Disodium Hydrogen Citrate is an oral systemic alkalizer and urinary alkalinizing agent. It is a sodium salt of citric acid that, upon metabolism, increases the plasma bicarbonate concentration, buffers excess hydrogen ion concentration, raises blood pH, and reverses metabolic acidosis. It also alkalinizes urine, increasing the solubility of uric acid and cystine, thereby preventing crystal formation and aiding in the dissolution of existing stones. It is a cornerstone therapy for metabolic acidosis and urinary stone prophylaxis in the Indian clinical setting.
Adult: 10-20 ml (3.06 - 6.12 gm) diluted in a glass of water, 3-4 times daily. Dose must be individualized based on urinary pH (target 6.5-7.5) and clinical response.
Note: Must be diluted in a full glass of water (at least 120-240 ml) before ingestion to minimize GI upset and ensure proper absorption. Administer after meals. Monitor urinary pH with pH strips to titrate dose to target range (6.5-7.5).
Disodium Hydrogen Citrate acts as a systemic and urinary alkalinizer. After oral administration, the citrate anion is absorbed and metabolized in the liver to bicarbonate (HCO3-). This generated bicarbonate enters the systemic circulation, where it acts as a buffer, neutralizing excess hydrogen ions (H+) and raising the blood pH, thereby correcting metabolic acidosis. In the kidneys, the increased bicarbonate load leads to enhanced urinary excretion of bicarbonate, raising the urinary pH. A higher urinary pH increases the ionization and solubility of uric acid and cystine, preventing their crystallization and promoting the dissolution of existing stones.
Pregnancy: Category C: Use only if clearly needed. Animal reproduction studies not conducted. Sodium load may exacerbate pregnancy-induced hypertension or edema. Benefit should outweigh risk.
Driving: No known effects on driving ability.
| Potassium-Sparing Diuretics (Amiloride, Spironolactone) | Increased risk of severe hyperkalemia due to combined effect of reduced potassium excretion and alkalinization. | Major |
| Lithium | Increased urinary pH can decrease renal lithium clearance, leading to increased lithium levels and toxicity. | Major |
| Methenamine (Hexamine) | Urinary alkalinization inactivates methenamine, which requires acidic urine for its antibacterial effect. | Major |
| Quinidine, Flecainide | Alkalinization of urine can decrease renal excretion of these drugs, potentially increasing their plasma levels and toxicity. | Moderate |
| Salicylates (Aspirin) | Alkalinization increases renal excretion of salicylates, reducing their plasma levels. Used therapeutically in overdose. | Moderate |
| Anticholinergics | May enhance GI absorption of citrate due to delayed gastric emptying. | Minor |