Urokit

When potassium citrate is taken by mouth, the body breaks down the absorbed citrate and this produces an alkaline load. That alkaline load raises the pH of the urine, and it also raises urinary citrate, mainly by increasing how fast the kidneys clear citrate. The level of citrate in the blood that can be filtered does not change in any measurable way. So potassium citrate seems to raise urinary citrate mostly by changing how the kidneys handle it, not by putting more citrate through the filter. A larger amount of filtered citrate may still play a part, though. In a few small comparisons, oral citrate raised urinary citrate more than oral bicarbonate did.

Besides raising urinary pH and citrate, potassium citrate increases urinary potassium by roughly the amount of potassium in the medicine. In some patients it causes a short-lived drop in urinary calcium.

These changes make the urine less likely to let stone-forming salts crystallise. Those salts are calcium oxalate, calcium phosphate and uric acid. Citrate in the urine binds to calcium, which lowers the amount of free calcium ion and so reduces how saturated the urine is with calcium oxalate. Citrate also stops calcium oxalate and calcium phosphate (brushite) from forming crystals on their own.

A higher urinary pH also lowers free calcium ion, because more calcium binds to the anions that have dissociated. The same rise in pH turns more uric acid into urate ion, which is more soluble.

Potassium citrate does not change how saturated the urine is with calcium phosphate. The extra citrate binding calcium is cancelled out by the way higher pH causes phosphate to dissociate. Calcium phosphate stones are more stable in alkaline urine.

With normal kidney function, the rise in urinary citrate after a single dose starts within the first hour and lasts for 12 hours. With repeated doses, citrate excretion reaches its highest level by the third day. It also evens out the usual large swings in urinary citrate across the day, so the level stays higher and steadier. When treatment is stopped, urinary citrate starts falling back towards its level before treatment on the first day.

The rise in citrate excretion depends directly on the dose. After long-term use, a dose of 60 mEq a day raises urinary citrate by about 400 mg a day and raises urinary pH by about 0.7 units.

In patients with severe renal tubular acidosis or chronic diarrhoeal syndrome, urinary citrate can be very low (below 100 mg a day). Potassium citrate may then do little to raise it, so a higher dose may be needed to get a satisfactory citrate response. In patients with renal tubular acidosis whose urinary pH is already high, potassium citrate raises the pH only slightly.

Pregnant women: No animal studies on reproduction have been carried out, and it is not known whether potassium citrate can harm the fetus or affect fertility when taken by a pregnant woman. Potassium citrate extended-release tablets should be given to a pregnant woman only when clearly needed.

Nursing mothers: Human milk normally contains about 13 mEq/L of potassium ion. Whether potassium citrate affects this level is not known. Potassium citrate extended-release tablets should be given to a nursing mother only when clearly needed.

Treatment of overdosage: Potassium salts, including Potassium Citrate, rarely cause serious hyperkalemia at the recommended doses in people who have no predisposing conditions for it. Hyperkalemia is usually without symptoms. It may show up only as a raised serum potassium concentration and characteristic electrocardiographic changes: peaking of the T-wave, loss of the P-wave, depression of the S-T segment and prolongation of the QT interval. Late signs include muscle paralysis and cardiovascular collapse from cardiac arrest.

Treatment of hyperkalemia includes the following measures. Patients should be watched closely for arrhythmias and electrolyte changes. Any medicines containing potassium should be stopped, along with agents that have potassium-sparing properties, such as potassium-sparing diuretics, ARBs, ACE inhibitors, NSAIDs, certain nutritional supplements and many others. Foods high in potassium should also be removed from the diet, for example almonds, apricots, bananas, beans (lima, pinto, white), cantaloupe, canned carrot juice, figs, grapefruit juice, halibut, milk, oat bran, potato (with skin), salmon, spinach, tuna and many others.

Intravenous calcium gluconate is given if the patient is at no risk or low risk of developing digitalis toxicity. Another measure is intravenous 10% dextrose solution at 300-500 mL/hr, containing 10-20 units of crystalline insulin per 1,000 mL. If acidosis is present, it is corrected with intravenous sodium bicarbonate. Hemodialysis or peritoneal dialysis can be used. Exchange resins may be used too, but this measure alone is not enough for the acute treatment of hyperkalemia. In patients taking digitalis, lowering potassium levels too quickly can produce digitalis toxicity.

Store Potassium Citrate below 30°C, and keep it away from light and moisture. Keep it out of the reach of children.