(1R,3S)- 5-[2-[(1R,3aR,7aS)-1- [(2R)-6-hydroxy-6-methyl-heptan-2-yl]-7a-methyl-2,3,3a,5,6,7-hexahydro-1H- inden-4-ylidene]ethylidene]-4-methylidene-cyclohexane-1,3-diol

Absorption
Oral
Rapidly absorbed from the intestine. T max is 3 to 6 h.

Distribution
Approximately 99.9% protein bound. Excreted in breast milk in low levels.

Metabolism
The first pathway involves 24-hydroxylase to produce calcitroic acid; the second pathway involves hydroxylation and cyclization. Calcitrol also undergoes enterohepatic recycling.

Elimination
The t ½ is about 5 to 8 h. About 27% is excreted in the feces and 7% in the urine within 24 h.

Special Populations
Renal Function Impairment
The t ½ is increased by at least 2-fold.

Children
The t ½ is prolonged.

Calcium supplements
Avoid uncontrolled intake of additional calcium-containing preparations.

Cholestyramine
May reduce intestinal absorption of fat soluble vitamins.

Ketoconazole
May reduce endogenous calcitriol concentrations.

Magnesium
Magnesium-containing products may cause hypermagnesemia and should be avoided during calcitriol administration to patients on chronic renal dialysis.

Phenytoin/Phenobarbital
Inhibits endogenous synthesis of calcitriol, therefore may require higher doses if given simultaneously.

Phosphate-binding agents
Because phosphate transport in the intestine, kidneys, and bones may be affected, the dosage of phosphate-binding agents must be adjusted based on serum phosphate concentration.

Thiazides
Known to induce hypercalcemia by the reduction of calcium excretion.

Vitamin D
To avoid possible additive effects and hypercalcemia, withhold pharmacologic doses of vitamin D and its derivatives.