avoiding hypercalcemia (Ref).
Oral: Initial: 0.25 mcg once daily (Ref); some experts recommend more conservative initial doses (eg, 0.25 mcg 3 to 4 times weekly) (Ref); may increase to 0.5 mcg/day if needed.
Vitamin D-dependent rickets type 1/pseudovitamin D deficiency rickets (PDDR) (off-label use): Oral: Initial: 0.5 mcg twice daily; subsequent dosing adjusted to maintain normal serum calcium and PTH levels; median dose after 2 years: 0.25 mcg daily (range: 0.1 to 0.5 mcg daily) (Ref).
Discontinuation of therapy for hypercalcemia: Discontinue therapy if hypercalcemia occurs; monitor calcium and phosphorous daily until levels normalize. Upon normalization, treatment with calcitriol can be resumed, at a reduced dose than that previously used. Assess dietary calcium intake and adjust if indicated.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function: No dosage adjustment likely to be necessary for any degree of kidney dysfunction (primarily excreted in feces) (Ref).
Hemodialysis, intermittent (thrice weekly): Unlikely to be significantly dialyzed (highly protein bound) (Ref): No supplemental dose or dosage adjustment likely to be necessary (Ref).
Peritoneal dialysis: Unlikely to be significantly dialyzed (highly protein bound) (Ref): No dosage adjustment likely to be necessary (Ref).
CRRT: No dosage adjustment likely to be necessary (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment likely to be necessary (Ref).
There are no dosage adjustments provided in the manufacturer’s labeling.
Refer to adult dosing. Start at the lower end of the dosage range.
(For additional information see "Calcitriol (systemic): Pediatric drug information")
Chronic kidney disease-mineral and bone disorder (CKD-MBD): Limited data available: Note: In pediatric patients with CKD stages 3a through 5 with elevated parathyroid hormone (PTH), guidelines recommend consideration of calcitriol use to maintain serum calcium in age-appropriate normal range; optimal serum PTH concentration remains undefined (Ref).
CKD stages 3a to 4:
Children and Adolescents:
Note: Dosing recommendations based on the 2005 KDOQI Guidelines (Ref). Dosage should be adjusted based on patient response (eg, calcium, phosphorus, PTH levels).
Initial dose:
<10 kg: Oral: 0.05 mcg every other day.
10 to 20 kg: Oral: 0.1 to 0.15 mcg once daily.
>20 kg: Oral: 0.25 mcg once daily.
Dosage adjustment:
If intact parathyroid hormone (iPTH) decrease is <30% after 3 months of therapy and serum levels of calcium and phosphorus are within the target ranges based upon the CKD stage, increase dosage by 50%.
If iPTH decreases to < target range for CKD stage, hold calcitriol therapy until iPTH increases to above target range; resume therapy at half the previous dosage (if dosage <0.25 mcg capsule or 0.05 mcg liquid, use every other day therapy).
If serum levels of total corrected calcium exceed 10.2 mg/dL, hold calcitriol therapy until serum calcium decreases to <9.8 mg/dL; resume therapy at half the previous dosage (if dosage <0.25 mcg capsule or 0.05 mcg liquid, use every other day therapy).
If serum levels of phosphorus increase to > age-appropriate upper limits, hold calcitriol therapy; resume therapy at half the previous dosage.
CKD stage 5 requiring dialysis:
Children and Adolescents:
Note: Dosing recommendations based on the 2005 KDOQI Guidelines (Ref). Dosage should be adjusted based on patient response (eg, calcium, phosphorus, PTH levels) and concomitant therapies; to ensure adequate bone health in children, maintain calcium in normal range; avoid hypocalcemia (Ref).
Initial dose:
iPTH 300 to 500 pg/mL: Oral, IV: 0.0075 mcg/kg 3 times weekly; maximum dose: 0.25 mcg/dose.
iPTH >500 to 1,000 pg/mL: Oral, IV: 0.015 mcg/kg 3 times weekly; maximum dose: 0.5 mcg/dose.
iPTH >1,000 pg/mL: Oral, IV: 0.025 mcg/kg 3 times weekly; maximum dose: 1 mcg/dose.
Dosage adjustment: If iPTH decrease is <30% after 3 months of therapy and serum levels of calcium and phosphorus are within the target ranges for CKD stage 5, increase dosage by 50%.
Hypoparathyroidism/pseudohypoparathyroidism:
Note: Dosage should be adjusted based on patient response.
Infants: Limited data available: Oral: 0.02 to 0.06 mcg/kg once daily (Ref).
Children 1 to 5 years: Oral: 0.25 to 0.75 mcg once daily (Ref).
Children ≥6 years and Adolescents: Oral: 0.5 to 2 mcg once daily (Ref).
Vitamin D-dependent rickets: Infants, Children, and Adolescents: Oral: Initial: 0.25 to 2 mcg once daily; adjust dose based on clinical response to maintain low-normal serum calcium level, normal serum phosphorus level, and a high-normal serum PTH level; reduce dose once rickets has healed (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
No dosage adjustment necessary.
There are no dosage adjustments provided in the manufacturer's labeling (has not been studied).
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
>10%: Endocrine & metabolic: Hypercalcemia
1% to 10%:
Central nervous system: Headache
Dermatologic: Skin rash
Endocrine & metabolic: Polydipsia
Gastrointestinal: Abdominal pain, nausea
Genitourinary: Urinary tract infection
Frequency not defined:
Cardiovascular: Cardiac arrhythmia, hypertension
Central nervous system: Apathy, drowsiness, hyperthermia, metallic taste, psychosis, sensory disturbance
Dermatologic: Erythema, erythema multiforme, pruritus, urticaria
Endocrine & metabolic: Albuminuria, calcinosis, decreased libido, dehydration, growth suppression, hypercholesterolemia, weight loss
Gastrointestinal: Anorexia, constipation, pancreatitis, stomach pain, vomiting, xerostomia
Genitourinary: Hypercalciuria, nocturia
Hepatic: Increased serum ALT, increased serum AST
Hypersensitivity: Hypersensitivity reaction
Local: Pain at injection site (mild)
Neuromuscular & skeletal: Dystrophy, myalgia, ostealgia, weakness
Ophthalmic: Conjunctivitis, photophobia
Renal: Calcium nephrolithiasis, increased blood urea nitrogen, increased serum creatinine, polyuria
Respiratory: Rhinorrhea
<1%, postmarketing and/or case reports: Agitation, anaphylaxis, apprehension, hypermagnesemia, hyperphosphatemia, hypervitaminosis D, increased hematocrit, increased hemoglobin, increased neutrophils, increased serum alkaline phosphatase, insomnia, limb pain, lymphocytosis
Hypersensitivity to calcitriol, other vitamin D analogues, or any component of the formulation; hypercalcemia, vitamin D toxicity
Concerns related to adverse effects:
• Excessive vitamin D: Excessive vitamin D administration may lead to over suppression of parathyroid hormone (PTH), progressive or acute hypercalcemia, hypercalciuria, hyperphosphatemia and adynamic bone disease. Withhold pharmacologic doses of vitamin D and its derivatives during therapy to avoid the potential for hypercalcemia to develop. In addition, several months may be required for ergocalciferol levels to return to baseline in patients switching from ergocalciferol therapy to calcitriol.
• Hypercalcemia: Monitor calcium levels closely with initiation of therapy and with dose adjustments; discontinue use promptly in patients who develop hypercalcemia. Avoid abrupt dietary modifications (eg, increased intake of dairy products) which may lead to hypercalcemia; adjust calcium intake if indicated and maintain adequate hydration. Chronic hypercalcemia can result in generalized vascular and soft tissue calcification, exacerbate nephrolithiasis, and has been associated with increased mortality in adults with chronic kidney disease (CKD) (KDIGO 2017). Immobilized patients may be at a higher risk for hypercalcemia.
Disease-related concerns:
• Malabsorption syndrome: Use oral calcitriol with caution in patients with malabsorption syndromes; efficacy may be limited and/or response may be unpredictable.
• Renal impairment: Calcitriol can increase serum phosphate levels in patients with kidney impairment. Progressive or persistently increased serum phosphate levels in patients with CKD stage G3a to G5D may lead to ectopic calcification; phosphate-lowering treatment (eg, low phosphate diet alone or in combination with phosphate binders and/or dialysis) may be necessary (KDIGO 2017).
Dosage form specific issues:
• Aluminum: The parenteral product may contain aluminum; toxic aluminum concentrations may be seen with high doses, prolonged use, or renal dysfunction. Premature neonates are at higher risk due to immature renal function and aluminum intake from other parenteral sources. Parenteral aluminum exposure of >4 to 5 mcg/kg/day is associated with CNS and bone toxicity; tissue loading may occur at lower doses (Federal Register 2002). See manufacturer’s labeling.
• Coconut oil: Products may contain coconut oil (capsule).
• Palm seed oil: Products may contain palm seed oil (oral solution).
• Tartrazine: Some products may contain tartrazine.
Other warnings/precautions:
• Calcium: Adequate dietary (supplemental) calcium is necessary for clinical response to vitamin D. Patients with a tendency to develop hypercalcemia may require low doses of calcium or no supplementation at all.
Calcium, phosphorus, and parathyroid hormone levels should be monitored closely and the calcitriol dosage adjusted accordingly. The combination of hypercalcemia and hyperphosphatemia may result in adverse outcomes such as soft tissue or vascular calcification (KDOQI 2005; KDIGO 2017). Previously, expert opinion was that serum calcium times phosphorus product (Ca × P) should not exceed 65 mg2/dL2 for infants and children and 55 mg2/dL2 for adolescents (KDOQI 2005). Current guidelines do not recommend use of the calcium phosphorus product, but rather suggest that calcium and phosphorus values should be considered individually/evaluated together, with age-appropriate normal values targeted (KDIGO 2017).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Rocaltrol: 0.25 mcg, 0.5 mcg [contains fd&c yellow #6 (sunset yellow), methylparaben, propylparaben]
Generic: 0.25 mcg, 0.5 mcg
Solution, Intravenous:
Generic: 1 mcg/mL (1 mL)
Solution, Oral:
Rocaltrol: 1 mcg/mL (15 mL)
Generic: 1 mcg/mL (15 mL)
Yes
Capsules (Calcitriol Oral)
0.25 mcg (per each): $0.33 - $1.56
0.5 mcg (per each): $0.51 - $2.50
Capsules (Rocaltrol Oral)
0.25 mcg (per each): $2.05
0.5 mcg (per each): $3.22
Solution (Calcitriol Intravenous)
1 mcg/mL (per mL): $11.94
Solution (Calcitriol Oral)
1 mcg/mL (per mL): $11.93 - $31.73
Solution (Rocaltrol Oral)
1 mcg/mL (per mL): $17.17
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Rocaltrol: 0.25 mcg, 0.5 mcg
Generic: 0.25 mcg, 0.5 mcg
Solution, Intravenous:
Generic: 1 mcg/mL (1 mL)
IV: May be administered as a bolus dose IV through the catheter at the end of hemodialysis.
Oral: May be administered without regard to food. Administer with meals to reduce GI problems.
Oral: May be administered with or without meals.
Parenteral: May be administered undiluted as a bolus dose IV through the hemodialysis catheter at the end of hemodialysis.
Hypocalcemia associated with hypoparathyroidism/pseudohypoparathyroidism: Management of hypocalcemia in patients with hypoparathyroidism or pseudohypoparathyroidism (oral).
Secondary hyperparathyroidism in patients with chronic kidney disease: Management of secondary hyperparathyroidism in patients with moderate to severe chronic kidney disease not on dialysis (oral) or in patients on dialysis (oral or IV). Note: Although the manufacturer’s labeling states that calcitriol may be used specifically to treat hypocalcemia in dialysis patients, due to the risk of hypercalcemia, use should generally be reserved for patients with severe and progressive hyperparathyroidism (KDIGO 2017).
Hypophosphatemia, X-linked (ie, vitamin D-resistant rickets); Vitamin D-dependent rickets type I/pseudovitamin D deficiency rickets (PDDR)
Calcitriol may be confused with alfacalcidol, calcifediol, Calciferol, calcitonin, calcium carbonate, captopril, colestipol, paricalcitol, ropinirole
Dosage is expressed in mcg (micrograms), not mg (milligrams); rare cases of acute overdose have been reported
Substrate of CYP3A4 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Aluminum Hydroxide: Vitamin D Analogs may increase the serum concentration of Aluminum Hydroxide. Specifically, the absorption of aluminum may be increased, leading to increased serum aluminum concentrations. Management: Consider avoiding chronic use of aluminum and aluminum-containing products in patients who are also taking active vitamin D analogs. If coadministered, monitor aluminum status and for signs and symptoms of aluminum-related toxicities. Risk D: Consider therapy modification
Bile Acid Sequestrants: May decrease the serum concentration of Vitamin D Analogs. More specifically, bile acid sequestrants may impair absorption of Vitamin D Analogs. Management: Avoid concomitant administration of vitamin D analogs and bile acid sequestrants (eg, cholestyramine). Separate administration of these agents by several hours to minimize the potential risk of interaction. Monitor plasma calcium concentrations. Risk D: Consider therapy modification
Burosumab: Vitamin D Analogs may enhance the adverse/toxic effect of Burosumab. Risk X: Avoid combination
Calcium Salts: May enhance the adverse/toxic effect of Vitamin D Analogs. Risk C: Monitor therapy
Cardiac Glycosides: Vitamin D Analogs may enhance the arrhythmogenic effect of Cardiac Glycosides. Risk C: Monitor therapy
Corticosteroids (Systemic): May diminish the therapeutic effect of Calcitriol (Systemic). Risk C: Monitor therapy
CYP3A4 Inducers (Strong): May decrease the serum concentration of Calcitriol (Systemic). Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May increase the serum concentration of Calcitriol (Systemic). Risk C: Monitor therapy
Danazol: May enhance the hypercalcemic effect of Vitamin D Analogs. Risk C: Monitor therapy
Erdafitinib: Serum Phosphate Level-Altering Agents may diminish the therapeutic effect of Erdafitinib. Management: Avoid coadministration of serum phosphate level-altering agents with erdafitinib before initial dose increase period based on serum phosphate levels (Days 14 to 21). Risk D: Consider therapy modification
Magnesium Salts: Calcitriol (Systemic) may increase the serum concentration of Magnesium Salts. Management: Consider using a non-magnesium-containing antacid or phosphate-binding product in patients also receiving calcitriol. If magnesium-containing products must be used with calcitriol, serum magnesium concentrations should be monitored closely. Risk D: Consider therapy modification
Mineral Oil: May decrease the serum concentration of Vitamin D Analogs. More specifically, mineral oil may interfere with the absorption of Vitamin D Analogs. Management: Avoid concomitant, oral administration of mineral oil and vitamin D analogs. Consider separating the administration of these agents by several hours to minimize the risk of interaction. Monitor plasma calcium concentrations. Risk D: Consider therapy modification
Multivitamins/Fluoride (with ADE): May enhance the adverse/toxic effect of Vitamin D Analogs. Risk X: Avoid combination
Multivitamins/Minerals (with ADEK, Folate, Iron): May enhance the adverse/toxic effect of Vitamin D Analogs. Risk X: Avoid combination
Orlistat: May decrease the absorption of Vitamins (Fat Soluble). Management: Administer oral fat soluble vitamins at least 2 hours before or 2 hours after the administration of orlistat. Avoid concomitant administration due to the risk of impaired vitamin absorption. Risk D: Consider therapy modification
Sevelamer: May decrease the serum concentration of Calcitriol (Systemic). Risk C: Monitor therapy
Sucralfate: Vitamin D Analogs may increase the serum concentration of Sucralfate. Specifically, the absorption of aluminum from sucralfate may be increased, leading to an increase in the serum aluminum concentration. Management: Consider avoiding chronic use of aluminum and aluminum-containing products, such as sucralfate, in patients who are also taking active vitamin D analogs. If combined, monitor for signs and symptoms of aluminum-related toxicities. Risk D: Consider therapy modification
Thiazide and Thiazide-Like Diuretics: May enhance the hypercalcemic effect of Vitamin D Analogs. Risk C: Monitor therapy
Vitamin D Analogs: May enhance the adverse/toxic effect of other Vitamin D Analogs. Risk X: Avoid combination
Maternal calcitriol may be detected in the fetal circulation. Mild hypercalcemia has been reported in a newborn following maternal use of calcitriol during pregnancy. Adverse effects on fetal development were not observed with use of calcitriol during pregnancy in patients (N=9) with pseudovitamin D-dependent rickets. Doses were adjusted every 4 weeks to keep calcium concentrations within normal limits (Edouard 2011). If calcitriol is used for the management of hypoparathyroidism in pregnancy, dose adjustments may be needed as pregnancy progresses and again following delivery. Vitamin D and calcium levels should be monitored closely and kept in the lower normal range (Callies 1998).
Low levels of calcitriol are found in breast milk (~2 pg/mL)
May be taken without regard to food. Give with meals to reduce GI problems. Adequate calcium intake should be maintained during therapy; dietary phosphorous may need to be restricted.
Secondary hyperparathyroidism (patients with CKD): Note: The frequency of serum calcium, phosphate, and parathyroid hormone (PTH) measurements may be dependent upon the presence and magnitude of abnormalities, the rate of progression of chronic kidney disease (CKD), and the use of treatments for chronic kidney disease-mineral and bone disorder (KDIGO 2017).
During therapy initiation and dosage adjustments: Frequent monitoring of serum calcium and phosphate levels (eg, at least twice weekly) is recommended (manufacturer’s labeling).
KDIGO guidelines (2017): Note: During treatment or when biochemical abnormalities are identified more frequent monitoring may be reasonable.
CKD stage G3a to G3b: Serum calcium and phosphate: Every 6 to 12 months; PTH: Frequency based on baseline level and progression of CKD; alkaline phosphatase.
CKD stage G4: Serum calcium and phosphate: Every 3 to 6 months; PTH: Every 6 to 12 months; alkaline phosphatase every 12 months or more frequently in the presence of elevated PTH.
CKD stage G5 and G5D: Serum calcium and phosphate: Every 1 to 3 months; PTH: Every 3 to 6 months; alkaline phosphatase every 12 months or more frequently in the presence of elevated PTH.
Hypoparathyroidism: Note: Frequency of measurement is dependent upon on how stable a patient is to a given dosage regimen with more frequent measurements (eg, weekly) required initially during dosage titration. Once hypoparathyroidism is well controlled, monitoring may be required on a yearly or twice-yearly basis (ES [Brandi 2016]).
Serum calcium, phosphate, and magnesium; renal function (ie, 24-hour urinary calcium and creatinine, blood urea nitrogen [BUN], measured CrCl or estimated glomerular filtration rate [eGFR]); renal imaging (every 5 years in asymptomatic patients with a history of renal lithiasis or calcinosis or more frequently as indicated); CNS imaging (basal ganglia and other sites of calcification), ophthalmologic exam, and/or BMD as indicated (ES [Brandi 2016]).
Hypophosphatemia, X-linked (off-label use):Serum calcium, phosphorous, PTH, alkaline phosphatase (ALP) (elevation in ALP of bone-origin may indicate extensive osteomalacia), and creatinine and 24-hour urinary calcium and creatinine (4 to 6 weeks after initiation of therapy, 6 to 8 weeks after satisfactory biochemical response is achieved and then every 3 to 4 months for the first year and every 6 to 9 months thereafter (Carpenter 2011).
Note: Due to the complexity and interdependency of the laboratory parameters used for therapeutic decisions in chronic kidney disease-mineral and bone disorder (CKD-MBD) patients, serial assessments of phosphate, calcium, and parathyroid hormone (PTH) levels should be considered together (KDIGO 2017)
Calcium (total): Adults: Normal range: 8.6 to 10.2 mg/dL (SI: 2.2 to 2.6 mmol/L). Avoid hypercalcemia for chronic kidney disease (CKD) stages G3a to G5D (KDIGO 2017)
Phosphorus: 3 to 4.5 mg/dL (SI: 1 to 1.5 mmol/L). Lower elevated phosphorus levels toward the normal range for CKD stages G3a to G5D (KDIGO 2017)
PTH:
CKD stage G3a to G5: Optimal PTH level is unknown; evaluate patients with progressively elevated intact PTH levels or if levels are consistently above the normal range (assay-dependent) (KDIGO 2017)
Dialysis patients: Maintain intact parathyroid hormone (iPTH) within 2 to 9 times the upper limit of normal for the assay used (KDIGO 2017)
Calcitriol, the active form of vitamin D (1,25 hydroxyvitamin D3), binds to and activates the vitamin D receptor in kidney, parathyroid gland, intestine, and bone, stimulating intestinal calcium transport and absorption. It reduces parathyroid hormone (PTH) levels and improves calcium and phosphate homeostasis by stimulating bone resorption of calcium and increasing renal tubular reabsorption of calcium. Decreased renal conversion of vitamin D to its primary active metabolite (1,25 hydroxyvitamin D) in chronic renal failure leads to reduced activation of vitamin D receptor, which subsequently removes inhibitory suppression of parathyroid hormone (PTH) release; increased serum PTH (secondary hyperparathyroidism) reduces calcium excretion and enhances bone resorption.
Onset of action: Oral: 2 hours; maximum effect: 10 hours
Duration: Oral, IV: 3 to 5 days
Absorption: Oral: Rapid
Protein binding: 99.9%
Metabolism: Primarily to calcitroic acid and a lactone metabolite
Half-life elimination: Children 1.8-16 years undergoing peritoneal dialysis: 27.4 hours; Healthy adults: 5 to 8 hours; Hemodialysis: 16 to 22 hours
Time to peak, serum: Oral: 3 to 6 hours; Hemodialysis: 8 to 12 hours
Excretion: Feces (27%); urine (7%, unchanged in 24 hours)
Clearance: Children 1.8 to 16 years undergoing peritoneal dialysis: 15.3 mL/hour/kg
Altered kidney function: The half-life is increased by at least 2-fold.
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