Disodium Hydrogen Citrate is a systemic and urinary alkalizing agent. It is a sodium salt of citric acid that, upon metabolism, increases the plasma bicarbonate concentration, buffers excess hydrogen ion concentration, and raises blood and urinary pH. It is primarily used to correct metabolic acidosis and to alkalinize urine, which aids in the management of certain drug toxicities and prevents uric acid and cysteine stone formation in the urinary tract.
Adult: Individualized based on condition. For urinary alkalinization: 2-6 grams (approx. 20-60 mEq sodium) dissolved in water, 3-4 times daily. For chronic metabolic acidosis: 4-12 grams (40-120 mEq sodium) per day in divided doses. Dose must be titrated to achieve desired urinary pH (6.0-7.0) or serum bicarbonate level.
Note: Granules/powder must be completely dissolved in a full glass of water (or as directed) before ingestion. Take after meals to minimize GI upset. Do not take with antacids containing aluminum (risk of increased aluminum absorption). Maintain adequate fluid intake (2-3 L/day) unless contraindicated.
Disodium Hydrogen Citrate acts as a prodrug for bicarbonate. After oral administration, the citrate anion is absorbed and metabolized in the liver and other tissues via the Krebs cycle. This metabolism consumes a hydrogen ion (H+) and yields bicarbonate (HCO3-). The generated bicarbonate enters the systemic circulation, increasing the plasma bicarbonate buffer capacity. This helps neutralize excess hydrogen ions, raising blood pH in metabolic acidosis. In the kidneys, the increased filtered load of bicarbonate alkalinizes the urine, increasing the solubility of uric acid and cysteine, and promoting the renal excretion of weak acids like salicylates and barbiturates.
Pregnancy: Category C: Animal reproduction studies not conducted. Use only if clearly needed, weighing benefits against risks of sodium load and alkalosis. Monitor electrolytes.
Driving: No known effects. However, if alkalosis or electrolyte disturbances occur, they may cause dizziness or confusion, impairing ability.
| Lithium | Increased renal excretion of lithium, decreasing its serum levels and efficacy. | Major |
| Methenamine (e.g., Hiprex) | Alkalinized urine inactivates methenamine, rendering it ineffective for urinary tract infections. | Major |
| Quinolone Antibiotics (e.g., Ciprofloxacin) | Decreased solubility of some quinolones in alkaline urine, potentially increasing risk of crystalluria. | Moderate |
| Salicylates (Aspirin) | Increased renal excretion of salicylates, reducing their serum levels. Used therapeutically in overdose. | Moderate |
| Anticholinergics | Increased absorption of citrate due to delayed gastric emptying, potentially increasing systemic effects. | Moderate |
| Corticosteroids, ACTH | Enhanced sodium retention, increasing risk of edema and hypertension. | Moderate |
| Potassium-Sparing Diuretics (e.g., Spironolactone) | Increased risk of hyperkalemia, especially in renal impairment. | Moderate |
| Antacids containing Aluminum | Increased aluminum absorption, risk of toxicity. | Moderate |