A highly selective cation exchanger that entraps potassium in the intestinal tract in exchange for sodium and hydrogen.
Compared with placebo is associated with significant reductions in serum potassium levels within the first 48 hours of treatment in patients with stage III chronic kidney disease with estimated GFR 30-60 mls per minute per 1.73 m² of body surface area and a serum potassium of 5-6 mmol per liter.
In the above study sodium zirconium cyclosilicate in hyperkalemia maintained normokalemia during 12 days of maintenance therapy (Packham DK et al).
Clinically significant treatment effects are observed within one hour after administration.
The decline in the potassium level is rapid and dose-dependent.
The dose starts at 2.5 g TID.
Reduction in serum potassium levels is most pronounced in patients with the highest potassium levels at baseline.
The drug normalizes potassium levels in patients who are receiving or RAAS inhibitors for the treatment of cardiovascular and renal disease.
Normal potassium levels can be maintained with 5-10 g of this drug once daily.
The drug is effective in patients with heart failure, chronic kidney disease and diabetes.
The potassium lowering action is based on size-selective micropores in the zirconium silicate crystal structure, which traps potassium in the intestinal tract in exchange for protons and sodium.
The potassium-binding capacity is nine times that of organic polymer resins and is more selective by a factor of greater than 125 for potassium over calcium.
The drug is in soluble and does not swell on contact with water, and is not systemically absorbed, with fecal excretion of more than 99% after ingestion.
Its stable crystal structure enables potassium to bind throughout the intestinal tract, explaining the significant fall in serum potassium levels within one hour following the first dose of 10 g of medication.
The overall safety profile is similar to that of placebo.