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Pharmacology: Pharmacodynamics: Metabolism of absorbed Potassium Citrate produces an alkaline load, raising urinary pH and increasing urinary citrate by augmenting citrate clearance. Thus, Potassium Citrate therapy appears to increase urinary citrate mainly by changing the renal handling of citrate. Increased urinary citrate and pH, decreases calcium ion activity by increasing calcium complexion to dissociated anions. Thus, decreasing the saturation of calcium oxalate.
Potassium Citrate also inhibits the crystallization and spontaneous nucleation of calcium oxalate and calcium phosphate in hypocitraturic calcium oxalate nephrolithiasis. However, Potassium Citrate does not alter the urinary saturation of calcium phosphate, because the effect of increased citrate complexion of calcium is antagonized by the rise in pH-dependent dissociation of phosphate. Calcium phosphate stones are more stable in alkaline urine.
Mechanism of Action: Potassium Citrate, which works by restoring naturally occurring chemicals in the urine that stop crystals from forming and also inhibits the formation of 2 most common types of kidney stones, calcium oxalate and uric acid stones. In numerous studies, patients treated with Potassium Citrate have demonstrated significantly lower rates of kidney stone formation. In many patients, new stones do not form at all.
Pharmacokinetics: Potassium Citrate is administered orally. Potassium first enters the extracellular fluid and is then actively transported into cells. Skeletal muscle accounts for the bulk of the intracellular store of potassium. Renal excretion of potassium normally is equal to the amount being absorbed in the diet. Potassium is freely filtered at the glomerulus and also completely reabsorbed in the proximal tubule. Tubular secretion occurs, in the late distal convoluted tubule and collecting duct, and accounts for the potassium excreted in the urine, which is about 10% of the amount filtered. Fecal elimination of potassium is minimal and plays no significant role in potassium homeostasis.
When Potassium Citrate is used to alkalinize the urine, urinary citrate and urinary pH values are important. In the setting of normal renal function, the risk in urinary citrate following a single dose of extended-release Potassium Citrate 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 circadian fluctuation in urinary citrate, thus maintaining urinary citrate at a higher, more constant level throughout the day. The rise in citrate excretion is directly dependent on the Potassium Citrate dosage.
When the treatment is withdrawn, urinary citrate begins to decline toward the pre-treatment level on the first day.
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 acidosis or chronic diarrhea 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 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.
In addition to raising urinary pH and citrate, Potassium Citrate increases urinary potassium by approximately the amount contained in the medication. In some patients, Potassium Citrate causes a transient reduction of urinary calcium.
