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Edetate calcium disodium (CaNa2EDTA) is a chelating agent that is primarily used for the management of severe lead poisoning. Edetate calcium disodium has been replaced by succimer (2,3-dimercaptosuccinic acid) for the treatment of patients with lead concentrations between45 and 70 μg/dL. Although, in conjunction with dimercaprol, CaNa2EDTA retains a critical role in the management of serious lead poisoning and lead encephalopathy.

Edetate calcium disodium belongs to the family of polyaminocarboxylic acids. Although it is capable of chelating many metals, its current use is almost exclusively in the management of lead poisoning. The term chelate has its origin in the Greek word chele, which means "claw," implying an ability to tightly grasp the metal.42 Implicit in chelation is the formation of a ring-structured complex. When CaNa2EDTA chelates lead, the calcium is displaced and the lead takes its place, forming a stable ring compound.27

Edetate calcium disodium is an ionic, water-soluble compound with a molecular weight of 374 daltons. The volume of distribution is small (0.05–0.23 L/kg), and due to its polar nature approximates that of the extracellular fluid compartment in normal individuals,22,27 but is smaller in patients with renal dysfunction.33 Edetate calcium disodium appears to penetrate erythrocytes poorly,2,22 and less than 5% of CaNa2EDTA gains access to the spinal fluid.22,27 Oral administration of CaNa2EDTA is not practical because of an oral bioavailability of less than 5%. The half-life is about 20 to 60 minutes.4,22,27 Renal elimination approximates the glomerular filtration rate,32 which correlates with creatinine clearance,33 and results in the excretion of 50% of CaNa2EDTA in the urine within 1 hour, and more than 95% within 24 hours.22,27 When CaNa2EDTA combines with lead, it forms a stable, soluble, nonionized compound that is subsequently excreted in the urine. Following CaNa2EDTA administration, urinary lead excretion is increased 20- to 50-fold.9,34


Animal studies demonstrate a decrease in tissue lead stores, including brain concentrations, when measurements are performed following CaNa2EDTA therapy.25 A rat study examining the effect of a single dose of CaNa2EDTA on brain lead concentrations demonstrated a significant increase in brain lead concentrations,17 suggesting that CaNa2EDTA may initially mobilize lead and facilitate redistribution to the brain. Additional doses enhance lead elimination, reduce blood lead concentrations, and subsequently reduce brain lead concentrations. The initial increase in brain lead may explain why some human case reports demonstrate worsening lead encephalopathy when CaNa2EDTA is used without concomitant dimercaprol (British anti-Lewisite [BAL]) therapy.


Edetate calcium disodium is capable of reducing blood lead concentrations, enhancing renal excretion of lead, and reversing the effects of lead on hemoglobin synthesis.14 With chronic exposure, blood lead concentrations ...

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