Citric acid arrives two ways. As a food additive it slowly and permanently wears away tooth enamel. Taken deliberately as a citrate salt, it counteracts the acid produced by a typical diet: strong human evidence for fewer repeat calcium kidney stones and small gains in bone density in older adults. Costs include stomach upset, potassium load, enamel loss. (Full Review)
| Marker | Target | Why |
|---|---|---|
| 24-hour urinary citrate | > 600 mg/day, ideally > 800 mg/day | The direct target of therapy and the predictor of stone risk |
| 24-hour urine pH | 6.0–6.5 | Confirms alkali delivery without overshoot into calcium phosphate territory |
| 24-hour urinary calcium | < 200 mg/day | Citrate should lower calcium excretion; failure to do so suggests a separate cause |
| Serum potassium | 4.0–4.5 mmol/L | The dose-limiting safety marker for potassium citrate |
| Serum bicarbonate | 24–26 mmol/L | Confirms systemic alkali effect and detects low-grade acid retention |
| Estimated glomerular filtration rate | > 90 mL/min/1.73 m², minimum 60 | Sets the safe potassium ceiling and tracks the kidney benefit |
| Serum ferritin and transferrin saturation | Ferritin 50–100 ng/mL; saturation 20–40% | Citric acid enhances iron absorption, so overload can develop silently |
| Erosive tooth wear score | No established numeric target; change from the individual's own baseline | Erosion is the principal irreversible harm and is silent until advanced |
Cadence: Serum potassium and bicarbonate at 4 weeks; repeat 24-hour urine at 8–12 weeks; then both every 6–12 months. Bone density at 24 months; dental erosion scoring annually.