Endrate Disease Interactions

Severe cardiac arrhythmias associated with EDTA disodium are due to decreased serum calcium. EDTA also exerts a negative inotropic effect on the heart and can exacerbate congestive heart failure. EDTA disodium functions to reduce serum concentrations of calcium by forming stable soluble complexes with calcium. EDTA also chelates zinc, magnesium, and other trace metals and increases potassium excretion in the urine. Therapy with EDTA disodium should be used with caution in patients with limited cardiac reserve, congestive heart failure or arrhythmia. Clinical monitoring of cardiac function and electrolytes (including calcium, potassium, and magnesium) is recommended.

The use of disodium EDTA is contraindicated in patients with anuria and severe renal dysfunction. Dose-related nephrotoxicity (usually reversible) associated with EDTA has included polyuria, dysuria, oliguria, proteinuria, cast and cells in urine, renal insufficiency/failure, and rarely, acute tubular necrosis. EDTA disodium is eliminated by the kidney primarily chelated to calcium. Impaired renal function decreases the elimination of EDTA and may increase its nephrotoxicity.

The use of EDTA disodium is usually contraindicated in patients with active tuberculosis or healed calcified tubercular lesions. EDTA disodium forms stable soluble complexes with calcium.

EDTA disodium functions to reduce serum calcium concentrations by forming stable soluble complexes with calcium. Hypocalcemia may precipitate seizures. Therapy with EDTA disodium should be used with caution in patients with intracranial lesions or with or predisposed to seizure disorders. Clinical monitoring of electrolyte concentrations is recommended.

EDTA may chelate zinc present in exogenous insulin and alter glucose concentrations and insulin requirements in patients with diabetes. Insulin dosages may need to be adjusted in diabetic patients administered EDTA.