Kidney Stones

History, signs, and symptoms

The 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 with some containing calcium phosphate, and the majority of these are idiopathic; that is, not caused by a systemic disease, either genetic or acquired although some are due to a familial increase in urinary calcium excretion. 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. A significant proportion of kidney stones are recurrent with 15% recurring within one year, 40% within 5 years and greater than 50% after 10 years. As a result, patients should have at least an abbreviated work-up for metabolic risk factors.

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. It is important, if possible, to send the stone for analysis as this can guide future therapy.

Patients typically present with acute onset of flank pain which may radiate towards the pelvis. Occasionally, where complete obstruction of the ureter occurs, patients may have acute kidney injury or, in more severe cases, pyelonephritis. Recurrent kidney stones are a risk factor for future chronic kidney disease although the mechanism for this is unclear.

Risk factors for rapid stone recurrence or renal damage

All patients presenting with kidney stones should be questioned regarding the potential risks for stone formation. These include:

Medical and surgical risk factors
  • Bowel disease or resection which may increase oxalate absorption and thus increase the risk for calcium oxalate stones.

  • Bariatric surgery, especially gastric bypass procedures similarly increase oxalate absorption.

  • First stone in childhood or adolescence may suggest the presence of a primary metabolic or genetic disorder.

  • History of recurrent urinary tract infection.

  • History of prior stones in the patient’s family.

  • Patients with a history of gout are at risk for uric acid stones.

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

  • Stone composed of uric acid, cystine, or struvite.

  • Chronic kidney disease.

Medications that increase stone risk
  • Vitamin C is metabolized to oxalate and high doses may increase the risk of oxalate stones.

  • High vitamin D ingestion increases urinary calcium excretion.

  • Calcium supplements may increase or decrease risk depending on whether the primary issue is hypercalciuria or hyperoxaluria as calcium supplements can bind excess oxalate in the GI tract and are occasionally used to treat oxalate stones.

  • Acetazolamide or other carbonic anhydrase inhibitor increase the urine pH and thus increase the risk for both calcium phosphate stones and nephrocalcinosis.

  • Topiramate is an anticonvulsant medication that also acts as a carbonic anhydrase inhibitor.

Occupational/recreational risk factor
  • Dehydration due to hot environment, vigorous physical activity, lack of fluid intake

Dietary risk factors
  • Oxalate load – nuts, spinach, strawberries, dark leafy greens

  • High sodium intake – prepared foods and snacks which increases urinary calcium excretion

  • Unusual diets – high protein intake or protein supplements can increase urinary calcium excretion and also increase urinary uric acid

Genetic risk factors
  • Stones in a first-degree relative may suggest the presence of idiopathic familial hypercalciuria or 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, the 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. The utility of a 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. The 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 the accuracy of detection is poor compared with NCCT (sensitivity 24%) and is dependent 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 in the absence of alkali therapy suggests infection with a urea-splitting organism, commonly associated with struvite stones. The urine sediment may demonstrate crystals that help to identify stone types, such as calcium oxalate, uric acid, or cystine although this is neither sensitive nor specific.

Evaluation of patients with a kidney stone

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

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

  • Serum calcium and uric acid. Note that both of these can be normal in patients with calcium and uric acid stones respectively.

  • Hyperparathyroidism may be associated with hypercalciuria even in the absence of hypercalcemia and should be evaluated in all patients with suspected calcium stones. Secondary hyperparathyroidism is not associated with an increased risk of kidney stones.

  • Serum angiotensin converting enzyme or activated vitamin D levels may be elevated in patients with sarcoidosis.

  • 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.

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.

24 hour Urine analysis

A comprehensive urine analysis can allow for targeted management of stone risk factors. Some reporting agencies provide estimates of the supersaturation of salts in the urine. A fluid is considered to be supersaturated when the concentration of a salt exceeds the ability of the fluid to dissolve any additional salt. See Table I for the factors that should be assessed.

Table I.

24 hour Urine analysis: factors that should be assessed

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. 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

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 but may vary depending on the stone type

  • Medications are recommended for certain metabolic disturbances:

  • Primary hypercalciuria. Thiazide diuretics lower urinary calcium excretion. Hydrochlorothiazide 12.5-25 mg/day; indapamide 1.25-2.5 mg/day; chlorthalidone 12.5-50 mg/day. Care should be taken in patients on high sodium diets and both dietary sodium and protein should be reduced before starting a diuretic

  • Hypocitraturia – Potassium citrate 10-20 mmol taken 2 to 3 times/day. In patients with hypocitraturia and calcium stones, these may decrease the supersaturation of calcium oxalate. May increase the risk of calcium phosphate stones if the urine pH rises excessively.

  • Hyperuricosuria – Uric acid stones do not form in an alkaline urine so the first line therapy is to increase the urine pH using potassium citrate (or bicarbonate if this is not available). Goal pH is >6-6.5. If the supersaturation remains elevated despite adequate alkalinization, then patients may be treated with allopurinol to reduce production. This should be considered a second line therapy as it is not as effective.

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.

More than 90% of recurrent stones are preventable with adequate management of metabolic risk factors.

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 (e.g., increased intakes of fluid and potassium, decreased intakes of sodium and oxalate, normal intakes of calcium and protein with an emphasis on vegetable sources).

  • Medications (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 (

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