Scope of the Problem

Nephrolithiasis is a major cause of morbidity involving the urinary tract. The prevalence of nephrolithiasis in the US population increased from 3.8% in the late 1970s to 8.8% in the late 2000s. The increase in prevalence was observed in men and women and in whites and blacks. There were almost 2 million physician office visits for stone disease in 2000. It is estimated that more than $5 billion US dollars is spent on stone disease annually.

The lifetime risk of nephrolithiasis is about 19% in men and 9% in women. In men, the first episode of renal colic is most likely to occur after age 30, but it can occur earlier. The incidence for men who have never had a stone is about 0.3% per year between the ages of 30 and 60 years, and it decreases thereafter with age. For women, the rate is about 0.25% per year between the ages of 20 and 30 years and then declines to 0.15% for the next 4 decades.

The risk of the first recurrent stone after the incident stone in untreated patients remains controversial. Reported frequencies of stone recurrence in uncontrolled studies have ranged from 30% to 50% at 5 years. However, data from the control groups of randomized, controlled trials suggest much lower rates of first recurrence after an incident calcium oxalate stone, ranging from 2% to 5% per year. Sex-specific rates are not available from the randomized trials.

Acute Renal Colic

With the passage of a stone from the renal pelvis into the ureter resulting in partial or complete obstruction, there is sudden onset of unilateral flank pain of sufficient severity that the individual usually seeks medical attention. Despite the use of the misnomer “colic,” the pain does not completely remit but rather waxes and wanes. Nausea and vomiting may accompany the pain. The pattern of pain depends on the location of the stone: if it is in the upper ureter, pain may radiate anteriorly to the abdomen; if it is in the lower ureter, pain may radiate to the ipsilateral testicle in men or labium in women; if it is lodged at the ureterovesical junction (UVJ), the primary symptoms may be urinary frequency and urgency. A less common acute presentation is gross hematuria without pain.

The symptoms from a ureteral stone may mimic those of several other acute conditions. A stone lodged in the right ureteropelvic junction can mimic acute cholecystitis. A stone lodged in the lower right ureter as it crosses the pelvic brim can mimic acute appendicitis. A stone lodged at the UVJ on either side can mimic acute cystitis. A stone lodged in the lower left ureter as it crosses the pelvic brim can mimic diverticulitis. An obstructing stone with proximal infection can mimic acute pyelonephritis. Note that infection in the setting of obstruction is a medical emergency (“pus under pressure”) that requires emergent drainage by placement of a ureteral stent or a percutaneous nephrostomy tube. However, because nephrolithiasis is common, the simple presence of a stone in the kidney does not confirm the diagnosis of renal colic in a patient presenting with acute abdominal pain.

Other conditions to consider in the differential diagnosis of suspected renal colic include muscular or skeletal pain, herpes zoster, duodenal ulcer, abdominal aortic aneurysm, gynecologic causes, ureteral obstruction resulting from other intraluminal factors (e.g., blood clot, sloughed papilla), and ureteral stricture. Extraluminal factors causing compression tend not to result in a presentation with symptoms of renal colic.

The physical examination alone rarely allows for diagnosis, but clues guide the evaluation. The patient typically is in obvious pain and is unable to achieve a comfortable position. There may be ipsilateral costovertebral angle tenderness, or in cases of obstruction with infection, symptoms and signs of sepsis.

Although blood tests are typically normal, there may be a leukocytosis resulting from stress or infection. The GFR is typically normal, but it may be reduced in the setting of volume depletion, bilateral ureteral obstruction, or unilateral obstruction, particularly in a patient with a solitary functioning kidney. The urinalysis classically shows red blood cells and white blood cells, and occasionally crystals. If ureteral obstruction by the stone is complete, there may be no red blood cells because urine will not be flowing through that ureter into the bladder.

Because of the often nonspecific physical examination and laboratory findings, imaging studies play a crucial role in making the diagnosis. A recent study suggested that a kidney ultrasound can be used as the first imaging study in the emergency department. Ultrasonography, although avoiding radiation, can image only the kidney and proximal ureter. The imaging modality that provides the most detailed information is a noncontrast helical (spiral) computed tomography (CT), because it can detect stones as small as 1 mm. Even pure uric acid stones, traditionally considered “radiolucent,” are identified. Typically the study shows a ureteral stone ( Fig. 46.1 ) or evidence of recent passage, such as perinephric stranding or hydronephrosis. A plain abdominal radiograph of the kidney, ureter, and bladder (KUB) can miss a small stone in the ureter or kidney, even one that is radiopaque, and it provides no information on obstruction. Although KUB is often used to monitor the progress of a ureteral stone or the growth of asymptomatic kidney stones, its sensitivity is limited.

Non–contrast-enhanced computed tomography scan shows a radioopaque obstructing stone (arrow) in the left ureter.

Renal colic is one of the most excruciating types of pain, and pain control is essential. Narcotics and parenteral nonsteroidal antiinflammatory drugs are effective, with the latter preferable because they cause fewer side effects. Other treatments that may be effective for promoting stone passage include α-adrenergic blockers and calcium channel blockers, which have similar reported benefits on stone passage rates. Tadalafil and silodosin have been considered, but the data on these agents are limited. In the acute setting, urinary alkalinization may be effective for dissolving a uric acid stone, but this stone type is relatively rare, and there must be adequate urine flow past the stone.

Types of Stones

Almost 90% of stones in first-time stone formers contain calcium, most commonly as calcium oxalate ( Fig. 46.2 ). Other types of stones, such as cystine, pure uric acid, and struvite, are much less common. However, these types of stones also deserve careful attention because recurrences are common.

Types of stones in first-time and recurrent stone formers. (With gratitude to Professor Michel Daudon.)

Pathogenesis

The urinary concentrations of calcium, oxalate, and other solutes that influence stone formation are high enough that they should result in crystal formation in the urine of most individuals, but this is clearly not the case. This condition is termed supersaturation . Substances in the urine that prevent crystal formation are called inhibitors . The most clinically important inhibitor is citrate, which works by chelating calcium cations in the urine and decreasing the free calcium available to bind with oxalate or phosphate anions. If the supersaturation is sufficiently high or there are insufficient inhibitors, precipitation occurs with resulting crystalluria.

The causes of stone formation differ for different stone types. Cystine stones form only in individuals with the autosomal-recessive disorder of cystinuria. Uric acid stones form only in those who have persistently acidic urine, with or without hyperuricosuria. Struvite stones form only in the setting of an upper urinary tract infection with a urease-producing bacterium. These stones are seen in individuals with recurrent urinary tract infections, particularly those with abnormal urinary tract anatomy, such as patients who have urinary diversions or who require frequent catheterization. Stones may occasionally result from precipitation of medications, such as acyclovir, sulfadiazine, atazanavir, and triamterene, in the urinary tract.

Calcium-based stones have a multifactorial etiology. Traditionally, stone formation was believed to occur from (1) crystal formation in the renal tubule, followed by (2) attachment of the crystal to the tubular epithelium, usually at the tip of the papilla, and (3) growth of the attached crystal by deposition of additional crystalline material. However, it now appears that the initial event occurs when calcium phosphate deposits in the medullary interstitium. The calcium phosphate material may then erode through the papillary epithelium, on which calcium oxalate is subsequently deposited.

Calcium phosphate stones are more likely to form in the presence of high urine calcium, low urine citrate, and alkaline urine (urine pH 6.5 or higher). Systemic conditions that are present more frequently in patients with calcium phosphate stones include renal tubular acidosis and primary hyperparathyroidism. The remainder of this chapter focuses on calcium oxalate stones, except where noted.

Urinary variables that increase the risk of calcium oxalate stone formation are higher levels of calcium and oxalate, whereas higher levels of citrate and higher total volume decrease the risk ( Table 46.1 ). Risk of calcium oxalate stone formation does not vary with urine pH, unlike calcium phosphate and uric acid stones, which are pH dependent. Although higher urine uric acid concentration had been thought to increase the risk of calcium oxalate stone formation, results from a recent large study did not support this belief.

The traditional approach to urinary abnormalities is based on 24-hour urinary excretion. The reference ranges for urinary factors vary by laboratory; this is because there are no universally accepted normal ranges. Commonly used definitions of “abnormal values” are presented in Table 46.2 . After being evaluated, patients have typically been classified into categories according to their urinary abnormalities and treatment directed at correcting the abnormalities.

Table 46.2

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