Nephrology Hypertension

Kidney Stones

Does this patient have a kidney stone?

History, signs, and symptoms

Prevalence of kidney stones in the United States has been increasing for at least the past 30 years and is currently about 5%. Most kidney stones (85-90%) are composed primarily of calcium oxalate or calcium phosphate, and the majority of these are idiopathic; that is, not caused by a systemic disease, either genetic or acquired. The remaining stones - those composed of uric acid, cystine, or struvite - are usually associated with systemic diseases that increase risk of recurrence and the potential for renal injury.

The peak age of onset for idiopathic calcium stones is the third through fifth decades, while mean age of onset for cystine stones is 12 years and uric acid stones not associated with bowel disease are most likely to occur after age 50 years.

Adults who pass a single kidney stone, with no other stones seen on X-ray (preferably non-contrast computed tomography [CT]), are likely to have an idiopathic calcium stone, and need only an abbreviated evaluation to rule out systemic diseases that may result in renal damage or prompt stone recurrence. History of episodes of flank pain suspicious for colic may reflect earlier stone episodes where the stone was not retrieved. Rarely will physical findings be of help.

Risk factors for rapid stone recurrence or renal damage

Medical and surgical risk factors

  • Bowel disease or resection

  • Bariatric surgery, especially gastric bypass procedures

  • First stone in childhood or adolescence

  • History of recurrent urinary tract infection

  • History of prior stones in the patient's family

  • Gout

  • Renal structural anomalies (e.g. cystic or obstructive disorders)

  • Fractures

  • Stone composed of uric acid, cystine, or struvite

  • Chronic kidney disease

Medications that increase stone risk

  • Large intake of vitamins C or D

  • Calcium supplements

  • Acetazolamide or other carbonic anhydrase inhibitor

  • Topiramate

Occupational/recreational risk factor

  • Dehydration due to hot environment, vigorous physical activity, lack of fluid intake

Dietary risk factors

  • Oxalate load - nuts, spinach, vitamin C

  • High sodium intake - prepared foods and snacks

  • Eating disorders - laxative use, vomiting

  • Unusual diets - high protein intake

Genetic risk factors

  • Stones in a first-degree relative - hypercalciuria, hyperoxaluria

Other possible diagnoses

The classic presentation of ureteral stone passage, with flank pain and renal colic, is seldom mistaken for anything else; either microscopic or macroscopic hematuria is usually present as well. However, passage of clots or renal tissue (as in papillary necrosis) may cause similar symptoms.

Other diagnoses occasionally confused with renal colic

  • Diverticulitis

  • Biliary colic

  • Pelvic inflammatory disease

Stones lodged at the ureterovesical junction may cause frequency and urgency, and may be mistaken for symptoms of a urinary tract infection. When the stone passes into the bladder, pain or discomfort typically cease immediately.

Urinary tract stones may present without colic. Stones in the renal pelvis, even very large stones, may be asymptomatic, or may cause microscopic hematuria or vague costo-vertebral angle pain. Ureteral stones may also be asymptomatic on occasion, and can result in loss of renal function if the obstruction is left unrelieved for a long period. Stones may sometimes be retained in the bladder and grow to a large size; hematuria is often the only symptom.

What tests to perform?

Diagnosis of kidney stones

Radiologic tests for diagnosis of kidney stones

  • Non-contrast computed tomography (NCCT) is the preferred modality for visualization of kidney stones in symptomatic patients, having a sensitivity and specificity above 95% for assessment of stone size, number, and location; all types of stone visualize well. Ureteral obstruction and hydronephrosis can also be detected. Stone density, measured in Hounsfield units, may be able to distinguish uric acid from calcium stones. Concern about radiation dose may limit the use of NCCT for follow up.

  • Plain film radiography of the kidney, ureter, and bladder (KUB) can visualize stones containing calcium, including those composed of calcium oxalate or calcium phosphate. However, uric acid and cystine stones are usually radiolucent, and struvite stones may also visualize poorly, depending on their content of calcium phosphate. Utility of KUB also depends on stone size and location; ureteral stones may be missed if they overlie a vertebral transverse process, for example, or may be confused with a phlebolith in the pelvis. Sensitivity and specificity of KUB for diagnosis of stone is reported as 45-59% and 71-77%, respectively. KUB is of limited use in the initial evaluation of a patient with possible kidney stones but is helpful to follow the course of patients with known radio-opaque stones.

  • Renal ultrasound can detect renal stones, but accuracy of detection is poor compared with NCCT (sensitivity 24%) and is dependant on stone size, so a negative exam cannot exclude the presence of stones. It is especially limited at detecting stones in the ureter (sensitivity 19%), which is the location of most stones in patients with symptomatic stone passage. It is sensitive for hydronephrosis, a possible manifestation of ureteral obstruction. Its role in initial diagnosis of stones is limited, but it can be useful for follow up, particularly in those patient with radiolucent stones. It is also useful for evaluation of pregnant patients in whom radiation exposure should be avoided.

Other testing

  • Stone analysis. Patients experiencing renal colic should void into a container or a mesh sieve to catch the stone for analysis.

  • Urinalysis (preferably first morning void). Urine pH > 7 suggests infection with urea-splitting organism, commonly associated with struvite stones. Sediment may demonstrate crystals that help to identify stone types, such as calcium oxalate, uric acid, or cystine.

Evaluation of patients with a kidney stone

Single (first) kidney stone

Stone analysis is the sine qua non for diagnosis. If no stone analysis is available, in the absence of other risk factors, idiopathic calcium stone is the most likely diagnosis.

For a single (first) calcium stone, or if stone type unknown and no other risk factors:

  • A basic metabolic panel and serum calcium will evaluate for chronic kidney disease and hyperparathyroidism.

    • Parathyroid hormone testing is not indicated in the absence of hypercalcemia.

  • A urinalysis can detect infection with urea splitting organisms, which raise urine pH > 7.

For non-calcium stones, or in patients with systemic disease and high risk of recurrence or kidney damage, testing should follow suggestions as for recurrent stones.

Recurrent kidney stones

  • People with recurrent kidney stones should be evaluated for risk factors as described under "History, signs and symptoms."

  • Stone analysis is key to determine the type as well as to detect conversion. For example, those who begin with calcium oxalate stones may subsequently develop struvite stones due to infection or calcium phosphate stones if the urine ph has risen in response to treatment (eg, potassium citrate).

  • Imaging is indicated to assess whether old stones have passed and whether new ones have formed. In the case of the latter, improved preventive treatment is warranted. Either ultrasound or plain radiography may be used for follow-up considering the expense and radiation exposure with CT scanning.

  • Metabolic testing is recommended after the acute episode of stone passage to evaluate for disorders such as hyperparathyroidism, vitamin D excess, sarcoidosis, renal tubular acidosis, eating disorders or malabsorption, primary hypercalciuria, hyperoxaluria, high protein diet, calculation of supersaturation, and adequacy of urine collection.

    • Testing for systemic diseases (eg, levels of serum parathyroid hormone, vitamin D, angiotensin converting enzyme) is not indicated unless suggested by history, physical findings, or abnormal initial lab tests (listed below).

      • Blood tests (normal ranges)

        • Calcium (8.3-10.3 mg/dl)

        • Phosphate (2.5-5.0 mg/dl)

        • Creatinine (0.6-1.2 mg/dl)

        • Bicarbonate (20-28 mmol/liter)

        • Chloride (95-105 mmol/liter)

        • Potassium (2.5-5.0 mmol/liter)

      • 24-hour urine studies (normal ranges)

        • Volume (>1.5 liter/day)

        • Creatinine (20-25 mg/kg in men; 15-20 mg/kg in women)

        • Urea (g/day X 6.25/weight in kg = estimated protein intake; 0.8-1.0 g/kg per day)

        • Calcium (<300 mg/day in men; <250 mg/day in women; <140 mg/g creatiine per day)

        • Oxalate (< 40 mg/day)

        • pH (5.8-6.2)

        • Phosphate (500-1500 mg/day)

        • Citrate (>450 mg/day in men; >550 mg/day in women)

        • Uric acid (<800 mg/day in men; <750 mg/day in women)

        • Sodium (50-150 mmol/day)

        • Potasssium (20-100 mmol/day)

        • Magnesium (50-150 mg/day)

        • Sulfate (20-80 mmol/day)

        • Ammonium (15-60 mmol/day)

      • Spot urine

        • Cystine (cyanide nitroprusside test; negative result indicates cystine <75mg/liter)

How should a patient's kidney stone(s) be managed?

Medical management

Single (first) kidney stone

Conservative treatment to prevent or delay recurrence is appropriate in the absence of special risk factors (ie, single kidney).

Increased fluid intake to achieve urine volume of 2-2.5 liters daily. The optimal fluid is water, but other fluids are acceptable in moderation. Fluids containing large amounts of sugar or sodium may increase urine calcium excretion, and should be avoided. A clinical trial found that first-time idiopathic calcium oxalate stone formers that increased water intake and urine volume from 1 liter to 2.6 liters daily had significantly lower risk of recurrent stones over 5 years of follow up compared to a matched group who did not increase water intake (recurrence rates of 12% vs 27%, respectively).

Diet. Epidemiologic data suggests that diets high in sodium, sugar, and animal protein are associated with increased risk for kidney stones. In contrast, intake of potassium and dietary calcium are associated with lower risk, although use of calcium supplements may increase risk of stone formation. Therefore, low calcium diet is not advisable, as it may increase risk of bone disease, while failing to prevent stone recurrence.

Idiopathic stone formers

The following dietary recommendations are appropriate:

  • Lower intake of sodium (<100 mmol/day) and oxalate (<100 mg/day)

  • Higher intake of potassium (>100 mmol/day) and fluid (>2 liters/day)

  • Normal intakes of calcium (800-1000 mg/day) and protein (0.8-1 g/kg/day) with an emphasis on vegetable sources

No radiologic follow up is necessary in the absence of symptoms.

Patients with systemic disease or non-calcium stone should be managed as for recurrent stones.

Recurrent kidney stones

Untreated idiopathic calcium kidney stones have a recurrence rate of approximately 40% at 5 years, 50 % at 10 years, and 75% at 20 years.

  • Advice for fluid intake and diet is the same as for those with a single (first) kidney stone.

  • Medicines are recommended for certain metabolic disturbances:

    • Primary hypercalciuria - hydrochlorothiazide 12.5-25 mg/day; indapamide 1.25-2.5 mg/day; chlorthalidone 12.5-50 mg/day; may also be helpful in some with normocalciuria

    • Hypocitraturia - Potassium citrate 10-20 mmol taken 2 to 3 times/day; discontinue if urine pH rises and/or citrate does not increase due to increased risk of calcium phosphate stones

    • Hyperuricosuria - allopurinol 100-300 mg/day; dose should be adjusted downward for low eGFR

Surgical management

If a kidney stone does not pass, several surgical options are available for stone removal.

Ureteral stones

  • Shock wave lithotripsy

  • Ureteroscopy with laser lithotripsy

  • Stones lodged in the kidney

Smaller stones (≤2 cm)

  • Shock wave lithotripsy

  • Ureteroscopic lithotomy

Larger stones (>2 cm) or obstructing stones

  • Percutaneous nephrolithotomy

  • Open or laparoscopic stone removal for more difficult cases

What happens to patients with kidney stones?

After the passage of a first kidney stone, recurrences are common with rates of approximately 40 % at 5 years, 50 % at 10 years, and 75 % at 20 years. Stone formation is associated with increased rates of chronic kidney disease, hypertension, osteoporosis, and obesity. Although systemic diseases (eg, hyperparathyroidism, vitamin D intoxication, sarcoidosis, malabsorption) increase risk of kidney stones, the majority are idiopathic.

Most idiopathic stone formers have at least one metabolic abnormality that can be addressed as a preventive measure for stone recurrence.

Preventive measures include:

  • Lifestyle modifications (eg, increased intakes of fluid and potassium, decreased intakes of sodium and oxalate, normal intakes of calcium and protein with an emphasis on vegetable sources).

  • Medicines (thiazide diuretics, potassium citrate, and/or allopurinol depending on metabolic abnormalities)

How to utilize team care?

  • Urologists are key partners for determining need and methods of stone removal.

  • Nurses in the ambulatory care setting can provide patient education and reinforce advice for lifestyle modifications and/or medical therapy.

  • Pharmacists may assist with therapeutic monitoring such as following potassium levels in patients treated with thiazide diuretics or allopurinol dose adjustments for low estimated glomerular filtration rate (eGFR).

  • Dietitians provide important direction regarding dietary advice and practical tips for implementation and maintenance.

Are there clinical practice guidelines to inform decision making?

  • American Urological Association provides guidelines regarding benefits and risks of current methods for stone removal (www.auanet.org)

  • Guidelines for kidney stone evaluation and medical management are lacking.

Other considerations

DRG codes:

323 Urinary stones with complications, co-morbidities, and/or extracorporeal shock wave lithotripsy

324 Urinary stones without complications

What is the evidence?

Coe, FL, Evan, A, Worcester, E. "Pathophysiology-based treatment of idiopathic calcium kidney stones". Clin J Am Soc Nephrol. vol. 6. 2011. pp. 2083-2092.

(A comprehensive discussion of current concepts in pathophysiology of kidney stones, especially as related to patient management.)

Worcester, EM, Coe, FL. "Calcium kidney stones". N Engl J Med 3. vol. 63. 2010. pp. 954-963.

(A case-based overview of best practices in evaluation and treatment of kidney stones.)

Parks, JH, Coe, FL. "Evidence for durable kidney stone prevention over several decades". BJU Int. vol. 103. 2009. pp. 1238-1246.

Worcester, EM, Coe, FL. "New insights into the pathogenesis of idiopathic hypercalciuria hypercalciuria". Semin Nephrol. vol. 28. 2008. pp. 120-132.

Borghi, L, Schianchi, T, Meschi, T, Guerra, A, Allegri, F, Maggiore, U, Novarini, A. "Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria". N Engl J Med. vol. 346. 2002. pp. 77-84.

(Evidence to support normal (not low) calcium along with avoidance of high protein,oxalate, and sodium in the diet for stone prevention.)

Ettinger, B, Tang, A, Citron, JT, Livermore, B, Williams, T. "Randomized trial of allopurinol in the prevention of calcium oxalate calculi". N Engl J Med. vol. 315. 1986. pp. 1386-1389.

Laerum, E, Larsen, S. "Thiazide prophylaxis of urolithiasis: A double-blind study in general practice". Acta Med Scand. vol. 215. 1984. pp. 383-389.

Borghi, L, Meschi, T, Guerra, A, Novarini, A. "Randomized prospective study of a nonthiazide diuretic, indapamide, in preventing calcium stone recurrences". J Cardiovasc Pharmacol. vol. 22. 1993. pp. S78-S86.

Ettinger, B, Citron, JT, Livermore, B, Dolman, LI. "Chlorthalidone reduces calcium oxalate calculous recurrence but magnesium hydroxide does not". J Urol. vol. 139. 1988. pp. 679-684.

Ettinger, B, Pak, CY, Citron, JT, Thomas, C, Adams-Huet, B, Vangessel, A. "Potassium-magnesium citrate is an effective prophylaxis against recurrent calcium oxalate nephrolithiasis". Urol. vol. 158. 1997. pp. 2069-2073.

Barcelo, P, Wuhl, O, Servitge, E, Rousaud, A, Pak, CY. "Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis". J Urol. vol. 150. 1993. pp. 1761-1764.

Stamatelou, KK, Francis, ME, Jones, CA, Nyberg, LM, Curhan, GC. "Time trends in reported prevalence of kidney stones in the United States". Kidney Int. vol. 63. 2003. pp. 1817-1823.

(Data demonstrating that kidney stone prevalence has been rising over the past 30 years.)

Hofbauer, J, Hobarth, K, Szabo, N, Marberger, M. "Alkali citrate prophylaxis in idiopathic recurrent calcium oxalate urolithiasis - a prospective randomized study". Br J Urol. vol. 73. 1994. pp. 362-365.

Rule, AD, Bergstralh, EJ, Melton, LJ, Li, X, Weaver, AL, Lieske, JC. "Kidney stones and the risk for chronic kidney disease". Clin J Am Soc Nephrol. vol. 4. 2009. pp. 804-8011.

(Development of kidney stones is associated with increased rates of chronic kidney disease and hypertension.)

Madore, F, Stampfer, MJ, Rimm, EB, Curhan, GC. "Nephrolithiasis and risk of hypertension". Am J Hypertens. vol. 11. 1998. pp. 46-53.

Taylor, EN, Stampfer, MJ, Curhan, GC. "Obesity, weight gain, and the risk of kidney stones". JAMA. vol. 293. 2005. pp. 455-462.

(Obesity increases risks of kidney stones, chronic kidney disease, and hypertension. However, obesity does not fully account for these risks.)

Coe, FL, Favus, MJ, Crockett, T, Strauss, AL, Parks, JH, Porat, A, Gantt, CL, Sherwood, LM. "Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects". Am J Med. vol. 72. 1982. pp. 25-32.

Voss, S, Hesse, A, Zimmermann, DJ, Sauerbruch, T, von Unruh, GE. "Intestinal oxalate absorption is higher in idiopathic calcium oxalate stone formers than in healthy controls: measurements with the [(13)C2] oxalate absorption test". J Urol. vol. 175. 2006. pp. 1711-1715.

Taylor, EN, Curhan, GC. "Determinants of 24-hour urinary oxalate excretion". Clin J Am Soc Nephrol. vol. 3. 2008. pp. 1453-1460.

Parks, JH, Coe, FL, Evan, AP, Worcester, EM. "Urine pH in renal calcium stone formers who do and do not increase stone phosphate content with time". Nephrol Dial Transplant. vol. 24. 2009. pp. 130-136.

Parks, JH, Goldfisher, E, Asplin, JR, Coe, FL. "A single 24-hour urine collection is inadequate for the medfical evaluation of nephrolithiases". J Urol. vol. 167. 2002. pp. 1607-1612.

Wignall, GR, Canales, BK, Denstedt, JD, Monga, M. "Minimally invasive approaches to upper urinary tract urolithiasis". Urol Clin North Am. vol. 35. 2008. pp. 441-454.

Keeley, FX, Assimos, DG. "Clinical trials of the surgical management of urolithiasis: current status and future needs". Adv Chronic Kidney Dis. vol. 16. 2009. pp. 65-69.

Curhan, GC, Willett, WC, Speizer, FE, Stampfer, MJ. "Twenty-four-hour urine chemistries and the risk of kidney stones among women and men". Kidney Int. vol. 59. 2001. pp. 2290-2298.

Borghi, L, Meschi, T, Amato, F, Briganti, A, Novarini, A, Giannini, A. "Urinary volume, water and recurrences of idiopathic calcium nephrolithiasis: a 5-year randomized prospective study". J Urol. vol. 155. 1996. pp. 839-843.

Hiatt, RA, Ettinger, B, Caan, B, Quesenberry, CP, Duncan, D, Citron, JT. "Randomized controlled trial of low animal protein, high fiber diet in the prevention of recurrent calcium oxalate kidney stones". Am J Epidemiol. vol. 144. 1996. pp. 25-33.

Nouvenne, A, Meschi, T, Prati, B, Guerra, A, Allegri, F, Vezzoli, G, Soldati, L, Gambaro, G, Maggiore, U, Borghi, L. "Effects of a low-salt diet on idiopathic hypercalciuria in calcium-oxalate stone formers: a 3-mo radomized controlled trial". Am J Clin Nutr. vol. 91. 2010. pp. 565-570.

Heilberg, IP, Weisinger, JR. "Bone disease in idiopathic hypercalciuria". Curr Opin Nephrol Hypertens. vol. 15. 2006. pp. 394-402.

(Low calcium diets should be avoided in kidney stone formers because of reduction in bone density.)

Lauderdale, DS, Thisted, RA, Wen, M, Favus, MJ. "Bone mineral density and fracture among prevalent kidney stone cases in the Third National Health and Nutrition Examination Survey". J Bone Miner Res. vol. 16. 2001. pp. 1893-1898.

(Low calcium diets are associated with higher fracture rates in kidney stone formers.)

Mandel, N, Mandel, I, Fryjoff, K, Rejniak, T, Mandel, G. "Conversion of calcium oxalate to calcium phosphate with recurrent stone episodes". J Urol. vol. 169. 2003. pp. 2026-2029.

Kacker, R, Meeks, JJ, Zhao, L, Nadler, RB. "Decreased stone-free rates after percutaneous nephrolithotomy for high calcium phosphate composition kidney stones". J Urol. vol. 180. 2008. pp. 958-960.

Taylor, EN, Fung, TT, Curhan, GC. "DASH-style diet associates with reduced risk for kidney stones". J Am Soc Nephrol. vol. 20. 2009. pp. 2253-2259.

(The DASH diet, modified to reduce oxalate intake, largely reproduces dietary recommendations for kidney stone formers. However, it has not been specifically studied for stone prevention.)

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