Indication
Renal Tubular Acidosis (RTA) With Calcium Stones: Potassium?ÿcitrate is indicated for the management of renal tubular?ÿacidosisHypocitraturic Calcium Oxalate Nephrolithiasis Of Any Etiology: Potassium citrate is indicated for the management of Hypocitraturic calcium oxalate?ÿnephrolithiasisUric Acid Lithiasis With Or Without Calcium Stones: Potassium citrate is indicated for the management of?ÿUric acid?ÿlithiasis with or without calcium stones
Pharmacology
When Potassium Citrate is given orally, the?ÿmetabolism?ÿof absorbed citrate produces an alkaline load. The induced alkaline load in turn increases urinary pH and raises urinary citrate by augmenting citrate clearance without measurably altering ultrafilterable serum citrate. Thus, Potassium Citrate therapy appears to increase urinary citrate principally by modifying the renal handling of citrate, rather than by increasing the filtered load of citrate. The increased filtered load of citrate may play some role, however, as in small comparisons of oral citrate and oral?ÿbicarbonate, citrate had a greater effect on urinary citrate.In addition to raising urinary pH and citrate, Potassium Citrate increases urinary?ÿpotassium?ÿby approximately the amount contained in the medication. In some patients, Potassium Citrate causes a transient reduction in urinary calcium.The changes induced by Potassium Citrate produce urine that is less conducive to the crystallization of stoneforming salts (calcium oxalate, calcium phosphate and?ÿuric acid). Increased citrate in the urine, by complexing with calcium, decreases calcium ion activity and thus the saturation of calcium oxalate. Citrate also inhibits the spontaneous nucleation of calcium oxalate and calcium phosphate (brushite).The increase in urinary pH also decreases calcium ion activity by increasing calcium complexation to dissociated anions. The rise in urinary pH also increases the ionization of uric acid to the more soluble?ÿurate?ÿion.Potassium Citrate therapy does not alter the urinary saturation of calcium phosphate, since the effect of increased citrate complexation of calcium is opposed by the rise in pH-dependent?ÿdissociation?ÿof phosphate. Calcium phosphate stones are more stable in alkaline urine.In the setting of normal renal function, the rise in urinary citrate following a single dose begins by the first hour and lasts for 12 hours. With multiple doses the rise in citrate excretion reaches its peak by the third day and averts the normally wide?ÿcircadian?ÿfluctuation in urinary citrate, thus maintaining urinary citrate at a higher, more constant level throughout the day. When the treatment is withdrawn, urinary citrate begins to decline toward the pre-treatment level on the first day.The rise in citrate excretion is directly dependent on the Potassium Citrate dosage. Following long-term treatment, Potassium Citrate at a dosage of 60 mEq/day raises urinary citrate by approximately 400 mg/day and increases urinary pH by approximately 0.7 units.In patients with severe renal tubular?ÿacidosis?ÿor chronic diarrheal syndrome where urinary citrate may be very low (<100 mg/day), Potassium Citrate may be relatively ineffective in raising urinary citrate. A higher dose of Potassium Citrate may therefore be required to produce a satisfactory citraturic response. In patients with renal tubular acidosis in whom urinary pH may be high, Potassium Citrate produces a relatively small rise in urinary pH.
Dosage
Dosing Instructions: Treatment with extended release potassium citrate should be added to a regimen that limits salt intake (avoidance of foods with high salt content and of added salt at the table) and encourages high fluid intake (urine volume should be at least two liters per day). The?ÿobjective?ÿof treatment with Potassium Citrate is to provide Potassium Citrate in sufficient dosage to restore normal urinary citrate (greater than 320 mg/day and as close to the normal mean of 640 mg/day as possible), and to increase urinary pH to a level of 6.0 or 7.0.Monitor serum electrolytes (sodium, potassium, chloride and?ÿcarbon dioxide), serum creatinine and complete blood counts every four months and more frequently in patients with cardiac disease, renal disease or acidosis. Perform electrocardiograms periodically. Treatment should be discontinued if there is?ÿhyperkalemia, a significant rise in serum creatinine or a significant fall in blood hemocrit or?ÿhemoglobin.Severe Hypocitraturia: In patients with severe hypocitraturia (urinary citrate <150 mg/day), therapy should be initiated at a dosage of 60 mEq/day (30 mEq two times/day or 20 mEq three times/day with meals or within 30 minutes after meals or bedtime snack). Twenty-four hour urinary citrate and/or urinary pH measurements should be used to determine the adequacy of the initial dosage and to evaluate the effectiveness of any dosage change. In addition, urinary citrate and/or pH should be measured every four months. Doses of Potassium Citrate greater than 100 mEq/day have not been studied and should be avoided.Mild To Moderate Hypocitraturia: In patients with mild to moderate hypocitraturia (urinary citrate > 150 mg/day) therapy should be initiated at 30 mEq/day (15 mEq two times/day or 10 mEq three times/day within 30 minutes after meals or bedtime snack). Twenty-four hour urinary citrate and/or urinary pH measurements should be used to determine the adequacy of the initial dosage and to evaluate the effectiveness of any dosage change. Doses of Potassium Citrate greater than 100 mEq/day have not been studied and should be avoided.
Interaction
Contradiction
Potassium Citrate is contraindicated:
In patients with hyperkalemia (or who have conditions pre-disposing them to hyperkalemia), as a further rise in serum potassium concentration may produce cardiac arrest. Such conditions include:?ÿchronic renal failure, uncontrolled?ÿdiabetes mellitus, acute dehydration, strenuous physical exercise in unconditioned individuals, adrenal insufficiency, extensive tissue breakdown or the administration of a potassium-sparing agent (such as?ÿtriamterene, spironolactone or amiloride).
In patients in whom there is cause for arrest or delay in tablet passage through the?ÿgastrointestinal?ÿtract, such as those suffering from delayed?ÿgastric?ÿemptying, esophageal compression, intestinal obstruction or?ÿstricture, or those taking?ÿanticholinergic?ÿmedication.
In patients with?ÿpeptic ulcer?ÿdisease because of its ulcerogenic potential.
In patients with active?ÿurinary tract infection?ÿ(with either?ÿurea-splitting or other organisms, in association with either calcium or struvite stones). The ability of Potassium Citrate to increase urinary citrate may be?ÿattenuated?ÿby bacterial enzymatic degradation of citrate. Moreover, the rise in urinary pH resulting from Potassium Citrate therapy might promote further bacterial growth.
In patients with renal insufficiency (glomerular?ÿfiltration rate of less than 0.7 ml/kg/min), because of the danger of soft tissue?ÿcalcification?ÿand increased risk for the development of hyperkalemia.
Side Effect
Nausea, vomiting, diarrhea, and stomach pain may occur. Taking it after meals will help prevent these side effects. An empty tablet shell may appear in your stool. This is harmless because your body has already absorbed the medication.This drug may cause serious stomach or intestinal problems (e.g., bleeding, blockage, puncture). This medication may cause high potassium levels in the blood (hyperkalemia). A very serious allergic reaction to this drug is rare.
Pregnancy
Pregnancy Category C. Animal reproduction studies have not been conducted. It is also not known whether Potassium Citrate can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Potassium Citrate should be given to a pregnant woman only if clearly needed.Nursing Mothers: The normal potassium ion content of human milk is about 13 mEq/L. It is not known if Potassium Citrate has an effect on this content. Potassium Citrate should be given to a woman who is?ÿbreast feeding?ÿonly if clearly needed.
Precaution
This medication should not be used ifpatient have (Addison's disease), current bladder infection, uncontrolled diabetes, severe heart disease (e.g., recent heart attack, heart damage), certain stomach/intestinal problems (diabetic gastroparesis, conditions decreasing gut movement, peptic ulcer, blockage), severe kidney disease (e.g., inability to make urine), potassium-restricted diet, high potassium levels, severe loss of body water (dehydration).Before using this medication, tell your doctor or pharmacist your medical history, especially of: low calcium levels, severe diarrhea, heart problems (e.g., irregular heartbeat, heart failure), kidney disease, stomach/gut problems (e.g., irritable bowel), severe tissue damage (e.g., severe burns). Before having surgery, tell your doctor or dentist that you are taking this medication.
Overdose
Treatment Of Overdosage: The administration of?ÿpotassium?ÿsalts to persons without predisposing conditions for?ÿhyperkalemia?ÿrarely causes serious hyperkalemia at recommended dosages. It is important to recognize that hyperkalemia is usually asymptomatic and may be manifested only by an increased serum potassium concentration and characteristic electrocardiographic changes (peaking of T-wave, loss of P-wave, depression of S-T segment and prolongation of the QT interval). Late manifestations include muscle?ÿparalysis?ÿand?ÿcardiovascular?ÿcollapse from cardiac arrest.Treatment measures for hyperkalemia include the following:
Patients should be closely monitored for arrhythmias and?ÿelectrolyte?ÿchanges.
Elimination of medications containing potassium and of agents with potassium-sparing properties such as potassium-sparing?ÿdiuretics, ARBs,?ÿACE inhibitors,?ÿNSAIDs, certain nutritional supplements and many others.
Elimination of foods containing high levels of potassium such as almonds, apricots, bananas, beans (lima, pinto, white), cantaloupe, carrot juice (canned), figs,?ÿgrapefruit?ÿjuice, halibut, milk, oat bran, potato (with skin), salmon, spinach,?ÿtuna?ÿand many others.
Intravenous calcium gluconate if the patient is at no risk or low risk of developing digitalis toxicity.
Intravenous administration of 300-500 mL/hr of 10% dextrose solution containing 10-20 units of crystalline?ÿinsulin?ÿper 1,000 mL.
Correction of?ÿacidosis, if present, with intravenous sodium?ÿbicarbonate.
Hemodialysis?ÿor?ÿperitoneal dialysis.
Exchange resins may be used. However, this measure alone is not sufficient for the acute treatment of hyperkalemia.
Lowering potassium levels too rapidly in patients taking digitalis can produce digitalis toxicity.
Storage