Nephrolithiasis (kidney stones) develops when conditions are present to cause supersaturation of urine, crystal formation, and aggregation of those crystals into a sizable mass. Stones can develop anywhere along the urinary tract. Kidney stones are common in Western societies; more than 10% of Americans will develop a symptomatic kidney stone during their lifetime.[1] The rate of recurrence over 5 years is estimated to be as high as 35-50%.[2]

The 5 major stone compositions are calcium oxalate, calcium phosphate, magnesium ammonium phosphate (struvite), uric acid, and cystine. Calcium-based stones are the most common, causing more than 75% of cases; calcium oxalate is the most common type overall. Struvite stones can form when certain urease-producing bacteria are present in the urinary tract.

Most often, stones are due to increased concentrations of stone-forming material in the urine, either from increased excretion or decreased urinary volume. Stone formation occurs when a stone-forming material becomes supersaturated in the urine and begins the process of crystal formation.

Many stones are asymptomatic. Large stones that become trapped in a ureter may cause severe flank pain that can radiate to the lower abdomen, groin, testicles, or perineum. Stones that lodge at the ureterovesical junction can cause lower urinary tract symptoms, including dysuria, urgency, and frequency. Nausea, vomiting, hematuria (gross and/or microscopic), and costovertebral angle tenderness may also be present, even in the absence of pain.

Risk Factors

Race and ethnicity. There is a higher incidence among White individuals compared with Asian Americans, Latinos, and Blacks.

Age. Risk increases with increasing age.

Anatomic defects of the kidneys such as horseshoe kidney may increase risk.

Gender. While traditionally more common in males, the ratio of male to female occurrence is now estimated to be almost equal.

History of nephrolithiasis. Individuals who have developed a kidney stone have an approximate 35% chance of recurrence within 5 years.[3]

Geography. Areas of elevated temperatures and high humidity appear to have an increased incidence of stone disease, likely due to population hydration status.

Socioeconomic status. Developed countries have a much higher risk of nephrolithiasis compared with developing countries, presumably due to dietary factors.

Obesity. Compared with persons at or near ideal body weight (BMI = 21-23), obese men (BMI ≥ 30) have a 33% greater risk for stone formation, while obese women have a 200% greater risk.[4] Patients who have had bariatric surgery are at risk for hyperoxaluria, which increases risk for kidney stones and kidney failure.[5]

Diet (See below).

Family history. A family history of nephrolithiasis raises risk 2-3 times.

Metabolic conditions. Insulin resistance, diabetes, obesity, cystinuria, oxaluria, gout, and hyperparathyroidism increase risk.

Urinary stasis (e.g., bladder outlet obstruction), chronic urinary tract infections, dehydration (e.g., diarrhea or malabsorption), and certain antiviral medications (e.g., indinavir, acyclovir) may also raise risk of nephrolithiasis. In addition, a guaifenesin metabolite may bind with calcium to form stones.

Diagnosis

Clinical presentation is highly specific for kidney stones, especially in patients with a history of the condition.

Helical non-contrast CT scan is the preferred means for detecting stones and urinary tract obstructions. Abdominal (kidney-ureter-bladder) x-ray will identify many radiopaque stones but cannot detect small or radiolucent (uric acid and proteinaceous) stones or obstructions and should only be used when non-contrast CT is unavailable. The intravenous pyelogram has been largely replaced by the more sensitive CT scan, which also carries less radiation exposure.

Ultrasound and, rarely, magnetic resonance urography, are imaging options for patients who should avoid radiation (e.g., pregnant women).

Urinalysis will usually reveal hematuria. Sediment examination may reveal pathognomonic crystals, and pH may give clues about etiology. Twenty-four–hour urine collections (for creatinine, calcium, phosphorus, oxalate, uric acid, cystine, citrate) on 2 occasions, after complete resolution and recovery from the acute event and resultant treatments, can aid diagnosis.

A chemistry panel that includes calcium and uric acid may help reveal etiology (e.g., hyperuricemia and hyperparathyroidism). Renal function should be assessed as urinary tract obstruction can lead to acute renal failure.

If a stone is passed, it should be sent to the laboratory for analysis.

Treatment

Immediate urologic attention is necessary for patients who present with fever, renal failure, intractable pain, persistent nausea, or signs and symptoms consistent with a systemic inflammatory response.

Small (< 5 mm) stones often pass spontaneously. While increased fluid intake facilitates passage, there is conflicting evidence for medical expulsive therapy (see tamsulosin).

Selective alpha-blockers (e.g., tamsulosin) or calcium channel blockers (e.g., nifedipine), with or without the addition of steroids, also may facilitate stone passage. However, a recent multicenter study found no significant difference in time to stone passage or analgesic use or pain in patients with stones ≤ 10mm managed medically with tamsulosin or nifedipine.[6]

Nonsteroidal anti-inflammatory drugs (e.g., indomethacin, ketorolac) and/or narcotics may be administered for pain; however, NSAIDs may increase bleeding risk following ureteroscopy or shock wave lithotripsy.

About 10-20% of stones require surgical removal. Minimally invasive surgical techniques include shock wave lithotripsy, percutaneous nephrolithotomy, and ureteroscopy. Open renal and ureteral surgery is necessary in about 1% of cases.

Extracorporeal shock wave lithotripsy is the treatment of choice for proximal renal or ureteral calculi. For the majority of middle and distal ureteral stones, ureteroscopy is preferred. This method can also be used to manage proximal ureteral and intrarenal calculi, as well as for ureteral stones that have failed shock wave lithotripsy. Nephrolithotomy is as effective as open surgery and is generally indicated for large or complex stones and cystine or monohydrate calcium stones, which are relatively resistant to lithotripsy.

Pharmacologic treatment and diet or lifestyle modifications are recommended in most cases to prevent recurrence of stones and may be specific to stone composition.

Nutritional Considerations

The incidence of kidney stones increases with animal protein intake, obesity, and poor fluid intake. Oxalates appear to be problematic primarily in persons with low calcium intake, and a vegetarian diet may offer significant protection against stone formation.

In observational studies, the following factors are associated with reduced risk:

A high fluid intake. Published guidelines suggest that daily water intake should be high enough to achieve at least 2.5 L of urine volume in order to prevent kidney stones. In a recent meta-analysis, when compared with an intake of 1,500 m/d, consumption of more than 2,000 mL of water intake per day reduced the risk of first kidney stone occurrence by roughly 8% and the highest intake (3,100 mL) was associated with a 26% reduction of risk.[7]

A healthy weight. The increase in the prevalence of kidney stones has paralleled that of obesity. The insulin resistance that occurs in obesity is associated with a reduction in renal ammonium production and low urinary pH, which could lead to the development of both uric acid stones and calcium oxalate stones.[8] The Women’s Health Initiative Study found that nephrolithiasis risk increased incrementally with BMI.[9] A study of medical claims data from nearly 100,000 individuals found that obesity (BMI > 30 kg/m2) was associated with a significantly greater likelihood of being diagnosed with a kidney stone.[10]

Bariatric surgery may increase the likelihood of stones. A review of weight loss surgeries found that Roux-en-Y gastric bypass causes a 30% reduction in urine volume, a 40% reduction in urinary citrate, and 50% increase in urinary oxalate, and increases stone incidence two-fold in non-stone formers (8.5%) and four-fold in patients with previous stone history (16.7%).[11]

Reducing intake of animal protein and sodium. Diets high in animal protein are associated with increased risk of stone formation; conversely, protein restriction causes a reduction of urinary calcium oxalate and urate.[12] Compared with individuals eating 50 g or less of animal protein per day, those eating the most (77 g or more) had a 33% higher risk for kidney stones.[13] A diet restricted in animal protein and sodium, when compared with a standard (low-calcium) diet used for prevention of calcium oxalate stone formation, reduces the risk for stone recurrence by half. A recent Cochrane review concluded that adherence to low protein and low salt diets with normal calcium intakes may also reduce the numbers of stone recurrences in people with idiopathic hypercalciuria.[14]

Limiting oxalates. American Urological Association guidelines recommend that clinicians counsel patients with calcium oxalate stones and relatively high urinary oxalate to limit intake of oxalate-rich foods and maintain normal calcium consumption.[15] However, a recent review of diets that are considered optimal for prevention of nephrolithiasis concluded that the benefits of oxalate restriction are unproven, except for bariatric surgery patients.[16]

Calcium from foods (versus supplements). Calcium intake from foods lowers the risk for calcium oxalate stones presumably because calcium binds oxalates within the intestinal tract. Oxalate absorption decreases as calcium intakes increase over a range of 200-1,200 mg per day.[17][18] Individuals consuming the greatest amount of calcium from foods have about a 30% lower risk for stone formation compared with persons consuming the lowest amounts.[19] Current evidence does not suggest that calcium supplements significantly increase the risk for nephrolithiasis; nevertheless, it has been suggested these should be taken with rather than between meals in order to minimize risk.[20]

Limiting soft drinks. Sugar-sweetened drinks, including sodas and fruit punch, appear to increase the risk for kidney stones. In a study of 194,095 participants followed for more than 8 years, individuals who consumed the highest amount of sugar-sweetened cola had a 23% higher risk of developing kidney stones, compared with those consuming the lowest amount. Those who consumed the highest amount of sugar-sweetened non-cola beverages had a 33% higher risk of developing kidney stones compared with those consuming the least. The increased risk may be due to high fructose corn syrup, which increases urinary excretion of calcium, oxalate, and uric acid.[21] Previous research found that patients who avoid colas and other phosphoric acid–containing beverages have a 15% lower rate of stone recurrence than those who continue to consume these beverages.[22] Coffee, tea, and orange juice are associated with significantly lower risk.[23][24]

Plant-based diets. The risk for stone formation is 40-60% lower in individuals following vegetarian diets for a number of reasons.[25] These include the absence of animal protein and the presence of phytic acid, which forms insoluble complexes with calcium in the intestinal tract and inhibits crystal formation in the urine. Higher fruit and vegetable intakes, which increase urine volume, pH, potassium, magnesium, citrate, and other stone inhibitors, decrease the supersaturation of calcium oxalate and uric acid overall.[9]

Avoidance of high-dose vitamin C. In a study of over 150,000 health professionals followed for more than 11 years, the highest intakes of a combination of both dietary and supplemental vitamin C were associated with a nearly 20% greater risk for kidney stones in men only.[26] Similarly, in the Cohort of Swedish Men study involving nearly 50,000 individuals, taking vitamin C supplements on a daily basis was associated with a significantly greater risk for kidney stones compared with less than daily supplementation.[27]

Dietary citrates. Citrates inhibit the formation of calcium oxalate stones by binding to calcium and interfering with calcium oxalate crystallization. However, hypocitraturia is common, found in 20% of stone formers, and increases the risk of stones.[28] Citrate supplementation (e.g., potassium citrate or potassium-magnesium citrate) is commonly prescribed for these patients. Gastrointestinal disturbances may limit compliance and benefit.[29][30] A review of strategies for reduction of risk factors for kidney stones concluded that an increased intake of fruit and vegetables (excluding those with high oxalate content) increases citrate excretion and provides significant protection against the risk of stone formation.[12]

Alcohol. A recent meta-analysis found that the amount of alcohol found in one standard drink consumed daily was associated with a 20% lower risk, compared with abstinence,[7] but the risks of alcohol use must also be taken into consideration.

Orders

See Basic Diet Orders chapter.

For patients with suspected or documented oxalate stones, consult with registered dietitian for instructions on how to follow a low-oxalate, high-magnesium diet. Avoid vitamin C supplements over 1,000 mg/d.

Consume ≥ 2.5 L of fluid (mostly water) per day.

What to Tell the Family

The risk of kidney stones is influenced by dietary factors, particularly high intake of animal protein and salt, along with low fluid consumption. Family members can help the patient in making diet changes and may benefit from these changes themselves. It is helpful to avoid animal protein and oxalate-containing foods, get adequate intake of calcium-rich foods at mealtime to reduce oxalate absorption, and drink adequate fluids.

References