Genitourinary Conditions / Kidney Stones

An estimated 600,000 people in the United States develop kidney stones each year and about 100,000 are admitted to hospitals for treatment. Men are four to five times more likely to develop the disease than women. An estimated 10% of men and 5% of women between the ages of 30 to 50 will suffer from kidney stones. Kidney stones are four to five times more common in Caucasians than in African Americans.

Most people who develop kidney stones experience their first episode between the ages of 20 and 30.

Genetics may play a role in uric acid stone propensity. People of Mediterranean ancestries, particularly those of Portuguese extraction, appear to have a high incidence of uric acid stones. Calcium stones are more prevalent among people of Anglo Saxon descent.

Kidney stone disease usually continues throughout life, particularly in men. Up to two-thirds of men who have passed one stone experience a recurrence, with an average of 9 years between episodes.

Risk Factors

Why people do or do not develop kidney stones is unknown. The disease appears to run in families, but it is unclear whether this is associated with inherited physiological factors or the result of shared family dietary preferences that may predispose a person to stone formation.

Researchers suggest that the mineral composition of drinking water is a factor, but they disagree as to whether "hard" (containing excessive calcium sulfate) or "soft" (containing excessive sodium carbonate) water is to blame. Alcohol consumption also may play a role in stone formation, particularly among drinkers who suffer from gout (painful inflammation of the joints resulting from an imbalance in the body's uric acid metabolism).

Residents of the southeastern United States have the highest incidence of kidney stones in the country, so temperature and body dehydration may be key factors. Southern dietary staples of green vegetables, brewed tea, and fatty foods may also be contributing factors.

Certain diets, particularly those with high-protein, salt, milk, and animal fat, may promote stone formation in people susceptible to the disease.

Possible causes of kidney stones include the following:

• Supersaturation

The most prevalent theory is supersaturation crystallization. Dehydration causes an imbalance in the liquids and dissolved solids in the urine. The kidneys must maintain a proper amount of water in the body as they remove harmful waste materials. If dehydration occurs, the urine may become overloaded (supersaturated) with substances that will not dissolve in water. These chemicals and trace elements combine to form crystals that slowly build up and form a stone.

• Inhibitors

Urine normally contains chemicals called inhibitors (e.g., pyrophosphate, citrate, magnesium, zinc, macromolecules) that prevent the formation of crystals. Some people do not have a sufficient quantity of inhibitors to prevent crystallization, or their inhibitors may fail to induce the necessary chemical reactions that prevent the formation of crystals, the first step in the development of a kidney stone.

• Matrix

A chemical component of urine, noncrystalline mucoprotein called matrix, is thought to play a role in stone formation. Matrix seems to act as an inhibitor in people who do not develop stones. However, in patients who suffer from stones, matrix appears to initiate and possibly provide the chemical framework upon which crystals develop.

Hypercalciuria

Hypercalciuria (excessive calcium in the urine and kidneys) is the primary cause of calcium stones. There are three primary types of hypercalciuria.

• Resorptive Hypercalciuria

Resorptive hypercalciuria is the result of a rare metabolic disorder which causes the body to produce too much parathyroid hormone (hyperparathyroidism), causing bone tissue to dissolve. The dissolved tissue creates excessive calcium in the blood that accumulates in the kidneys and produces calcium stones. The condition may result from a tumor on the parathyroid gland, a genetic condition, cancerous tumors attached to bone tissue, myeloma (cancer of the bone marrow), Cushing's disease (a pituitary gland abnormality characterized by obesity and muscular weakness), or long term immobilization.

Treatment of Hypercalciuria

Resorptive hypercalciuria produces recurrent stone formation regardless of dietary restriction. Treatment consists of treating the underlying disorder that produces bone resorption.

• Absorptive Hypercalciuria

Absorptive hypercalciuria is the most common form and is found in more than one-half of patients with stones. It results from an excessive intestinal response to vitamin D, causing the absorption of too much calcium from ingested foods. The diuretic furosemide, antacids, and steroids, can produce absorptive hypercalciuria.

Treatment of Absorptive Hypercalciuria

Diet and Hydration - Patients with absorptive hypercalciuria usually are placed on diets that restrict calcium and sodium. They are encouraged to add cereal bran to their diet because bran binds calcium in the gastrointestinal tract and helps excrete it from the body. Drinking 3-4 liters of water a day reduces the patient's urinary calcium concentration and discourages the formation of urinary crystals.

Cellulose Phosphate- Another treatment for absorptive hypercalciuria is adding cellulose phosphate to the diet. This calcium-binding resin exchanges sodium for calcium in the gastrointestinal tract. Cellulose phosphate lowers magnesium levels in the blood and raises urinary oxalate levels so patients must take oral magnesium supplements and restrict their intake of oxalate-rich foods.

Orthophosphate- Adding orthophosphate to the diet helps patients decrease the urinary excretion of calcium and increase the excretion of citrate and pyrophosphate, which inhibits stone formation. Diarrhea is the most common side effect.

• Renal Hypercalciuria

About 1 in 10 cases of hypercalciuria are the result of an inability by the kidney to resorb calcium resulting in urine that is overloaded with calcium. Restricting the patient's dietary calcium intake does not decrease urinary calcium, and adding calcium to the diet makes the condition worse.

Treatment of Renal Hypercalciuria

Renal hypercalciuria is treated with thiazide diuretics that increase the kidneys' resorption of calcium. Daily doses of hydrochlorothiazide are prescribed and patients undergoing this therapy must supplement dietary potassium and restrict salt consumption. Patients who do not respond to thiazide diuretics alone may also be given orthophosphates with dietary calcium restrictions.

Hyperuricosuria

Patients who form pure uric acid stones typically suffer from hyperuricosuria, a condition characterized by excessively acidic urine. About 25% of these patients have gout, but most simply have highly acidic urine, perhaps exacerbated by dehydration. About 20% of patients with recurrent calcium stones also have hyperuricosuria.

Treatment of Hyperuricosuria

Patients with hyperuricosuria are advised to drink three liters of water a day. A daily dosage of 650 milligrams of bicarbonate of soda is prescribed to neutralize the urine's acidity. Patients on salt-restricted diets may be given potassium bicarbonate. If these measures do not produce the desired result, dietary protein restrictions and allopurinol, which reduces uric acid excretion, may be prescribed.

Hyperoxaluria

Hyperoxaluria is a disorder in which the body produces too much insoluble oxalic acid. Oxalic acid is not metabolized but excreted in the urine. The cause is related to a metabolic irregularity. There are three types of hyperoxaluria:

• Primary Hyperoxaluriais a rare genetic disorder that leads to excess of calcium in the kidneys and soft tissue at a young age.

• Enteric Hyperoxaluriais a condition in which large quantities of fatty acid in the bowel bind with calcium producing excessive oxalate which is absorbed into the blood stream and leads to calcium stones. Patients with bowel disease and inflammation, or those who have undergone small bowel bypass surgery, are likely to suffer from enteric hyperoxaluria.

• Exogenous Hyperoxaluriais a rare disorder caused when the body metabolizes ingested substances to oxalate. Such substances include ethylene glycol (antifreeze), ascorbic acid (a vitamin found in citrus fruits, tomatoes, potatoes, and green, leafy vegetables) and methoxyflurane, an anesthetic.

Treatment of Hyperoxaluria

Treatment of primary hyperoxaluria consists of daily doses of pyridoxine, which has been found to reduce oxalate excretion. Limiting consumption of milk, eggs, ice cream, yogurt, cheese, tea, coffee, chocolate, peanuts, spinach, rhubarb, and beets and increased fluid consumption may also be prescribed.

A low-oxalate, low-fat diet with plenty of hydration and calcium supplementation is the prescribed treatment of enteric hyperoxaluria. Cholestryamine can also be used to bind oxalate in some patients.

Treatment of exogenous hyperoxaluria consists of preventing the patient from consuming the substances or restricting their dietary intake.

Renal Tubular Acidosis (RTA)

RTA accounts for about 1% of calcium kidney stones. There are several forms of RTA, but the type 1 disorder is responsible for stone formation. In this condition, a defect in the kidney's distal tubule renders it unable to maintain adequate hydrogen ion levels causing patients to form calcium phosphate, calcium oxalate, or mixed stones.

Treatment of RTA

Treatment reduces the patient's urinary acidity with sodium bicarbonate or potassium citrate.

Kidney stones develop slowly and often give little warning of their presence until they reach a stage where their size and/or position cause acute symptoms.

Occasionally, a patient undergoing a routine x-ray examination will be found to have a "silent" stone, one that is attached to the kidney, and has not grown large enough to impede kidney function.

A silent stone may continue growing until it begins to block the flow of urine. Patients often endure months, even years, of chronic back pain without associating their discomfort with a kidney problem. By the time the stone is discovered, it may have caused substantial impairment, and permanent damage to the kidney.

Sometimes a small stone will pass without producing any symptoms, or the symptoms are so mild that the patient attributes them to backache, muscle strain, or the onset of a flu-type illness. Such patients are considered asymptomatic and often experience recurrent urinary tract infections before the cause is accurately diagnosed.

Classic symptoms associated with a lodged stone that causes urinary tract irritation and/or obstructs the flow of urine are more common and the symptoms are immediate and severe. This condition is known as acute ureteral colic.

Acute ureteral colic comes on suddenly, often at night or early in the morning. It may feel like an attack of appendicitis, gastroenteritis, or colitis. Pain usually starts in the back, at the waist, or in the flank, stomach or groin. ("Teeth-gritting agony" is the way one expert characterizes it.) The pain can radiate down the leg or into a man's testes or tip of the penis, depending on where the stone has lodged.

Nausea, vomiting, chills, fever, and elevated blood pressure are common, and despite the discomfort, the patient often cannot sit or lie still. There may be an urgent need to urinate frequently, accompanied by a burning sensation during urination.

Hematuria (blood in the urine) is another classic symptom. The blood may be clearly visible, or it may be seen only through microscopic examination. Often, the patient's urine is unusually dark and/or cloudy and has a strong odor.

The physician typically uses diagnostic imaging to confirm that a stone is causing the symptoms. X-ray or ultrasound can help locate the stone and determine its size and shape. Blood and urine analyses identify the presence of infection and establish the stone's chemical composition. These procedures help determine whether passive treatment or surgery is likely to produce the best results.

Urinalysis

Patients whose medical history and/or symptoms suggest the presence of kidney stones, as well as those suffering from acute ureteral colic, are asked to provide a urine specimen for analysis. The specimen is examined microscopically for the presence of urinary crystals or minute amounts of blood (i.e., microhematuria). Either finding provides strong evidence of kidney stones.

Further diagnostic tests are conducted to rule out other medical problems, such as an inflammation of the appendix (appendicitis) or large bowel (diverticulitis).

If kidney stones are diagnosed, the doctor must establish several facts about the stone before deciding on a course of action, such as:

• Location

• Number

• Size

• Type

X-rays and intravenous pyelogram (IVP)

X-ray of the abdomen can provide this information. The doctor may also prescribe an intravenous pyelogram (IVP), which involves injecting a special dye into the bloodstream. The dye collects in the urinary system and improves the contrast for x-rays, giving the doctor a better image of the kidneys, ureters, and bladder.

Because most kidney stones are composed of calcium, they absorb more x-rays than surrounding soft tissue and appear as a white mass on an x-ray. Such stones are described as radiopaque.

Not all radiopaque stones (up to 34%) can be seen on an x-ray; some are too small and others may be obscured by bones or overlying bowel gas.

Some stones, particularly those composed of uric acid, do not absorb enough x-rays to produce a useful image. These stones are described as radiolucent and must be detected by other means.

CT ("CAT") Scan

A CT or CAT scan is a type of x-ray that generates a cross-sectional image. It is useful in detecting stones that are obscured by bones or other radiopaque matter.

Ultrasound

Kidney stones produce an acoustic "shadow" when subjected to ultrasound. In this painless procedure, a gel is applied to the patient's pelvic and kidney areas, and a small device that emits ultrasonic pulses is slowly passed over the area. The sonic image produced is viewed on a monitor.

Ultrasound has its limits. Obese patients often generate poor results, because they have more tissue through which the sound impulses must pass. Very small stones (i.e., those under 3 mm) may produce an acoustic shadow too small to be detected.

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