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Urinary
calculi are solid particles in the urinary system. They may cause
pain, nausea, vomiting, hematuria, and, possibly, chills and fever from
secondary infection. Diagnosis is based on urinalysis and radiologic
imaging, usually noncontrast helical CT. Treatment is with analgesics,
antibiotics for infection, and, sometimes, extracorporeal shock
wave lithotripsy or endoscopic procedures.
About 1/1000 adults is hospitalized annually in the US because of urinary calculi, which are also found in about 1% of all autopsies. Up to 12% of men and 5% of women will develop a urinary calculus by age 70. Calculi vary from microscopic crystalline foci to calculi several centimeters in diameter. A large calculus, called staghorn calculus, can fill an entire renal calyceal system.
Etiology
About 85% of calculi in the US are composed of Ca, mainly Ca oxalate (see Table 1: Urinary Calculi: Composition of Urinary Calculi ); 10% are uric acid; 2% are cystine; and the remainder are Mg ammonium phosphate (struvite).
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Table 1
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Composition of Urinary
Calculi
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Composition
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Percentage of All Calculi
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Common Causes
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Calcium oxalate
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70
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Hypercalciuria
Hyperparathyroidism
Hypocitruria
Renal tubular acidosis
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Calcium phosphate
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15
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Hypercalciuria
Hyperparathyroidism
Hypocitruria
Renal tubular acidosis
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Cystine
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2
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Cystinuria
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Magnesium ammonium phosphate (struvite)
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3
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UTI caused by urea-splitting bacteria
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Uric acid
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10
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Hyperuricosuria
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Increased urine acidity
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General risk factors include disorders that increase urinary salt concentration, either by increased excretion of Ca or uric acid salts, or by decreased excretion of urine or citrate.
For Ca calculi, risk factors vary by population. The main risk factor in the US is hypercalciuria, a hereditary condition present in 50% of men and 75% of women with Ca calculi; thus, patients with a family history of calculi are at increased risk for recurrent calculi. These patients have normal serum Ca but elevated urinary Ca: > 250 mg/day (> 6.2 mmol/day) in men and > 200 mg/day (> 5.0 mmol/day) in women. Hypocitruria (urinary citrate < 350 mg/day [1820 μmol/day]), present in about 40 to 50% of Ca calculi-formers, promotes Ca calculi formation because citrate normally binds urinary Ca and inhibits the crystallization of Ca salts. About 5 to 8% of calculi are caused by renal tubular acidosis. About 1 to 2% of patients with Ca calculi have primary hyperparathyroidism. Rare causes are sarcoidosis, vitamin D intoxication, hyperthyroidism, multiple myeloma, metastatic cancer, and hyperoxaluria. Hyperoxaluria (urinary oxalate > 40 mg/day [> 440 μmol/day]) can be primary or caused by excess ingestion of oxalate-containing foods (eg, rhubarb, spinach, cocoa, nuts, pepper, tea) or by excess oxalate absorption due to various enteric diseases (eg, bacterial overgrowth syndromes, chronic pancreatic or biliary disease) or ileojejunal surgery. Other risk factors include taking high doses of vitamin C, a Ca-restricted diet (possibly because dietary Ca binds dietary oxalate), and mild hyperuricosuria. Mild hyperuricosuria, defined as urinary uric acid > 750 mg/day (> 4 mmol/day) in women or > 800 mg/day (> 5 mmol/day) in men, is almost always caused by excess intake of purine (in proteins, usually from meat, fish, and poultry); it may cause Ca oxalate calculus formation (hyperuricosuric Ca oxalate nephrolithiasis).
Uric
acid calculi develop with increased urine acidity (urine pH < 5.5), or rarely with severe hyperuricosuria (urinary uric acid > 1500 mg/day [> 9 mmol/day]), which crystallizes undissociated uric acid. Uric acid crystals may comprise the entire calculus or, more commonly, provide a nidus on which Ca or mixed Ca and uric acid calculi can form.
Cystine
calculi occur only in the presence of cystinuria (see Renal Transport Abnormalities: Cystinuria).
Mg
ammonium phosphate calculi (struvite, infection calculi) indicate the presence of a UTI caused by urea-splitting bacteria (eg, Proteus sp, Klebsiella sp). The calculi must be treated as infected foreign bodies and removed in their entirety. Unlike other types of calculi, Mg ammonium phosphate calculi occur 3 times more frequently in women.
Pathophysiology
Urinary calculi may remain within the renal parenchyma or renal pelvis or be passed into the ureter and bladder. During passage, calculi irritate the ureter and may become lodged, obstructing urine flow and causing hydroureter and sometimes hydronephrosis. Common areas of lodgment include the ureteropelvic junction, the distal ureter (at the level of the iliac vessels), and the ureterovesical junction. Typically, a calculus must have a diameter > 5 mm to become lodged. Calculi ≤ 5 mm are likely to pass spontaneously.
Even partial obstruction causes decreased glomerular filtration, which may persist briefly after the calculus has passed. With hydronephrosis and elevated glomerular pressure, renal blood flow declines, further worsening renal function. Generally, however, permanent renal dysfunction occurs only after about 28 days of complete obstruction.
Secondary infection can occur with long-standing obstruction, but most patients with Ca-containing calculi do not have infected urine.
Symptoms and Signs
Even large calculi remaining in the renal parenchyma or renal pelvis are usually asymptomatic unless they cause obstruction. Symptoms, such as severe pain, often accompanied by nausea and vomiting, and sometimes gross hematuria, usually occur when calculi pass into the ureter, cause obstruction, or both. Pain (renal colic) is of variable intensity but is typically excruciating and intermittent, often occurs cyclically, and lasts 20 to 60 min. Nausea and vomiting are common. Pain in the flank or kidney area that radiates across the abdomen suggests upper ureteral or renal pelvic obstruction. Pain that radiates along the course of the ureter into the genital region suggests lower ureteral obstruction. Suprapubic pain along with urinary urgency and frequency suggests a distal ureteral, ureterovesical, or bladder calculus.
On examination, patients may be in obvious extreme discomfort, often ashen and diaphoretic. Patients with renal colic may be unable to lie still and may pace, writhe, or constantly shift position. The abdomen may be somewhat tender on the affected side as palpation increases pressure in the already-distended ureter, but peritoneal signs (guarding, rebound, rigidity) are lacking. For some patients, the first symptom is hematuria or either gravel or a calculus in the urine. Other patients may have symptoms of a UTI, such as fever, dysuria, or cloudy or foul-smelling urine.
Diagnosis
Clinical differential diagnosis
Urinalysis
Imaging
Determination of calculus composition
The symptoms and signs suggest the diagnosis. With peritonitis (eg, due to appendicitis, ectopic pregnancy, or pelvic inflammatory disease), pain is usually constant, and patients lie still because movement worsens pain. Patients often have rebound tenderness or rigidity. Cholecystitis may cause colicky pain, usually in the epigastrium or right upper quadrant, often with Murphy's sign. Bowel obstruction may cause colicky abdominal pain and vomiting, but the pain is usually bilateral and not located primarily in the flank or along the ureter. Pancreatitis may cause upper abdominal pain and vomiting, but the pain is usually constant, may be bilateral, and is usually not along the flank or ureter. With most of these disorders, urinary symptoms are uncommon and other symptoms may suggest which organ system is actually involved (eg, vaginal discharge or bleeding in pelvic disorders among females). Dissecting aortic aneurysm must be considered, particularly in the elderly, because, if a renal artery is affected, it can cause hematuria, pain that radiates along a ureteral distribution, or both. Other considerations in the general evaluation of acute abdominal pain are discussed elsewhere (see Acute Abdomen and Surgical Gastroenterology: Evaluation).
Patients suspected of having a calculus causing colic require urinalysis and usually an imaging study. If calculus is confirmed, evaluation of the underlying disorder, including calculus composition testing, is required.
Urinalysis:
Macroscopic or microscopic hematuria is common, but urine may be normal despite multiple calculi. Pyuria with or without bacteria may be present. Pyuria suggests infection, particularly if combined with suggestive clinical findings, such as foul-smelling urine or a fever. A calculus and various crystalline substances may be present in the sediment. If so, further testing is usually necessary because the composition of the calculus and crystals cannot be determined conclusively by microscopy. The only exception is when typical hexagonal crystals of cystine are found in a concentrated, acidified specimen, confirming cystinuria.
Imaging tests:
Noncontrast helical CT should be done. This study can detect the location of a calculus as well as the degree of obstruction. Moreover, helical CT may also reveal another cause of the pain (eg, aortic aneurysm). For patients who have recurrent calculi, cumulative radiation exposure from multiple CT scans is a concern. For those with typical symptoms, ultrasound or plain abdominal x-ray can usually confirm presence of a stone with minimal or no radiation exposure.
Although most urinary calculi are demonstrable on plain x-ray, neither their presence nor their absence obviates the need for more definitive imaging, so this study can be avoided. Both renal ultrasonography and intravenous urography (IVU) can identify calculi and hydronephrosis, but ultrasonography is less sensitive for small calculi in patients without hydronephrosis, and IVU is time consuming and exposes the patient to the risk of IV contrast agents; these studies are generally used if helical CT is unavailable.
Identifying the
cause:
The calculus is obtained by straining the urine (or, if necessary, during operative removal) and sent to the laboratory for crystallography. Some calculi are brought in by patients. Urine specimens that show microscopic crystals can also be sent for crystallography. Patients with a single Ca calculus without additional risk factors for calculi require only urinalysis and plasma Ca concentration on two occasions to exclude hyperparathyroidism. Predisposing factors, such as a high-protein diet or vitamin C or D supplements, should be sought. Patients with a strong family history of calculi, conditions that might predispose to calculi formation (eg, sarcoidosis, bone metastases, multiple myeloma), or conditions that would make it difficult to treat calculi (eg, solitary kidney, urinary tract anomalies) require evaluation for all possible causative disorders and risk factors. This evaluation should include serum electrolytes, uric acid, and Ca on two separate occasions. Follow-up determination of parathyroid hormone levels is done if necessary. Urine tests should include routine urinalysis and two separate 24-h urine collections for urine volume, pH, and excretion of Ca, uric acid, citrate, oxalate, Na, and creatinine.
Treatment
Analgesia
Facilitate calculus passage (eg, with α-receptor blockers or Ca channel blockers)
For persistent or infection-causing calculi, removal using extracorporeal shock wave lithotripsy or endoscopic techniques
Analgesia:
Renal colic may be relieved with opioids, such as morphine and, for a rapid onset, fentanyl . Ketorolac 30 mg IV is rapidly effective and nonsedating. Vomiting usually resolves as pain decreases, but persistent vomiting can be treated with an antiemetic (eg, ondansetron 10 mg IV).
Facilitating
calculus passage:
Although increasing fluids (either oral or IV) has traditionally been recommended, it has not been proved to speed the passage of calculi. Patients with calculi with a diameter of < 1 cm who have no infection or obstruction, whose pain is controlled with analgesics, and who can tolerate liquids can be treated at home with analgesics and with α-receptor blockers (eg, tamsulosin 0.4 mg once/day) or Ca channel blockers to facilitate calculus passage. Calculi that have not passed within 6 wk typically require removal. In patients with infection and obstruction, calculi should be removed as soon as possible.
Calculus removal:
The technique used for removal depends on the location and size of the calculi. Techniques include extracorporeal shock wave lithotripsy and endoscopic techniques. Endoscopic techniques may involve rigid or flexible scopes and may involve direct-vision removal (basketing), fragmentation with some sort of lithotripsy (eg, pneumatic, electrohydraulic, or laser), or both. For symptomatic calculi < 1 cm in diameter in the renal pelvis or proximal ureter, extracorporeal shock wave lithotripsy is a reasonable first option for therapy. For larger calculi or if lithotripsy is unsuccessful, ureteroscopy (done in a retrograde fashion) with holmium laser lithotripsy is usually used. Sometimes removal is possible using an endoscope inserted anterograde through the kidney. For mid-ureteral calculi, ureteroscopy with holmium laser lithotripsy is usually the treatment of choice. Shock wave lithotripsy is an alternative. For distal ureteral calculi, endoscopic techniques, such as direct removal and use of lithotripsy (eg, pneumatic, electrohydraulic, or laser), are considered by many to be the procedures of choice. Shock wave lithotripsy can also be used.
Calculus dissolution:
Uric acid calculi in the upper or lower urinary tract occasionally may be dissolved by prolonged alkalinization of the urine with K citrate 20 mEq po bid to tid, but chemical dissolution of other calculi is not possible.
Prevention
In a patient who has passed a first Ca calculus, the likelihood of forming a 2nd calculus is about 15% at 1 yr, 40% at 5 yr, and 80% at 10 yr. Recovery and analysis of the calculus, measurement of calculus-forming substances in the urine, and the clinical history are needed to plan prophylaxis. In < 3% of patients, no metabolic abnormality is found. These patients seemingly cannot tolerate normal amounts of calculus-forming salts in their urine without crystallization. Thiazide diuretics, K citrate, and increased fluid intake may reduce their calculus production rate.
For hypercalciuria, patients may receive thiazide diuretics (eg, chlorthalidone 25 mg po once/day or indapamide 1.25 mg po once/day), to lower urine Ca excretion and thus prevent urinary supersaturation with Ca oxalate. Patients are encouraged to increase their fluid intake to ≥ 3 L/day. A diet that is low in Na and high in K is recommended. Restriction of dietary animal protein is also recommended.
For patients with hypocitruria, K citrate (20 mEq bid) enhances citrate excretion. A normal Ca intake is recommended, and Ca restriction is avoided. Oral orthophosphate has not been thoroughly studied.
Hyperoxaluria prevention varies. Patients with small-bowel disease can be treated with a combination of high fluid intake, Ca loading (usually in the form of Ca citrate 400 mg po bid), cholestyramine , and a low-oxalate, low-fat diet. Hyperoxaluria may respond to pyridoxine 5 to 500 mg po once/day, possibly by increasing transaminase activity, because this activity is responsible for the conversion of glyoxylate, the immediate oxalate precursor, to glycine.
In hyperuricosuria, intake of meat, fish, and poultry should be reduced. If the diet cannot be changed, allopurinol 300 mg each morning lowers uric acid production. For uric acid calculi, the urine pH must be increased to between 6 and 6.5 by giving an oral alkalinizing drug that contains K (eg, K citrate 20 mEq bid) along with increased fluid intake.
Infection with urea-splitting bacteria requires culture-specific antibiotics and complete removal of all calculi. If eradication of infection is impossible, long-term suppressive therapy (eg, with nitrofurantoin ) may be necessary. In addition, acetohydroxamic acid can be used to reduce the recurrence of struvite calculi.
To prevent recurrent cystine calculi, urinary cystine levels must be reduced to < 250 mg cystine/L of urine. Any combination of increasing urine volume along with reducing cystine excretion (eg. with α-mecaptopropionylglycine or d- penicillamine ) should reduce the urinary cystine concentration.
Last full review/revision August 2007 by Glenn M. Preminger
Content last modified August 2007
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