A. Epidemiology

The peak incidence of urinary calculi is in the third to fifth decades. Stones are more prevalent in men than in women. Stone incidence is increased during the late summer months. Dietary factors leading to stone formation include low water intake and high protein or oxalate (leafy green vegetable) consumption. Calcium restriction is not recommended as a means of preventing stone formation; however, a low-sodium diet may decrease calciuria. Citrus juices, particularly lemonade, may increase urinary levels of citrate, an inhibitor of stone formation (J Urol 1996;156:907). Various drugs, including high-dose vitamins C and D, acetazolamide, triamterene, and some protease inhibitors (indinavir) (Lancet 1997;349:1294), have been associated with stone formation. Disease states, such as inflammatory bowel disease, and metabolic disorders, such as type I renal tubular acidosis or cystinuria, can also contribute to stone formation.

B. Clinical features

Acute onset of severe flank pain or renal colic, often associated with nausea and vomiting, results from urinary obstruction by the stone. Common locations for stones to become impacted include the renal infundibulum, the ureteropelvic junction, the crossing of the iliac vessels, and the ureterovesical junction, which is the most constricted area through which the stone must pass. Patients may present with microscopic or gross hematuria, but 15% of patients may have no hematuria.

C. Types of calculi

Calcium stones make up approximately 70% of all stones. Disorders of calcium metabolism, such as increased intestinal absorption or increased renal excretion of calcium or oxalate, can cause calcium stones. Systemic disorders, such as hyperparathyroidism, sarcoidosis, immobilization (causing calcium resorption from bone), and type I renal tubular acidosis, can lead to these derangements of calcium metabolism.

Uric acid stones make up approximately 10% of all stones. They occur as a result of hyperuricosuria, persistently acidic pH, and low urine volumes.

Cysteine stones account for 4% of stones. They are caused by a defect in tubular reabsorption of cysteine that is inherited in an autosomal recessive manner. Hexagonal crystals in the urine are highly suggestive of cysteine stones.

Magnesium ammonium phosphate or struvite stones account for 15% of stones and are associated with urinary tract infection, commonly with urea-splitting organisms, and a chronically alkaline urinary pH (>7.2). Urinalysis may demonstrate rectangular “coffin lid” crystals.

D. Evaluation of urinary calculi

Urinalysis, including microscopic examination and urine culture, should be performed on all patients suspected of having calculi.

Serum electrolytes, including calcium, and creatinine levels are also part of the standard workup. In addition, uric acid levels and parathyroid hormone levels may be helpful. A CBC with differential can be obtained in patients with signs of concurrent infection.



Noncontrast spiral CT has replaced IVP as the diagnostic study of choice in the acute setting (J Urol 1998;160:679). For patients with suspected nephrolithiasis but atypical symptoms, CT may elucidate other causes of abdominal pain. Signs of obstruction include hydroureteronephrosis and perinephric fat stranding.

KUB (kidneys, ureters, bladder) should be used to monitor stone passage in patients with already documented nephrolithiasis and to evaluate whether the stone is amenable to extracorporeal shock-wave lithotripsy (ESWL).

E. Management of urinary calculi

Hydration. Intravenous fluids are required if the patient is nauseated and cannot take oral fluids. Normal saline usually is initiated at 150 mL/hour in appropriate patients.

Pain management. Patients whose pain is not adequately managed with oral analgesics require hospitalization for administration of parenteral narcotics. Parenteral nonsteroidal compounds, such as ketorolac, can be effective in reducing the pain of renal colic but should not be used in patients who may undergo lithotripsy. ESWL is contraindicated within 72 hours of administration of nonsteroidal analgesics to minimize the risk of renal hematoma.

Urine should be collected and strained to retrieve the stone. The stone should be analyzed for composition.

Any patient found to have an obstructing stone in the presence of infection or fever needs emergent decompression with percutaneous nephrostomy tube or stent placement. This situation can deteriorate quickly into a life-threatening crisis, particularly in the diabetic or immunosuppressed patient.

Ninety-five percent of stones 4 mm or smaller in size pass spontaneously (J Urol 1997;158:1915). Patients may be given up to 4 weeks to pass a partially obstructing stone without permanent renal damage. Patients with stones larger than 4 mm or with intractable symptoms of pain, nausea, or vomiting may need early surgical treatment to relieve obstruction with a ureteral stent, shock-wave lithotripsy, or ureteroscopy with stone ablation or retrieval.

Patients who have had one episode of nephrolithiasis do not require further workup. Those who have recurrent episodes require a 24-hour urine collection for volume, creatinine, pH, sodium, calcium, magnesium, phosphorous, oxalate, citrate, uric acid, and protein measurement.

Potassium citrate may help to prevent stone recurrence by increasing urinary citrate levels and alkalizing the urine. Uric acid stones may dissolve by increasing urinary pH, and calcium stones may be prevented with thiazide diuretics.