Kidney Stones--Treatment

Treatments that can benefit all stone formers

Certain conservative treatments are available to help stone formers prevent further episodes of stone disease.

If a patient with a history of kidney stones does nothing else, increasing fluid intake can decrease stone formation rates by 60%. Stone formers should drink enough fluid so as to make 2,500 to 3,000 ml of urine per day. We tell our patients that if the urine is yellow, they are not drinking enough. The urine should be clear. The more dilute the urine, the less concentrated it is with respect to the minerals that can form stones.

Calcium oxalate stone formers should be on a diet limited in oxalate and sodium (salt). Foods that result in a significant increase in urinary oxalate excretion, and therefore should be avoided, are:

spinach

rhubarb

beets

nuts

chocolate

tea

wheat bran

strawberries

Excess salt in the diet will lead to excess sodium being excreted in the urine. As excess sodium is excreted, it drags calcium with it in the urine, thereby raising the concentration of calcium in the urine. We tell our patients to avoid canned foods and not reach for the salt shaker at the table at home, as this cuts down on the amount of salt ingested.

In patients with suggested absorptive hypercalciuria, a limitation of dairy products may help.

In patients with too much uric acid in the urine, animal proteins should be restricted.

With these conservative measures alone, a significant number of patients may be able to decrease their urinary risk factors for stone formation and keep their stone disease in check.

There are many patients who have had multiple attacks of kidney stones over the years or are at an increased risk for developing more kidney stones in the future. For these patients, more in-depth diagnostic testing is indicated. These improved diagnostic tests have identified many different causes of kidney stones. This has made possible the adoption of specific treatment programs. These treatments should:

	reverse the underlying problem causing the stone disease
	prevent new stone formation
	be free of serious side effects

Treatments for specific abnormalities

Absorptive hypercalciuria

There is no treatment capable of correcting the basic abnormality of absorptive hypercalciuria type I, which is too much of the calcium in the intestine being absorbed into the body and excreted in the urine. However, several medications can help restore normal calcium excretion in the urine.

Sodium cellulose phosphate--This medication is taken by mouth, and it works by binding calcium in the gut, thereby leaving less calcium available in the gut for absorption. However, this medication may have a few side effects. It may cause a negative calcium balance, meaning that so much calcium is bound by the medication, not enough calcium is available to the body for normal function. Sodium cellulose phosphate may bind magnesium and cause magnesium depletion. Since calcium is bound by sodium cellulose phosphate, not enough calcium remains to bind with oxalate in the gut, making more oxalate available for absorption by the bowels, leading to an excess of oxalate being excreted in the urine. This could result in further calcium oxalate stone formation. These side effects can be avoided by having the patient take oral magnesium and restricting oxalate intake in the diet while taking sodium cellulose phosphate.

Thiazide--Thiazide is a diuretic medication. It does not treat the primary defect in absorptive hypercalciuria since it does not decrease calcium absorption by the bowels. However, thiazide is used to treat absorptive hypercalciuria type I because it does decrease the amount of calcium excreted in the urine and is more convenient to take than sodium cellulose phosphate. In addition, the medication may lose its ability to decrease calcium excretion in the urine during long-term use. The patient should also be taking potassium citrate medication while on thiazide, to prevent low blood levels of potassium and low urine levels of citrate which may occur with this medication. Urinary citrate is a powerful inhibitor of calcium oxalate stone formation and decreased levels in the urine may counteract the benefits of thiazide medication.

Therefore, these are our recommendations for treating absorptive hypercalciuria type I and type II.

Fluid intake is increased so as to make 2,500 to 3,000 ml per day

In patients with absorptive hypercalciuria type I, thiazide medication is the first choice. The patient must be on a low sodium diet (restrict salt intake), as too much dietary sodium lessens the effect of thiazide in reducing calcium excretion. Potassium citrate medication is given to prevent the loss of potassium and citrate which occurs with thiazide therapy. When thiazide loses its ability to decrease calcium excretion in the urine after long-term use, sodium cellulose phosphate may be temporarily substituted for about six months. Magnesium supplementation is given while the patient is on sodium cellulose phosphate and a low oxalate diet is instituted. Thiazide therapy may be restarted after six months.

In patients with absorptive hypercalciuria type II, no specific drug treatment may be necessary. Since urinary calcium is increased only when the patient is on a high calcium diet, a low calcium intake is started. Many patients have concentrated urine because of limited fluid intake, and therefore, patients are told to increase their fluid intake as discussed above.

Renal hypercalciuria

Thiazide is an effective treatment of renal hypercalciuria. This diuretic medication corrects the renal leak of calcium by increasing the amount of calcium reabsorbed back into the bloodstream from the urine. The urine becomes less saturated with respect to calcium oxalate and calcium phosphate because of the reduced calcium excretion. Potassium citrate medication should be given while the patient is on thiazide medication as discussed above.

Primary hyperparathyroidism

The treatment for primary hyperparathroidism is removal of the enlarged, overactive parathyroid gland. There should follow a decrease in the level of calcium in the blood to within normal limits and urinary calcium excretion should return to normal.

Hyperuricosuric calcium oxalate stones

The abnormality in this case is an excess of uric acid in the urine. Since the cause of excess uric acid in the urine is often purine excess in the diet, dietary modification is the main aspect of treatment. Food high in purine content, such as animal protein, is limited. The medication Allopurinol is very effective in this disorder because Allopurinol reduces the formation of uric acid in the body and therefore lowers the level of uric acid in the urine. The lower amount of uric acid in the urine allows more calcium oxalate to exist in the urine before it comes out of solution and forms stones. This makes it more difficult for calcium oxalate stones to form.

Gouty diathesis

Since the main reason for uric acid or calcium oxalate stone formation in a patient with gout is an acidic urine, the goal in the management of gouty diathesis is to make the urine more alkaline, or less acidic. Potassium citrate is a very useful medication for doing this. If the level of uric acid in the blood or urine is elevated above normal, the medication Allopurinol can be added to the treatment regimen.

Hyperoxaluria

Treatment for hyperoxaluria consists of dietary and medical therapy.

Dietary changes include decreasing the amount of fat consumed and avoiding foods high in oxalate (see the list of high oxalate foods at the beginning of this page). Since some of these patients have problems absorbing fats from their intestines, fats in the diet can be replaced by medium-chain trigycerides. Many of these patients are also dehydrated due to excess fluid loss from the bowels, and antidiarrheal medications and a high fluid intake may be of great benefit.

Medical therapy consists of giving calcium in the form of calcium carbonate medication. The calcium binds the oxalate in the gut, making less oxalate available for absorption into the body and therefore less oxalate is excreted in the urine. Even though urinary levels of calcium may increase with this regimen, the decrease in urinary oxalate levels is greater than the increase in urinary calcium levels, lowering the overall concentration of calcium oxalate in the urine.

Hypocitraturic calcium oxalate stones

Urinary citrate is an inhibitor of calcium stones and acts by lowering the urinary saturation of calcium salts and by preventing calcium salt from forming crystals. Low levels of citrate in the urine can be found in several different conditions.

Distal renal tubular acidosis--In this disease, the patient has difficulty excreting the acid waste products made by the body's natural metabolism. It is also associated with low levels of potassium in the blood. Potassium citrate medication can correct the build-up of acid in the blood and replace the potassium. It can also restore normal levels of citrate in the urine. When the acidosis is corrected, the high levels of calcium in the urine should drop down to normal levels.

Chronic diarrheal conditions--Patients who suffer from long-term, frequent episodes of diarrhea have low levels of citrate in the urine because bicarbonate (the precursor of citrate) is lost from the intestinal tract during the episodes of diarrhea. Potassium citrate medication replaces the lost citrate and can lessen the rate of stone formation.

Hypocitraturia due to thiazide medication--Thiazide medication causes low levels of potassium in the blood. The body tries to replace the potassium by releasing potassium from cells into the bloodstream. Hydrogen molecules then move into the cells to replace the lost potassium, and this excess of hydrogen inside the cells causes a state of acidosis inside the cells. The body uses citrate to counteract the acidosis, and by conserving most of the citrate, leaves little citrate to be excreted in the urine. To correct this problem, potassium should be prescribed whenever a patient is receiving thiazide therapy. Potassium citrate medication will not only replace potassium, but would also enhance citrate excretion.

Idiopathic hypocitraturic calcium oxalate stones--In this stone forming condition, there is no underlying cause for the low levels of citrate in the urine. The low urinary citrate levels can exist alone or with elevated levels of urinary calcium. If only low levels of citrate in the urine are found, then potassium citrate therapy is appropriate. If high levels of urinary calcium are also present, then thiazide medication is administered along with potassium citrate medication.

Cystinuria

The goal of treatment for elevated levels of cystine in the urine is to lower the concentration of cystine in the urine to below its solubility limit. This is accomplished by doing the following:

	Dietary restrictions--Patients are told to refrain from eating foods containing methionine, which is a source of cystine. These methionine-rich foods include meat, poultry, and dairy products.
	Salt retriction
	Hydration--Patients are told to drink more than 4 liters of fluid each day.
	Alkalinization of urine--This means making the urine less acidic. Cystine is better able to dissolve in urine when the urine is less acidic. To accomplish this, the patient will usually need both potassium citrate and sodium bicarbonate (baking soda) and the medication acetazolamide.
	When all these treatments fail, there are two medications which combine with cystine in the urine and make the cystine better able to dissolve in the urine. One medication is D-peicillamine. However, the side effects of this medication may make it difficult to tolerate. Therefore, the medication alpha-mercaptopropionylglycine is often used, as it is better tolerated the D-penicillamine and has less severe side effects.

Struvite (infection) stones

The bacteria which cause the urinary conditions that promote infection stones live inside the stones. Therefore, it is difficult to completely eliminate the urinary tract infection with just antibiotics alone. That is why these stones should be removed surgically. If a patient with infection stones is not a candidate for stone removal surgery due to medical problems, the medication acetohydroxamic acid can be used. However, this medication will not work well if the patient has slow kidney function. In addition, most patients cannot tolerate this medication because of its many side effects.

	Distal renal tubular acidosis--In this disease, the patient has difficulty excreting the acid waste products made by the body's natural metabolism. It is also associated with low levels of potassium in the blood. Potassium citrate medication can correct the build-up of acid in the blood and replace the potassium. It can also restore normal levels of citrate in the urine. When the acidosis is corrected, the high levels of calcium in the urine should drop down to normal levels.
	Chronic diarrheal conditions--Patients who suffer from long-term, frequent episodes of diarrhea have low levels of citrate in the urine because bicarbonate (the precursor of citrate) is lost from the intestinal tract during the episodes of diarrhea. Potassium citrate medication replaces the lost citrate and can lessen the rate of stone formation.
	Hypocitraturia due to thiazide medication--Thiazide medication causes low levels of potassium in the blood. The body tries to replace the potassium by releasing potassium from cells into the bloodstream. Hydrogen molecules then move into the cells to replace the lost potassium, and this excess of hydrogen inside the cells causes a state of acidosis inside the cells. The body uses citrate to counteract the acidosis, and by conserving most of the citrate, leaves little citrate to be excreted in the urine. To correct this problem, potassium should be prescribed whenever a patient is receiving thiazide therapy. Potassium citrate medication will not only replace potassium, but would also enhance citrate excretion.
	Idiopathic hypocitraturic calcium oxalate stones--In this stone forming condition, there is no underlying cause for the low levels of citrate in the urine. The low urinary citrate levels can exist alone or with elevated levels of urinary calcium. If only low levels of citrate in the urine are found, then potassium citrate therapy is appropriate. If high levels of urinary calcium are also present, then thiazide medication is administered along with potassium citrate medication.