New York Urological Associates, PC
R. Ernest Sosa, MD
880 5th Ave.
New York, NY 10021
Tel (212) 570-6800 Fax (212) 861-7964
Prevention of Renal Stones
Approximately 12% of the American population will suffer from a kidney stone at some point in their lives. Kidney stones are more common in men than in women, occurring in men twice as often as in women. Caucasians are more likely to suffer from kidney stones than African-Americans. The prevalence of urinary calculi increases with age, peaking in the 35 to 60 year range. Once you form a urinary stone, there is, on average, a 10% risk per year of forming a second stone. In five years, on average a stone former has a 50-50 chance of having a new stone. There are patients that may be even more prone to form stones due to their life style, their diet, or due to an underlying medical condition that afflicts them. Kidney stones are painful and they are costly.
Prevention of renal stones is possible in most patients. For this, it is important to investigate the potential underlying factors that could cause a stone to form in an individual and correct any anomalies that may be detected. In the United States, a large number of patients form stones due to dietary abundance and a lack of adequate water intake.
For the patient that is found to have a stone in the urinary tract, there are often several options for treatment. Conservative management with hydration and pain medication will often support of patient as they pass their stone spontaneously. Over half of the symptomatic stones that are diagnosed can pass without intervention. For those patients with stones too large to pass on their own, there are a variety of treatment options, many of which are minimally invasive and can be rendered in the outpatient setting.
Prevention of Kidney Stones
Kidney stones can form for a variety of reasons. Whatever the mechanism at play, for a stone to form, urine has to become too concentrated with a certain chemical to keep that substance in solution. In the body, the chemical elements most commonly found in kidney stones arecalcium, oxalate, phosphates, uric acid and cystine.
A stone can form because there is too much of one these elements in the urine. For example, salt (which is made of sodium chloride) dissolves in water as long as there is enough water present. If the water begins to evaporate, salt crystals begin to form that we can see as a powdery solid. In the urinary tract it is calcium containing or uric acid crystals that form. First a few crystals precipitate. If the urine remains concentrated than more crystals are deposited and a small stone begins to take shape. On this small nidus (of calcium or uric acid) additional crystals are deposited and the stone grows larger and larger. One can see that drinking plenty of water could help prevent a stone from forming or from growing.
Calcium Stones
The most common stones that form in the kidney are made of calcium and oxalate. When calcium and oxalate join, they bind very tightly and are difficult if not impossible to dissolve. In the past, advice to patients who suffered form calcium containing kidney stones was to decrease the calcium in their diet. A growing body of evidence, however, suggests that calcium restriction is inappropriate in patients with calcium stones. The reason for this surprising finding has to do with several other factors responsible for stone formation. One of these factors is oxalate. Oxalate in the urine is a very powerful stone former. It is a more powerful stone former than is calcium! Unattached oxalate, (see appendix 1 for foods rich in oxalate), is normally absorbed into the blood stream from the intestines. Calcium and oxalate, once bonded together are not easily absorbed from the gut. By maintaining an adequate amount of calcium in the diet, one may decrease the oxalate absorption from the gastrointestinal tract and thus decrease the urinary excretion of oxalate. Moreover, calcium intake is a very important factor for the prevention of bone loss as we age.
Dietary manipulation is one of the most important tools for preventing new calcium oxalate stone formation. However, adequate fluid intake is the single most important factor in the prevention of urinary stones. How much water should one drink to prevent stones? It is advisable to drink enough fluids to make about two liters of urine a day (a little over 2 quarts). For most people this means emptying a full bladder 7 times a day. On a cold day one would need to drink less water to achieve this volume of urine than on a hot day. The endpoint of fluid intake, therefore, should be determined by the volume of urine made. Colas, coffee, tea, and beer do not help prevent stones. Cranberry juice, which may have a role in preventing urinary infections, does not help prevent stones. Cranberry, like many other berries, metabolizes to form oxalates that are an ingredient for stone formation. It is important to drink water for most of the fluid volume one consumes.
The second most important factor in the prevention of stone formation is to keep the animal protein intake to less than 6 ounces a day. Animal proteins are metabolized into purines, which increase the risk for uric acid stone formation. Animal proteins also make the urine more acid, which makes uric acid more likely to crystallize and also lowers the production of citrate by the kidneys. Citrate is a naturally occurring stone inhibitor that serves to prevent the formation of uric acid and calcium stones. Finally, glycine, an amino acid found in proteins is metabolized to oxalate; methionine, another amino acid, drives more calcium into the urine. Reducing the animal protein content of one’s diet has an impact on decreasing stone recurrence, while helping to prevent bone loss.
Beyond adequate fluid intake, avoidance of high animal protein intake, what else can be done to prevent calcium stone formation?
There are several mechanisms for calcium oxalate stone formation. The role of diet in calcium stone formation has been outlined above. Many patients with calcium stones can prevent further stone formation by drinking plenty of fluids and eating small portions of animal protein. Lowering one’s salt intake is also important in decreasing stone formation. The higher the sodium contents of a diet, the greater the renal excretion of calcium into the urine, even if the calcium intake stays the same.
A number of folks will form calcium oxalate stones because they absorb more calcium from their diet than is normal. These “hyperabsorbers” of calcium are the only ones that need to watch their calcium intake carefully. Another subgroup of patients will leak calcium into their urine. The urinary calcium level is always elevated, regardless how little calcium may be found in their diet. In fact, lowering calcium in the diet of these patients will result in leaching of calcium from their bones, producing osteoporosis. Management of these patients involves the use of medications to diminish the renal calcium leak. Finally, less than 1% of calcium stone formers will suffer from oversecretion of parathyroid hormone. The parathyroid glands produce this hormone, which is important for the regulation of calcium metabolism. An adenoma may form on one of the parathyroid glands resulting in overproduction of parathyroid hormone. The treatment is the identification of the adenoma and its removal.
About 15% percent of calcium oxalate stones form on a uric acid nidus. In these patients, keeping the urinary uric acid level under control is therefore important for stone prevention (see next section).
Uric Acid Stones
Uric acid stones account for approximately 10% of all urinary stones. They affect men four times more often than they affect women. Although patients with gout suffer from uric acid elevation, the majority of patients with uric acid stones do not have gout. The typical patient who presents with a uric acid stone will fit the following scenario:
The afflicted patient will generally be a male, over forty, who works hard all day not stopping to drink water, eats lightly because of lack of time. He arrives home after work feeling ravenous; he consumes a large dinner, drinks very little water and is more inclined to have wine or a cocktail. The total calorie intake of this patient may not be excessive, but he is presenting most of the calories to his body at one time. The fluid intake is abysmal, as this man has been dehydrated all day. He is a prime candidate for uric acid stone formation.
Preventing future stones for this patient will call for a more even distribution of calories during the day, a much greater consumption of fluids. Animal proteins (chicken, beef, pork, and fish) contribute to an increase in uric acid stone formation (see low purine diet for other foods that contribute to uric acid stone formation). Eating large amounts of salt will also increase the risk for uric acid stones.
Other factors, besides diet and gout that may contribute to a high uric acid excretion in the urine include myeloproliferative disorders being treated with chemotherapy, weight loss on a high calorie diet or due to low caloric intake. Acid urine also increases the risk of uric acid stone formation. At a pH of <5.5 uric acid crystallizes in the urine. This may occur with high protein intake, with distal small bowel disease or resection (regional enteritis) where there is loss of base, and with terminal ileostomies.
Unlike the calcium renal stones, uric acid stones can be dissolved by adding base to the urine to raise the urine pH to a range of 6-7. Of course, plenty of water is sure to help a great deal. If a large amount of uric acid is found in the urine, medical treatment to prevent uric acid formation will be necessary to complement hydration, dietary manipulation and alkalinization of the urine. Allopurinol will decrease uric acid formation.
Of note, uric acid stones are not visible on a standard x-ray like calcium stones are. To diagnose uric acid stones an unenhanced helical CT of the abdomen and pelvis will permit visualization of the entire urinary system for uric acid stones. Alternatively, a renal sonogram will allow inspection of the kidney, but leave the ureters unexplored. Once a uric acid stone is diagnosed, if there is no blockage to the urinary tract, medical management can be started to try to dissolve the uric acid stone. For this, potassium citrate is given by mouth to raise the urine pH of to a 6-7 range, which increases the solubility of uric acid. A low purine diet is observed (see appendix B), salt intake is kept low (less than 150 mEq/day) and hydration to make 2 liters of urine a day is maintained.
Cystine Stones
Cystine stones make up less than 5% of all urinary calculi. Cystine stone formation results from the impaired reabsorption of the amino acids cystine, lysine, ornithine and arginine from the renal tubules. Cystine is the only amino acid of this group that is poorly soluble and therefore results in urinary stone formation. Cystinuria, an autosomal recessive disease, results from excessive excretion of the four basic amino acids, cystine, ornithine, lysine, and arginine (COLA) into the urine. Cystine is relatively insoluble in acid urine. Patients with cystinuria (>250mg/24 hr.) produce supersaturated urine and are at risk for crystallization and stone formation. Cystine is not very radiodense and can be difficult to find on a flat plate of the abdomen. Moreover, it is resistant to Shock Wave Lithotripsy and must be fragmented by ultrasonic, laser or electrohydrualic lithotripsy.
Prevention and medical management of cystine stones depends on decreasing the total urinary cystine concentration by fluid hydration; increasing the solubility of cystine by alkalinizing the urine to a pH of 7.5 or higher using potassium citrate and by binding cystine with penicillamine to form a much more soluble cystine - S - penicillamine complex. This latter molecule is 50 times more soluble than cystine in urine. Another agent that can be substituted for penicillamine is Thiola.
Struvite Stones:
Struvite stones, commonly called infectious stones, are composed of magnesium, ammonium and phosphate, mixed with carbonate. Struvite stones form as a result of the effects of certain bacteria on the urine. Species of bacteria, such as Proteus and Klebsiella, produce an enzyme called urease. The urea in the urine is split by urease to cause an increase in the pH of the urine to a value of 7.2 or higher.
Prevention of Struvite stones depends on maintaining sterile urine, and of course, a good state of hydration. Management of Struvite stones already present requires a multimodal therapy. First, the stone must be removed as completely as possible from the kidney. After the stone has been removed from the kidney, medication, called Renacidin is instilled into the kidney to dissolve any residual stone fragments. Medical management with antimicrobial therapy, chemolysis with Renacidin, and urinary acidification helps to prevent stone recurrence.
Patient Evaluation:
A urinary calculus that obstructs the flow of urine will produce a renal or ureteric colic. The pain can be very severe, often starting in the flank with radiation to the groin of the same side. Patients with renal colic find it impossible to be still. No relief from the pain is found in any position. The colic may be associated with blood in the urine. The amount of blood may be small and not visible to the naked eye, its detection requiring use of a microscope to study the urine. The urinalysis can also tell a physician about the urine pH (a measure of the acid-base content of the urine), the presence of bacteria and infection, and can help detect crystals to suggest the composition of the stone.
The most effective test to document the presence of a urinary stone is the Unenhanced Helical CT. This test is rapid, requires no contrast to be injected so it is safe for everyone and it is the most reliable imaging modality for stone disease. Sonography can be helpful but it is less reliable in the kidney than the Unenhanced CT. Moreover, Sonography cannot image a ureteral stone. Intravenous pyelography is another useful test, less reliable than the Unenhanced CT and it requires contrast.
Once the diagnosis of a urinary stone is known, plans for treatment and prevention of further stones are initiated.
Treatment options:
For the patient in acute renal colic, the first order of business is to make the diagnosis, provide medication to control the pain, hydrate the patient and treat the stone if it is not likely to pass spontaneously. Treatment options to render the patient stone free are discussed below.
Dietary
For the patient afflicted with stones, a high water intake, a low salt and animal protein intake (see above) is important to decrease recurrent stones. For patients with uric acid stones, a low Purine diet is recommended (see appendix B); for patients with oxalate stones, a low oxalate diet is appropriate (see appendix A).
Medications
Patients with uric acid stones benefit from alkalinization of the urine. For this, potassium citrate, to maintain the urine pH in the 6-7 ranges, is important. Allopurinol decreases the uric acid production.
Patients with calcium stones with associated high calcium levels in the urine benefit from a low sodium diet and hydrochlorothiazide. This medication lowers the calcium content of the urine, moving it into the blood stream where it can be utilized by the body.
In cystine stones, the use of urinary alkalinization with potassium citrate as well as increasing the solubility of cystine with medications such as penicillamine and Thiola tends to decrease the risk for new stone formation.
Infection stones are treated in part by antibiotics to kill urea-splitting bacteria. Use of medications to inhibit the splitting of urea, such as acetohydraximic acid (Lithostat) is useful but side effects, like the formation of blood clots in the legs are undesirable.
Interventional Treatments to Remove Renal and Ureteral Stones
Shock-wave lithotripsy (SWL) is a non-invasive technique that fragments urinary stones using high-energy waves that are focused on a targeted stone. For most renal stones of less than 2 cm in size, SWL is the preferred treatment. The overall success rate is about 80 % (see figure 5). For stones less than one centimeter in size, found in the ureter the success rate is about 85%, with a retreatment rate of 10-15%. SWL can be performed under monitored anesthesia care in an outpatient setting.
SWL does not work well for:
- Stones > 2 cm stones
- Stones in a calyceal diverticulum
- Stones is a horshoe kidney
- Stones in a patient who is bed-ridden
- Kidneys or ureters with obstruction distal to the stone
- Stones impacted into the wall of the ureter
- Stones composed of calcium oxalate monohydrate and cystine stones.
These problem stones that cannot be broken up by SWL are fragmented and removed by percutaneous nephrolithotomy or sometimes, by ureteroscopy (see below).