Overview and Risk Factors
Nephrolithiasis is characterized by the formation of crystalline aggregates ("kidney stones") that can develop anywhere along the urinary tract. Kidney stones are common in Western societies; nearly 10% of Americans will develop a symptomatic kidney stone during their lifetime.
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, and calcium oxalate is the most common type of stone overall. A rare but increasingly recognized cause of nephrolithiasis is the use of the protease inhibitor indinavir in treating HIV patients.
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.
Severe flank pain, known as renal colic, occurs with stones that become lodged in the ureter. It may radiate to the lower abdomen, groin, testicles, or perineum. Lower urinary tract symptoms, including dysuria, urgency, and frequency, occur with stones that become lodged at the ureterovesical junction. Nausea, vomiting, hematuria, and costoverterbral angle tenderness may also be present, even in the absence of pain.
Risk Factors
- Male gender. Males are 3 times more likely to develop stones than females.
- History of nephrolithiasis. Individuals who have developed a kidney stone have an 80% chance of recurrence within 10 years.
- Geography. Areas of elevated temperatures and high humidity appear to have an increased incidence of stone disease.
- Nationality. Developing countries have a much lower risk of nephrolithiasis, compared with developed countries. This is presumed to be due to dietary factors, specifically the absence of a Western-style, meat-based diet.
- 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.1
- Diet. Diet plays an important role in nephrolithiasis risk, as described below in Nutritional Considerations.
- Family history of nephrolithiasis. Patients with a family history of kidney stones have a 2 to 3 times higher risk.
- History of cystinuria. Cystinuria is an autosomal recessive disorder that increases risk of cystine stone formation.
- Urinary stasis (eg, bladder outlet obstruction).
- Chronic urinary tract infections.
- Dehydration (eg, diarrhea).
Diagnosis and Treatment
Diagnosis
Clinical presentation is highly specific for kidney stones, especially in patients with a history of the condition.
Noncontrast abdominal CT scan is the preferred test to detect stones and urinary tract obstructions. Abdominal x-ray (kidney-ureter-bladder film) will identify many radiopaque stones, but will not detect small or radiolucent stones or urinary tract obstructions.
The intravenous pyelogram has largely been replaced by abdominal CT scan. While the intravenous pyelogram has high sensitivity and specificity for detecting stones, its use is restricted by the risk of contrast reactions and by the fact that evaluation time is very limited when obstruction is present.
Ultrasound is used in patients who should avoid radiation, including pregnant women.
Urinalysis will usually reveal hematuria.
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 urinary tract infections.
Small (<5 mm) stones will often pass spontaneously, and increased fluid intake will facilitate stone passage. In some cases, tamsulosin (Flomax) or an alpha blocker (eg, terazosin) can also facilitate stone passage. Nonsteroidal anti-inflammatory drugs (NSAIDs) or narcotics may be administered for pain. However, urologists may prefer not to use NSAIDs because of the increased risk of bleeding in the event that the patient should need urteroscopy or shock wave lithotripsy.
About 10% to 20% of stones require surgical removal. Minimally invasive surgical techniques include shock wave lithotripsy, percutaneous nephrostolithotomy, and ureteroscopy. Open renal and ureteral surgery is necessary for stone removal in about 1% of cases.
Extracorporeal shock wave lithotripsy is the treatment of choice for most renal caculi. Percutaneous nephrostolithotomy is as effective as open surgery and is generally indicated for large or complex stones and cystine stones, which are relatively resistant to lithotripsy. Ureterorenoscopy with holmium laser lithotripsy is the treatment of choice for ureteral stones and stones that have failed lithotripsy.
Recurrence is common. Patients who tend to form stones should be instructed in methods of stone prevention, including increased fluid intake, restriction of animal protein and salt, avoidance of oxalate-containing foods (eg, tea, dark greens, chocolate), and consumption of citrates (eg, lemons, citrus juices, potassium citrate supplement). For stones caused by indinavir antiretroviral therapy, hydration and temporary interruption of therapy (1 to 3 days) may decrease recurrence.2
Nutritional Considerations
Kidney stones are increasingly common. Their incidence 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:
Reducing Intake of Animal Protein and Sodium
A high animal protein intake causes a significant increase in the urinary excretion of calcium, oxalate, and uric acid, 3 of the 6 main urinary risk factors for calcium stone formation.3 Compared with individuals eating 50 grams or less of animal protein per day, those eating the most (77 g or more) have a 33% higher risk for kidney stones.4Compared with a standard (low-calcium) diet used for prevention of calcium oxalate stone formation, a diet restricted in animal protein and sodium reduces the risk for stone recurrence by half.5
Limiting Oxalates
Although calcium intake was previously considered a culprit, current evidence indicates that urinary oxalate is the most important determinant of calcium oxalate crystallization.6 Individuals who tend to form stones of this type experience a significant increase in urinary oxalate excretion with even small increases in oxalate intake, whereas persons who do not form these stones do not experience a similar increase in urinary oxalate excretion with increased oxalate intake.7 Patients should be advised to avoid high-oxalate foods, such as rhubarb, spinach, strawberries, chocolate (especially dark), wheat bran, nuts, beets, and tea. Alternatively, certain food preparation methods may be used to reduce oxalate content. Boiling, for example, reduces soluble oxalate content by 30% to 87%, compared with steaming, which achieves a 5% to 53% reduction.8
Calcium at Mealtime
Calcium intake from foods lowers the risk for calcium oxalate stones,9 presumably because calcium binds oxalates within the intestinal tract. Oxalate absorption decreases as calcium intakes increase over a range of 200 to 1,200 mg per day.10 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.11 Research findings are mixed regarding the potential for calcium supplements to affect risk for urolithiasis. In the Nurses Health Study, women taking calcium supplements experienced a 20% increase in risk for stone formation, compared with not using supplements.9 But individuals taking doses of > 500 mg per day have been associated with decreased risk.12 Whether taking calcium supplements contributes to stone formation may depend on timing, with between-meal dosing associated with the risk for stone formation, while supplements taken with meals may reduce risk by binding dietary oxalates in the digestive tract.9
Limiting Colas, Coffee, and Tea
Although further research is required, evidence indicates that cola consumption significantly increases urinary calcium13 and oxalate excretion.14 Patients who avoid colas and other phosphoric acid-containing beverages have been found to have a 15% lower rate of stone recurrence than those who continue to consume these beverages.15 The association of coffee and tea intake with risk for stone formation appears to be less controversial, with findings of an inverse association with risk.16,17 Overall fluid consumption appears to be most important. Individuals who consume the highest amount of fluid each day (~2.6 L) have a 30% to 40% lower risk for stone formation than those consuming the least amount (~1.4 L).4,16
Vegetarian Diets
Vegetarian diets are associated with low excretion of calcium, oxalate, and uric acid3 and may lower the risk for urolithiasis in a number of ways. These include the absence of animal protein and provision of higher amounts of magnesium and potassium, both of which are associated with lower risk for stone formation.12,18 Vegetarian diets also provide ample amounts of whole grains high in phytic acid, a plant constituent that is associated with about a 40% lower risk for stone formation in persons eating the most (about 900 mg/day), compared with those eating the least amount (about 600 mg/day).19 Nationwide surveys have determined that the risk for stone formation is 40% to 60% lower in individuals following vegetarian diets.20 Compared with individuals following self-selected or Western diets, those on a vegetarian diet also have a decreased risk for uric acid crystallization.21
Wine
In a prospective study, each 8-oz serving of wine decreased the risk for stone formation by 39% to 59%.16,17 However, the potent diuretic effects of alcohol give it the potential to cause dehydration and increase stone risk if adequate consumption of other fluids is not maintained.
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 diet.
Consume ≥2.5 L of fluid 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. Persons with recurrent stones may benefit from avoiding animal protein and oxalate-containing foods, getting adequate intake of calcium-rich foods at mealtime to reduce oxalate absorption, and drinking adequate fluids.
References
1. Taylor EN, Stampfer MJ, Curhan GC. Obesity, weight gain, and the risk of kidney stones. JAMA. 2005;293:455-462.
2. Condra JH, Schleif WA, Blahy OM, Gabryelsi LJ, Graham DJ, Quintero JC, et al. In vivo emergence of HIV-1 variants resistant to multiple protease inhibitors. Nature.1995;374:569-571.
3. Robertson WG, Peacock M, Heyburn PJ, et al. Should recurrent calcium oxalate stone formers become vegetarians? Br J Urol. 1979;51:427-431.
4. Curhan GC, Willett WC, Rimm EB, et al. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med. 1993;328:833-838.
5. Borghi L, Schianchi T, Meschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med. 2002;346:77-84.
6. Lewandowski S, Rodgers AL. Idiopathic calcium oxalate urolithiasis: risk factors and conservative treatment. Clin Chim Acta. 2004;345:17-34.
7. de O G Mendonca C, Martini LA, Baxmann AC, et al. Effects of an oxalate load on urinary oxalate excretion in calcium stone formers. J Ren Nutr. 2003;13:39-46.
8. Chai W, Liebman M. Effect of different cooking methods on vegetable oxalate content. J Agric Food Chem. 2005;53:3027-3030.
9. Curhan GC, Willett WC, Speizer FE, et al. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Ann Intern Med. 1997;126:497-504.
10. von Unruh GE, Voss S, Sauerbruch T, et al. Dependence of oxalate absorption on the daily calcium intake. J Am Soc Nephrol. 2004;15:1567-1573.
11. Taylor EN, Stampfer MJ, Curhan GC. Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up. J Am Soc Nephrol. 2004;15:3225-3232.
12. Hall WD, Pettinger M, Oberman A, et al. Risk factors for kidney stones in older women in the southern United States. Am J Med Sci. 2001;322:12-18.
13. Iguchi M, Umekawa T, Takamura C, et al. Glucose metabolism in renal stone patients. Urol Int. 1993;51:185-190.
14. Rodgers A. Effect of cola consumption on urinary biochemical and physicochemical risk factors associated with calcium oxalate urolithiasis. Urol Res. 1999;27:77-81.
15. Shuster J, Jenkins A, Logan C, et al. Soft drink consumption and urinary stone recurrence: a randomized prevention trial. J Clin Epidemiol. 1992;45:911-916.
16. Curhan GC, Willett WC, Speizer FE, et al. Beverage use and risk for kidney stones in women. Ann Intern Med. 1998;128:534-540.
17. Curhan GC, Willett WC, Rimm EB, et al. Prospective study of beverage use and the risk of kidney stones. Am J Epidemiol. 1996;143:240-247.
18. Hirvonen T, Pietinen P, Virtanen M, Albanes D, Virtamo J. Nutrient intake and use of beverages and the risk of kidney stones among male smokers. Am J Epidemiol. 1999;150:187-194.
19. Curhan GC, Willett WC, Knight EL, et al. Dietary factors and the risk of incident kidney stones in younger women: Nurses' Health Study II. Arch Intern Med. 2004;164:885-891.
20. Robertson WG, Peacock M, Marshall DH. Prevalence of urinary stone disease in vegetarians. Eur Urol. 1982;8:334-339.
21. Siener R, Hesse A. The effect of a vegetarian and different omnivorous diets on urinary risk factors for uric acid stone formation. Eur J Nutr. 2003;42:332-337.
