Sodium citrate; citric acid oral solution is a urinary, gastric, and systemic alkalinizing agent. Sodium citrates are used for urinary alkalinization to prevent renal stone formation or to treat chronic metabolic acidosis associated with chronic renal insufficiency or renal tubular acidosis. Sodium citrate salts may be an alternative urinary alkalinizing agent when potassium citrate is contraindicated. Potassium citrate is generally preferred to sodium citrate for the prevention of renal stones, especially in patients requiring potassium supplementation or those with sodium restrictions. Once absorbed, citrate salts are metabolized to bicarbonates. Citrate salts have also been used to neutralize or buffer gastric hydrochloric acid prior to general anesthesia, however, they have generally been replaced by H2-blockers. Some guidelines recommend the use of sodium citrate before an emergent Cesarean delivery if general anesthesia is planned, as aspiration of gastric contents may occur in these patients and the emergent nature of such procedures cannot be delayed to avoid these risks. Other commonly used names for sodium citrate; citric acid solutions include Albright's solution and modified Shohl's solution.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
Route-Specific Administration
Oral Administration
-Administer each dose immediately after a meal or within 30 minutes after a meal or bedtime snack to minimize side effects (e.g., GI pain or saline laxative effect).
-When administering to treat or prevent renal stones, it is important for the patient to maintain a high fluid intake (at least 2 to 3 L/day) to prevent supersaturation of urine and to assure a minimum urine volume of at least 2.5 L/day.
-Have the patient avoid high-sodium foods (e.g., tomato juice) during treatment.
Oral Liquid Formulations
-Sodium citrate; citric acid oral solution should be diluted with water or juice prior to oral administration. May follow with additional water after swallowing mixture, if desired.
-Sodium citrate; citric acid solutions contain the equivalent of 1 mEq/mL sodium ion and 1 mEq/mL bicarbonate ion.
-The oral solution may be chilled before swallowing to enhance palatability. Do not freeze.
Sodium citrate; citric acid is generally well-tolerated, with few unpleasant side effects, when given in recommended doses to patients with normal renal function and urinary output. Due to a laxative effect, diarrhea may occur. Excessive doses or overdosage with sodium citrate salts may cause abdominal pain, diarrhea, metabolic alkalosis, nausea/vomiting, and seizures. If sodium intake is excessive while taking sodium citrate, especially in patients at risk, it is possible to develop hypernatremia, hypertension, heart failure, pulmonary edema or peripheral edema. Serious metabolic alkalosis rarely occurs during treatment with sodium citrate; citric acid. Metabolic alkalosis is more likely to occur in patients receiving excessive doses or in patients with impaired renal function. If untreated, metabolic alkalosis could result in compensatory hypoventilation, which can aggravate hypoxemia in patients with chronic obstructive lung disease. Clinical manifestations of metabolic alkalosis may include neuromuscular irritability such as hyperreflexia, tremor or muscle twitching, tetany, or seizures. Severe metabolic alkalosis (e.g., blood pH more than 7.6) can result in cardiac arrhythmias, especially in patients with cardiac disease.
Sodium citrate; citric acid is contraindicated in patients with a known hypersensitivity to citric acid or citrate salts.
Serious metabolic alkalosis rarely occurs during treatment with sodium citrate; citric acid. Metabolic alkalosis is more likely to occur in patients receiving excessive doses or in patients with impaired renal function. As with other alkalinizing agents, use potassium citrate with caution in patients which lack normal renal mechanisms to avoid the development of metabolic alkalosis, especially in the presence of hypocalcemia. Sodium citrate; citric acid is contraindicated in patients who on sodium-restricted diets. Sodium citrate; citric acid is also contraindicated for patients with renal failure or severe renal impairment with oliguria, azotemia, or anuria. Citrate salts may increase the risk of aluminum toxicity in patients at risk such as those taking aluminum antacids, especially in patients with renal impairment. Potassium citrate salts may serve as an alterative therapy in patients with sodium restrictions. Due to the sodium content, sodium citrate products should be used with caution in patients with cardiac disease, heart failure, hypernatremia, hypertension, renal impairment, renal disease, peripheral edema, or pulmonary edema. If untreated, metabolic alkalosis could result in compensatory hypoventilation, which can aggravate hypoxemia in patients with chronic obstructive pulmonary disease (COPD).
Conversion of sodium citrate; citric acid to bicarbonate may be impaired in patients with severe hepatic disease or hepatic failure. Due to the sodium content, sodium citrate products should be used with caution in patients with cirrhosis and associated ascites.
Sodium citrate; citric acid may generally be used cautiously during pregnancy when the potential maternal benefit justifies the potential for risk to the fetus. Closely monitor acid-base status and electrolytes. Due to the sodium content, the products should be used with caution in patients with toxemia of pregnancy (preeclampsia and eclampsia).
It is not known whether sodium citrate; citric acid is distributed into breast milk. No specific breast-feeding precautions are provided. Sodium citrate is absorbed and metabolized to sodium bicarbonate. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.
For urinary alkalinization:
Oral dosage (oral solution containing sodium citrate dihydrate 500 mg and citric acid monohydrate 334 mg per 5 mL):
NOTE: 1 mL provides 1 mEq of sodium and 1 mEq of bicarbonate.
Adults: 10 to 30 mEq PO 4 times daily.
Children and Adolescents: 5 to 15 mEq PO 4 times daily.
Oral dosage (solution containing hydrous sodium citrate 490 mg and citric acid 640 mg per 5 mL):
NOTE: 1 mL provides 1 mEq of sodium and 1 mEq of bicarbonate.
Adults: 10 to 30 mEq PO 4 times daily. Titrate dose to desired effects.
For the treatment of metabolic acidosis, including renal tubular acidosis (RTA):
Oral dosage (oral solution containing sodium citrate dihydrate 500 mg and citric acid monohydrate 334 mg per 5 mL):
NOTE: 1 mL provides 1 mEq of sodium and 1 mEq of bicarbonate.
Adults: 10 to 30 mEq PO 4 times daily.
Children and Adolescents: 5 to 15 mEq PO 4 times daily.
Oral dosage (solution containing hydrous sodium citrate 490 mg and citric acid 640 mg per 5 mL):
NOTE: 1 mL provides 1 mEq of sodium and 1 mEq of bicarbonate.
Adults: 10 to 30 mEq PO 4 times daily. Titrate dose to desired effects.
For the treatment of pyrosis (heartburn):
Oral dosage (oral solution containing sodium citrate dihydrate 500 mg and citric acid monohydrate 334 mg per 5 mL):
NOTE: 1 mL provides 1 mEq of sodium and 1 mEq of bicarbonate.
Adults: 15 mEq PO as a single dose.
Children and Adolescents: 15 mEq PO as a single dose.
For acid aspiration prophylaxis* before an emergent Cesarean delivery if general anesthesia is planned:
Oral dosage:
Pregnant persons presenting for emergent C-section: 30 mEq PO as a single dose. Citrate salts have been used to neutralize or buffer gastric acid prior to general anesthesia; however, they have generally been replaced by H2-blockers for most patients. Some guidelines recommend the use of these products before an emergent Cesarean delivery if general anesthesia is planned, as aspiration of gastric contents may occur in these patients and the emergent nature of such procedures cannot be delayed to avoid these risks.
Maximum Dosage Limits:
-Adults
120 mEq/day PO.
-Geriatric
120 mEq/day PO.
-Adolescents
60 mEq/day PO.
-Children
60 mEq/day PO.
-Infants
Safety and efficacy have not been established.
-Neonates
Safety and efficacy have not been established.
Patients with Hepatic Impairment Dosing
No specific dosage guidelines are available; however, caution is advised for patients with severe hepatic impairment. Conversion of citrate salts to bicarbonate may be impaired in patients with hepatic failure. Due to the sodium content, sodium citrate products should be used with caution in patients with cirrhosis and associated ascites.
Patients with Renal Impairment Dosing
CrCl >= 10 mL/min: No specific guidelines for dosage adjustment are available. Contraindicated for patients with severe renal impairment with oliguria, azotemia, or anuria.
CrCl < 10 mL/min: Contraindicated for patients with severe renal impairment with oliguria, azotemia, or anuria.
*non-FDA-approved indication
Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Acetaminophen; Aspirin, ASA; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Acetaminophen; Aspirin: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Acetaminophen; Aspirin; Diphenhydramine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Acetaminophen; Chlorpheniramine; Dextromethorphan; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acetaminophen; Dextromethorphan; Guaifenesin; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acetaminophen; Dextromethorphan; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acetaminophen; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Acrivastine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Aluminum Hydroxide: (Contraindicated) Avoid coadministration of antacids with citrate salts since increased absorption of aluminum can occur. In addition, some antacids like calcium carbonate, share the potential with the citrate salts for development of metabolic alkalosis, when given in higher dosage.
Aluminum Hydroxide; Magnesium Carbonate: (Contraindicated) Avoid coadministration of antacids with citrate salts since increased absorption of aluminum can occur. In addition, some antacids like calcium carbonate, share the potential with the citrate salts for development of metabolic alkalosis, when given in higher dosage.
Aluminum Hydroxide; Magnesium Hydroxide: (Contraindicated) Avoid coadministration of antacids with citrate salts since increased absorption of aluminum can occur. In addition, some antacids like calcium carbonate, share the potential with the citrate salts for development of metabolic alkalosis, when given in higher dosage.
Aluminum Hydroxide; Magnesium Hydroxide; Simethicone: (Contraindicated) Avoid coadministration of antacids with citrate salts since increased absorption of aluminum can occur. In addition, some antacids like calcium carbonate, share the potential with the citrate salts for development of metabolic alkalosis, when given in higher dosage.
Aluminum Hydroxide; Magnesium Trisilicate: (Contraindicated) Avoid coadministration of antacids with citrate salts since increased absorption of aluminum can occur. In addition, some antacids like calcium carbonate, share the potential with the citrate salts for development of metabolic alkalosis, when given in higher dosage.
Amphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Amphetamine; Dextroamphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Amphetamines: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Antacids: (Contraindicated) Avoid coadministration of antacids with citrate salts since increased absorption of aluminum can occur. In addition, some antacids like calcium carbonate, share the potential with the citrate salts for development of metabolic alkalosis, when given in higher dosage.
Aspirin, ASA: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Butalbital; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Caffeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Caffeine; Orphenadrine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Carisoprodol; Codeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Citric Acid; Sodium Bicarbonate: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Dipyridamole: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Omeprazole: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Aspirin, ASA; Oxycodone: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Benzoic Acid; Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form.
Benzphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Bismuth Subsalicylate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Bismuth Subsalicylate; Metronidazole; Tetracycline: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Brompheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Brompheniramine; Pseudoephedrine; Dextromethorphan: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Butalbital; Aspirin; Caffeine; Codeine: (Moderate) Concurrent administration of high doses of alkalinizing agents may increase urine pH and decrease serum salicylate levels by decreasing renal tubular reabsorption of salicylic acid.
Cetirizine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlophedianol; Dexchlorpheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlorpheniramine; Dextromethorphan; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlorpheniramine; Ibuprofen; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlorpheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Chlorpropamide: (Moderate) Urinary alkalinizing agents may increase the excretion of chlorpropamide by increasing renal clearance. Monitor for decreased efficacy of chlorpropamide (i.e., increased blood glucose) during coadministration.
Choline Salicylate; Magnesium Salicylate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Codeine; Guaifenesin; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Desloratadine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dexbrompheniramine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dexchlorpheniramine; Dextromethorphan; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dextroamphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Dextromethorphan; Guaifenesin; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Dextromethorphan; Quinidine: (Major) Urinary alkalinization increases the renal tubular reabsorption of quinidine, resulting in higher quinidine serum concentrations which may lead to toxicity. Avoid citric acid; potassium citrate; sodium citrate administration to any patient receiving treatment with quinidine.
Donepezil; Memantine: (Moderate) Urinary alkalinizing agents may decrease the elimination of memantine, resulting in drug accumulation and potential toxicity. The clearance of memantine is reduced by about 80% under alkaline urine conditions at pH 8. Memantine should be used with caution with drugs known to increase urinary pH.
Ephedrine: (Minor) The renal clearance of certain drugs can be affected by the administration of sodium citrate due to urinary alkalinization. Drug-induced urinary alkalization can increase the half-life of ephedrine by increasing tubular reabsorption.
Ephedrine; Guaifenesin: (Minor) The renal clearance of certain drugs can be affected by the administration of sodium citrate due to urinary alkalinization. Drug-induced urinary alkalization can increase the half-life of ephedrine by increasing tubular reabsorption.
Fexofenadine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Flecainide: (Moderate) Urinary alkalinization can decrease the renal clearance of flecainide, resulting in an increased elimination half-life and AUC for flecainide.
Guaifenesin; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Hydrocodone; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Hyoscyamine; Methenamine; Methylene Blue; Phenyl Salicylate; Sodium Biphosphate: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form.
Ibuprofen; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Lisdexamfetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Lithium: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with lithium, especially patients who are stabilized on lithium, as urinary alkalinization increases the renal clearance of lithium. If coadministration can not be avoided, monitor lithium serum concentrations and patient clinical response very closely. Also of note, lithium clearance is increased if hypernatremia occurs.
Loratadine; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Magnesium Hydroxide: (Contraindicated) Avoid coadministration of antacids with citrate salts since increased absorption of aluminum can occur. In addition, some antacids like calcium carbonate, share the potential with the citrate salts for development of metabolic alkalosis, when given in higher dosage.
Magnesium Salicylate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Memantine: (Moderate) Urinary alkalinizing agents may decrease the elimination of memantine, resulting in drug accumulation and potential toxicity. The clearance of memantine is reduced by about 80% under alkaline urine conditions at pH 8. Memantine should be used with caution with drugs known to increase urinary pH.
Methamphetamine: (Moderate) Monitor for an increase in the incidence and severity of amphetamine-related adverse effects during concomitant use of urinary alkalinizing agents. Increasing urine pH may increase amphetamine exposure by reducing urinary excretion of amphetamine. A urine pH more than 7.5 has been observed to increase the half-life of amphetamine from 8 to 10.5 hours to 16 to 31 hours when compared to a pH less than 6. Additionally, a urine pH more than 8 has been observed to reduce the amount of amphetamine excreted in the urine over 16 hours to less than 3% of the original dose; a 5-fold reduction compared to controls.
Methenamine: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form.
Methenamine; Sodium Acid Phosphate; Methylene Blue; Hyoscyamine: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form.
Methenamine; Sodium Salicylate: (Major) Avoid the administration of Alkalinizing agents to patients who are being treated with methenamine, as an acidic urine is required for methenamine therapeutic efficacy. Alkalinized urine decreases methenamine efficacy by increasing the amount of non-ionized drug available for renal tubular reabsorption and inhibits the conversion of methenamine to formaldehyde, which is the active bacteriostatic form.
Naproxen; Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Pseudoephedrine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Pseudoephedrine; Triprolidine: (Minor) Pseudoephedrine renal elimination is susceptible to changes in urinary pH. Urinary alkalinizers allow for increased tubular reabsorption of pseudoephedrine. Concomitant administration of pseudoephedrine with urinary alkalinizers may increase the likelihood of pseudoephedrine adverse reactions.
Quinidine: (Major) Urinary alkalinization increases the renal tubular reabsorption of quinidine, resulting in higher quinidine serum concentrations which may lead to toxicity. Avoid citric acid; potassium citrate; sodium citrate administration to any patient receiving treatment with quinidine.
Quinine: (Moderate) Use caution if using citric acid and quinine concomitantly. Urinary alkalinizing agents may increase plasma quinine concentrations because quinine is reabsorbed when the urine is alkaline.
Salsalate: (Moderate) Urinary alkalinizing agents may increase the excretion of salicylates by increasing renal clearance.
Following absorption, sodium citrate generates sodium bicarbonate, which raises the blood and urine pH. Citric acid is a temporary neutralizing buffer. Sodium citrate; citric acid is used as a urinary alkalinizer to prevent nephrolithiasis for certain renal stones (e.g., uric acid or cystine calculi). Urine alkalinization raises the solubility of cystine in the urine and also ionizes uric acid to a more soluble urate ion. Sodium citrate; citric acid is also used to treat metabolic acidosis associated with chronic renal insufficiency or renal tubular acidosis.
In treating metabolic acidosis, the resulting bicarbonates buffer excess hydrogen ion concentrations and raise blood pH. As a urinary alkalinizer, the generated bicarbonates increase urinary pH by promoting the urinary excretion of free bicarbonate ions. In 5 patients with uric acid lithiasis, sodium citrate and potassium citrate were equally effective in preventing uric acid stone formation due to their alkalinizing effect. However, in contrast to potassium citrate which decreases urinary calcium, sodium citrate does not significantly decrease urinary calcium. Therefore, sodium citrate may be less effective in preventing the complication of calcium nephrolithiasis in patients with uric acid stones.
Sodium citrate; citric acid solution is administered orally. The drug is systemically absorbed and subsequently oxidized to sodium bicarbonate. Citric acid is a temporary buffer. The majority of plasma citrate is oxidized by the Krebs cycle; about 10% to 35% of filtered plasma citrate is excreted renally.