A slow intravenous treatment that binds metals like lead and cadmium so the body can clear them. Lowering metal burden is its one proven effect; whether that renews arteries stays unresolved. Human evidence is mixed. Main drawbacks: dangerously low blood calcium, kidney strain, mineral loss, and a costly, demanding schedule. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Serum creatinine / eGFR | Creatinine 0.7–1.0 mg/dL; eGFR > 90 mL/min/1.73 m² | Kidneys clear EDTA and the metals it binds; detects injury early |
| Serum calcium | 9.0–10.0 mg/dL (ionized 4.6–5.3 mg/dL) | Disodium EDTA lowers calcium; guards against hypocalcemia and tetany |
| Serum / RBC magnesium | Serum 2.0–2.5 mg/dL | Chelation depletes magnesium; low levels raise rhythm risk |
| Blood lead | As low as achievable; < 2 µg/dL | Primary metal target of the toxicity hypothesis |
| Cadmium (blood or urine) | Urine < 0.5 µg/g creatinine | Cadmium is linked to blood-vessel disease |
| Potassium and electrolytes | Potassium 4.0–4.5 mmol/L | Long infusions can shift fluids and electrolytes |
| Fasting glucose / HbA1c | HbA1c < 6.5% | Diabetes modifies response and raises hypoglycemia risk during infusions |
Cadence: Renal function and calcium before each infusion or at least every few infusions early in the course; reassess key markers at ~4 weeks, then every 3–6 months for extended or maintenance schedules.