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Overview

Kidney stones (calculi) are hardened mineral deposits that form in the kidney. They originate as microscopic particles and develop into stones over time. The medical term for this condition is nephrolithiasis, or renal stone disease.

The kidneys filter waste products from the blood and add them to the urine that the kidneys produce. When waste materials in the urine do not dissolve completely, crystals and kidney stones are likely to form.

Small stones can cause some discomfort as they pass out of the body. Regardless of size, stones may pass out of the kidney, become lodged in the ureter (tube that carries urine from the kidney to the bladder), and cause severe pain that begins in the lower back and radiates to the side or groin. A lodged stone can block the flow of urine, causing pressure to build in the kidneys.

Stone Formation

Kidney stones form when there is a high level of calcium (hypercalciuria), oxalate (hyperoxaluria), or uric acid (hyperuricosuria) in the urine; a lack of citrate in the urine; or insufficient water in the kidneys to dissolve waste products. The kidneys must maintain an adequate amount of water in the body to remove waste products. If dehydration occurs, high levels of substances that do not dissolve (e.g., calcium, oxalate, uric acid) may form crystals that slowly build up into kidney stones.

Urine normally contains chemicals— citrate, magnesium, pyrophosphate— that prevent the formation of crystals. Low levels of these inhibitors can contribute to the formation of kidney stones. Of these, citrate is thought to be the most important.

Types

The chemical composition of stones depends on the chemical imbalance in the urine. The four most common types of stones are comprised of calcium, uric acid, struvite, and cystine.

Calcium Stones Approximately 85% of stones are composed predominantly of calcium compounds. The most common cause of calcium stone production is excess calcium in the urine (hypercalciuria). Excess calcium is normally removed from the blood by the kidneys and excreted in the urine. In hypercalciuria, excess calcium builds up in the kidneys and urine, where it combines with other waste products to form stones. Low levels of citrate, high levels of oxalate and uric acid, and inadequate urinary volume may also cause calcium stone formation.

Calcium stones are composed of calcium that is chemically bound to oxalate (calcium oxalate) or phosphate (calcium phosphate). Of these, calcium oxalate is more common. Calcium phosphate stones typically occur in patients with metabolic or hormonal disorders such as hyperparathyroidism and renal tubular acidosis.

Increased intestinal absorption of calcium (absorptive hypercalciuria), excessive hormone levels (hyperparathyroidism), and renal calcium leak (kidney defect that causes excessive calcium to enter the urine) can cause hypercalciuria. Prolonged inactivity also increases urinary calcium and may cause stones.

Renal tubular acidosis (inherited condition in which the kidneys are unable to excrete acid) significantly reduces urinary citrate and total acid levels and can lead to stone formation, usually calcium phosphate.

Uric Acid StonesThe digestion of protein produces uric acid. If the acid level in the urine is high or too much acid is excreted, the uric acid may not dissolve and uric acid stones may form. Genetics may play a role in the development of uric acid stones, which are more common in men. Approximately 10% of patients with kidney stone disease develop this type of stone.

Struvite StonesThis type of stone, also called an infection stone, develops when a urinary tract infection (e.g., cystitis) affects the chemical balance of the urine. Bacteria in the urinary tract release chemicals that neutralize acid in the urine, which enables bacteria to grow more quickly and promotes struvite stone development.

Struvite stones are more common in women because they have urinary tract infections more often. The stones usually develop as jagged structures called "staghorns" and can grow to be quite large.

Cystine StonesCystine is an amino acid in protein that does not dissolve well. Some people inherit a rare, congenital (present from birth) condition that results in large amounts of cystine in the urine. This condition (called cystinuria) causes cystine stones that are difficult to treat and requires life-long therapy.

Incidence and Prevalence
People who live near large bodies of water (e.g., Great Lakes, Gulf of Mexico), those who live in "soft" water areas, and those who have a sibling or parent with the condition experience a higher incidence of renal stone disease. According to the U.S. National Institutes of Health, 1 person in 10 develops kidney stones during their lifetime and renal stone disease accounts for 7–10 of every 1000 hospital admissions. Kidney stones are most prevalent in patients between the ages of 30 and 45, and the incidence declines after age 50.

Causes and Risk Factors

Several factors increase the risk for developing kidney stones, including inadequate fluid intake and dehydration, reduced urinary flow and volume, certain chemical levels in the urine that are too high (e.g., calcium, oxalate, uric acid) or too low (e.g., citrate), and several medical conditions. Anything that blocks or reduces the flow of urine (e.g., urinary obstruction, genetic abnormality) also increases the risk.

Chemical risk factors include high levels of the following in the urine:

• Calcium (hypercalciuria)
• Cystine (cystinuria; caused by a genetic disorder)
• Oxalate (hyperoxaluria)
• Uric acid (hyperuricosuria)
• Sodium (hypernatremia)

A low level of citrate is a risk factor for hypocitraturia.

The following medical conditions are also risk factors:

• Arthritis (painful joint inflammation)
• Colitis (inflammation of the colon that causes chronic diarrhea, dehydration, and chemical imbalances)
• Crohn’s disease (intestinal disorder that causes chronic diarrhea, dehydration, and low citrate)
• Gout (caused by excessive uric acid in the blood)
• Hypertension (high blood pressure)
• Hyperparathyroidism (excessive parathyroid hormone, which causes calcium loss)
• Medullary sponge kidney (congenital kidney defect that may increase urinary calcium loss and stone formation)
• Renal tubular acidosis (inherited condition in which the kidneys are unable to excrete acid)
• Urinary tract infections (affect kidney function)

Diet plays an important role in the development of kidney stones, especially in patients who are predisposed to the condition. A diet high in sodium, fats, meat, and sugar, and low in fiber, vegetable protein, and unrefined carbohydrates increases the risk for renal stone disease. Recurrent kidney stones may form in patients who are sensitive to the chemical byproducts of animal protein and who consume large amounts of meat.

High doses of vitamin C (i.e., more than 500 mg per day) can result in high levels of oxalate in the urine (hyperoxaluria) and increase the risk for kidney stones. Oxalate is found in berries, vegetables (e.g., green beans, beets, spinach, squash, tomatoes), nuts, chocolate, and tea. Stone formers should limit their intake of cranberries, which contain a moderate amount of oxalate.

Signs and Symptoms

Small, smooth kidney stones may remain in the kidney or pass without causing pain (called “silent” stones). Stones that lodge in the ureter (tube that carries urine from the kidneys to the bladder) cause the urinary system to spasm and produce pain. The pain is unrelated to the size of the stone and often radiates from the lower back to the side or groin.

A "small" stone (usually 4 mm in diameter or less) has a 90% chance of spontaneous passage. Stones that are 8 mm in diameter or larger usually require medical intervention.

Other symptoms of kidney stones may include the following:

• Blood in the urine (hematuria)
• Increased frequency of urination
• Nausea and vomiting
• Pain during urination (stinging, burning)
• Tenderness in the abdomen and kidney region
• Urinary tract infection (fever, chills, loss of appetite)

Treatment

Treatment depends on the size and type of stone, the underlying cause, the presence of urinary infection, and whether the condition recurs. Stones 4 mm and smaller (less than 1/4 inch in diameter) pass without intervention in 90% of cases; those 5 – 7 mm do so in 50% of cases; and those larger than 7 mm rarely pass without intervention. Patients are advised to avoid becoming sedentary, because physical activity, especially walking, can help move a stone.

If possible, the kidney stone is allowed to pass naturally and is collected for analysis. The patient is instructed to strain their urine to obtain the stone(s) for analysis. It is important to analyze the chemical composition of kidney stones to determine how to prevent recurrent stone formation. The urine may be strained using an aquarium net or another device. Each voiding should be strained until the physician instructs the patient otherwise.

Dietary changes may be required and fluid intake should be increased. Patients with stones must increase their urinary output. Generally, 2000 cc of urine per day (slightly more than 1/2 gallon) is recommended and patients should drink enough water to produce this amount of urine daily. In some cases (e.g., some cystine stone formers), even higher levels of fluid intake are required.

Dietary calcium usually should not be severely restricted. Reducing calcium intake often causes problems with other minerals (e.g., oxalate) and may result in a higher risk for calcium stone disease.

Hypercalciuria
Thiazides, water pills (diuretics), are sometimes prescribed to reduce high levels of urinary calcium (hypercalciuria) and to increase urinary volume. Patients with hypercalciuria who do not respond to thiazide therapy may be prescribed orthophosphates to reduce calcium absorption and may be given dietary calcium restrictions. Patients should not reduce their calcium intake unless their physicians advise them to do so.

Hyperuricosuria
Patients with elevated uric acid levels (hyperuricosuria) are advised to drink 3 liters of water a day and reduce excessive dietary protein. Potassium citrate (medication that maintains the antacid level in urine) or allopurinol (medication that stops the production of uric acid) may also be prescribed.

Hyperoxaluria
Hyperoxaluria (high levels of urinary oxalate) may be mild, enteric, or primary. Mild hyperoxaluria is usually caused by an excess of dietary oxalate (found in tea, chocolate, cola, nuts, and green leafy vegetables). Prevention consists of daily doses of pyridoxine (vitamin B-6), which reduces oxalate excretion, increased fluids, phosphate therapy, and sometimes, calcium citrate supplementation.

A low-oxalate, low-fat diet, increased fluid intake, and calcium supplementation is prescribed for enteric hyperoxaluria. This rare condition is often severe and is usually caused by an intestinal disorder (e.g., Crohn’s disease, colitis). Calcium citrate, magnesium, iron, and cholestyramine may be given to reduce oxalate levels.

Primary hyperoxaluria is rare, severe, and caused by an inherited liver disorder. Primary hyperoxaluria requires aggressive treatment to prevent severe renal stone disease and kidney failure. High doses of vitamin B-6, orthophosphates, magnesium supplements, and increased fluid intake (to produce 2 liters of urine/day) are prescribed. Rarely, kidney and liver transplants are necessary.

Hypocitraturia
Hypocitraturia (low level of urinary citrate) usually requires a prescribed supplement, such as potassium citrate. The dosage depends on the level of urinary citrate, which is determined by the 24-hour urine test. Patients with renal tubular acidosis usually respond well to treatment with potassium citrate supplements. Citrus fruits and lemon juice also can be used as supplements.

Medication
Over-the-counter pain relievers (e.g., aspirin, Tylenol®, Advil®) usually are not effective for severe pain caused by kidney stones. Oral analgesics such as acetaminophen/codeine (Tylenol with Codeine&174), propoxyphene HCL (Darvon®), and oxycodone/acetaminophen (Percocet®) may be prescribed to minimize moderate pain associated with stones.

Injectable medications such as morphine sulfate (Duramorph PF®), meperidine HCL (Demerol®), and tramadol HCL (Ultram®) may be administered intravenously (IV) or intramuscularly (by injection) for severe pain. There is a risk for dependency with oral narcotic analgesics and a risk for accidental overdose if injectable medications are given directly into a vein. Side effects of these medications include the following:

• Constipation
• Drowsiness
• Nausea
• Slowed breathing (respiration)
• Vomiting

Nausea and vomiting can be reduced using medications such as prochlorperazine edisylate (Compazine®), promethazine HCL (Phenergan®), and metoclopramide HCL (Reglan®). Pentosan polysulfate sodium (Elmiron®) may be prescribed in severe cases to prevent stone formation by blocking crystal formation.

Surgery

If a kidney stone does not move through the ureter within 30 days, surgery is considered. Urologists use several procedures to break up, remove, or bypass kidney stones.

UreteroscopyThis procedure can be used to remove or fragment (break up) stones located in the lower third of the ureter. A ureteroscope (fiberoptic instrument resembling a long, thin telescope) is inserted through the urethra and passed through the bladder to the stone. Once the stone is located, the urologist either removes it with a small basket inserted through the ureteroscope (called basket extraction) or breaks the stone with a laser or similar device. The fragments are then passed by the patient. Ureteroscopy is performed under general or local anesthesia on an outpatient basis.

LithotripsyThis procedure is effective for stones in the kidney or upper ureter. It uses an instrument, machine, or probe to break the stone into tiny particles that can pass naturally. Lithotripsy is not appropriate for patients with very large stones or other medical conditions.

• Ultrasonic lithotripsy uses high frequency sound waves delivered through an electronic probe inserted into the ureter to break up the kidney stone. The fragments are passed by the patient or removed surgically.
• Electrohydraulic lithotripsy (EHL) uses a flexible probe to break up small stones with shock waves generated by electricity. The probe is positioned close to the stone through a flexible ureteroscope. Fragments can be passed by the patient or extracted. EHL requires general anesthesia and can be used to break stones anywhere in the urinary system.
• Extracorporeal shock wave lithotripsy (ESWL) uses highly focused impulses projected from outside the body to pulverize kidney stones anywhere in the urinary system. The stone usually is reduced to sand-like granules that can be passed in the patient's urine. Large stones may require several ESWL treatments. The procedure should not be used for struvite stones, stones over 1 inch in diameter, or in pregnant women.

Patients undergoing lithotripsy are given a sedative and general or local anesthesia, and the procedure takes over an hour. More than one treatment may be required.

Percutaneous Nephrostolithotomy (PCN)This surgical procedure is performed under local anesthesia and intravenous sedation. Percutaneous (through the skin) removal of kidney stones (lithotomy) is accomplished through the most direct route to stones through the kidney. A needle and guidewire are used to access the stones. The surgeon then threads various catheters over the guidewire and into the kidney and manipulates surgical instruments through the catheters to fragment and remove kidney stones. This procedure achieves a better stone-free outcome in the treatment of medium and large stones than shock wave lithrotripsy. This procedure usually requires hospitalization, and most patients resume normal activity within 2 weeks.

Ureteroscopic Stone RemovalThis procedure is performed under general anesthesia to treat stones located in the middle and lower ureter. A ureteroscope (small, fiberoptic instrument) is passed through the urethra and bladder and into the ureter. Small stones are removed and large stones are fragmented using a laser or similar device. A small tube (or stent) may be left in the ureter for a few days after treatment to promote healing and prevent blockage from swelling or spasm.

Open SurgeryThis procedure requires general anesthesia. An incision is made in the patient's back and the stone is extracted through an incision in the ureter or kidney. Most patients require prolonged hospitalization and recovery takes several weeks. This procedure is now rarely used for kidney stones.

Prevention

Prevention of renal stone disease depends on the type of stone produced, underlying urinary chemical risk factors, and the patient’s willingness to undergo a long-term prevention plan. The patient may be asked to make lifestyle modifications such as increased fluid intake and changes in their diet. Medication may be prescribed and treatment for an underlying condition that causes renal stone disease may be necessary.

24-Hour Urine Test Effective preventative measures are based on the patient’s chemical risk factors, which can often be uncovered with a 24-hour urine test and a blood test.

1.       The patient strains their urine to collect stones for chemical analysis.

2.       The physician performs a blood test to evaluate the serum calcium, uric acid, phosphate, electrolytes, and bicarbonate content.

3.       Urine is collected during a 24-hour period and analyzed for calcium, citrate, uric acid, magnesium, phosphate, sodium, oxalate, pH (acid level), and total volume.

The physician evaluates the data and recommends dietary modifications, supplements, and medications to minimize the risk for developing kidney stones. The 24-hour urine test may be repeated several months after treatment has begun to determine the success of the therapy and any adjustments that should be made. Long-term strict compliance and periodic retesting may substantially reduce the risk for future stone formation.

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