Renal stones are common, with lifetime prevalence estimates as high as 15%. Historically, men are affected more often than women, with a ratio of 2 or 3:1, although recent evidence suggests the gender gap may be closing. Stones can form at any age, but most occur in adults between 30 and 60 years of age. The clinical and economic impact of stone disease is substantial, with an estimated $2 billion spent in the United States in 2000.
Bladder stones are also associated with signiﬁcant morbidity but occur far less frequently than renal stones. Because the causes of renal and bladder stones are distinct, their associated symptoms, treatments, and prevention strategies are considered separately.
Pathogenesis. The majority of renal stones (80%) are calcium-based, most frequently calcium oxalate and less commonly calcium phosphate. Other less common stone compositions are uric acid, struvite, and cystine. When stone-forming salts reach a urinary concentration that exceeds the point of equilibrium between dissolved and crystalline components, crystallization will occur. Although certain chemicals in the urine can delay stone formation, there is a concentration of stone-forming salts above which crystallization becomes inevitable. Thus factors that increase the propensity for stone formation do so by reducing urine volume, increasing the quantity of stone-forming salts, or decreasing the quantity of crystallization inhibitors.
The process by which crystal formation leads to stone formation remains incompletely understood. Recent evidence, however, suggests that routine calcium oxalate stones originate on calcium phosphate deposits, known as Randall plaques, that are located at the tips of renal papillae and act as niduses for crystal overgrowth.
Risk Factors. Calcium stones are associated with a variety of genetic, environmental, and dietary risk factors. Elevated urinary calcium levels, one of the most common causes of calcium stones, can occur in the setting of increased bone resorption, intestinal hyperabsorption of calcium, or impaired renal tubular reabsorption of calcium. Elevated urinary oxalate levels, either dietary or the result of enhanced intestinal oxalate absorption, increase the urinary saturation of calcium oxalate and promote stone formation.
Depressed urinary citrate levels, often idiopathic but in some cases associated with systemic acidosis or hypokalemia, are also associated with an increased risk of calcium stones because citrate is an important inhibitor of stone formation. Finally, elevated urinary uric acid levels promote calcium oxalate stone formation and are associated with excessive intake of animal protein, conditions that lead to overproduction/overexcretion of uric acid (e.g., Lesch-Nyhan syndrome), or use of uricosuric medications.
Noncalcium stones are also associated with speciﬁc metabolic, genetic, and infectious disorders. Uric acid stones primarily occur in the setting of overly acidic urine, in which uric acid crystallizes. These stones are more common among patients with insulin resistance and type II diabetes mellitus, in whom production and excretion of ammonia in the renal proximal tubule is impaired, leading to insufﬁcient buffering of protons in urine. Magnesium ammonium phosphate (struvite) stones, in contrast, occur in the setting of overly alkaline urine, in which struvite and calcium carbonate precipitate. These stones primarily occur in patients who have urinary tract infections with urea splitting bacteria, such as Proteus, Pseudomonas, Klebsiella, and Staphylococcus. The hydrolysis of urea produces high concentrations of ammonia, which buffers protons. Incorporation of bacteria into these stones may cause chronic infections. Finally, cystine stones occur because of an inherited disorder of amino acid transport in which proximal tubular reabsorption of dibasic amino acids (cystine, lysine, ornithine, arginine) is impaired, leading to high urinary concentrations. Because cystine is poorly soluble in urine, it crystallizes and forms stones at relatively low urinary concentrations.
Presentation and Diagnosis. The symptoms associated with renal stones depend on their location. Typically, stones located within the calyces are asymptomatic. When these stones become detached and are propelled down the narrow ureter, however, they frequently become impacted. Stones generally become lodged in the narrowest portions of the ureter, which are located at the ureteropelvic junction, the crossing of the iliac vessels, and the ureterovesical junction (see Plate 6–4). The ﬁrst sign of a stone in the ureter is often the acute onset of severe ﬂank pain. The stone obstructs urine outﬂow from the kidney, and the acute increase in renal pelvic pressure causes distention of the collecting system and stretching of the renal capsule, producing pain that classically starts in the ﬂank and radiates to the ipsilateral groin. For reasons that are incompletely understood, the pain of a ureteral stone is typically intermittent, rather than constant. Other symptoms include nausea, vomiting, and gross or microscopic hematuria. This constellation of symptoms is known as renal colic. Occasionally, the movement of a stone into the ureter can be associated with obstruction and infection, culminating in pyelonephritis (see Plate 5–5) and/or sepsis. In this situation, urgent relief of obstruction is required to decompress the collecting system and allow antibiotics to be excreted into the urine.
Most renal stones can be detected on plain abdominal radiographs because of their calcium content, although calcium-poor stones such as pure uric acids stones are radiolucent. The primary diagnostic imaging tool, however, is non–contrast enhanced CT, which has a 98% sensitivity for the detection of stones. If intravenous contrast is administered and excreted into the urine collecting system, stones may be obscured, since both stones and contrast have high attenuation.
If a stone is identiﬁed, microscopic analysis of urine may be helpful to determine stone composition, as characteristic crystals are sometimes seen.
|MAJOR SITES OF RENAL STONE IMPACTION|
Treatment. The treatment of a renal stone depends on its size, location, and associated symptoms. The majority of stones that enter the ureter will pass on their own, given enough time. The likelihood of spontaneous stone passage is higher for stones that are small and/or located in the distal ureter. The time interval to stone passage is variable, and intermittent episodes of pain may accompany stone transit. Once they reach the bladder, most stones can easily be voided, as the lumen of the urethra is much larger than that of the ureter.
Medications such as calcium channel blockers and -receptor antagonists have been shown to inﬂuence ureteral contractility and promote stone passage, thereby increasing the likelihood of spontaneous passage, reducing the time interval to passage, and decreasing the need for pain medication. A trial of these medications is indicated in patients with ureteral stones less than 1 cm in size, particularly if they are located in the lower part of the ureter at the time of diagnosis.
When a ureteral stone fails to pass or is too large to pass, or when pain becomes intolerable, surgical intervention is warranted. Many small to moderate-sized stones can be treated noninvasively, using shock waves focused on the stone under ﬂuoroscopic or ultrasound guidance (extracorporeal shockwave lithotripsy, see Plate 10-12). Repeated application of focused shock-waves causes stone fragmentation, which enables painless passage of fragments in the urine. Alternatively, stones can be removed using a ureteroscope (see Plate 10-33), which is passed through the urethra and bladder up to the site of the stone in the ureter. The stone is then fragmented with a laser or other device inserted through the working channel of the ureteroscope.
For large and/or complex stones, such as staghorn calculi (which occupy all or a large portion of the collecting system), a large endoscope is introduced percutaneously into the kidney through a small incision in the ﬂank. The stone is then fragmented and the fragments removed (percutaneous nephrostolithotomy, see Plate 10-13).
Prognosis. After a ﬁrst renal stone is diagnosed, there is a nearly 50% likelihood of recurrence over the next 5 to 10 years. With medical and dietary therapy, however, the recurrence rate can be signiﬁcantly reduced.
Prevention strategies generally aim to correct under-lying risk factors with diet or medication. Dietary changes that can lower the risk of calcium stones include an increase in ﬂuid intake (sufﬁcient to produce a urine volume of >2 L daily), limitation of salt intake (which reduces urinary calcium excretion), modest restriction of animal protein, and a reduction in consumption of oxalate-rich foods (such as nuts, chocolate, brewed tea, and dark green leafy vegetables). Severe dietary calcium restriction is discouraged in any stone former, but for patients with elevated urinary calcium levels, a modest reduction in calcium intake is recommended.
Medications can also help prevent stone formation. For patients with calcium stones, thiazide diuretics can help reduce urinary calcium excretion. For patients with uric acid stones, alkalizing agents such as potassium citrate can increase uric acid solubility. In the minority of patients with elevated urine uric acid levels, allopurinol may also be used.
Finally, underlying medical disorders that favor stone formation should also be treated, such as hypercalcemia associated with hyperparathyroidism.
Primary bladder stones form within the bladder and are distinct from stones that originate in the kidney and pass into the bladder. Although bladder stones were common in the past, improvements in nutrition have substantially reduced their incidence, since dietary phosphate deﬁciency and excess ammonia excretion can contribute to stone formation. In developing countries, however, bladder stones remain common.
In industrialized nations, bladder stone formation is usually related to urinary stasis or urinary infection with urea-splitting bacteria (e.g., Proteus mirabilis). Indeed, these conditions often coexist, since urinary stasis predisposes to infection. Bladder stones are typically com- posed of calcium phosphate, uric acid, or struvite.
The most common disorder associated with incomplete bladder emptying and bladder stone formation is benign prostatic hyperplasia (BPH). In affected patients, treatment consists of transurethral prostate resection and laser or pneumatic stone fragmentation. In the case of a very large prostate, open prostatectomy and bladder stone removal may be necessary.
Another disorder associated with bladder stone formation is neurogenic bladder (see Plate 8-2), which occurs when neurologic disorders such as spinal cord injury, multiple sclerosis, or spina biﬁda interfere with normal voiding. Patients with neurogenic bladder who have long-term indwelling catheters are particularly prone to bladder calculi because of their increased rate of infection with urea-splitting organisms. The bladder stones are most commonly treated with endoscopic fragmentation and removal, with open surgery only rarely performed. The risk of further stone formation can be decreased with intermittent rather than indwelling catheterization, increased hydration, and bladder irrigation with weakly acidic solutions, such as acetic acid. Antibiotics are rarely indicated because bacteriuria is essentially unavoidable, and overuse of anti- biotics may promote resistance.
The symptoms of bladder calculi are typically less obvious than those associated with kidney stones. Some patients may be completely unaware that they have a stone, while others may complain of urgency and frequency of urination, pelvic pain, or hematuria. These symptoms are also commonly associated with the underlying condition that leads to stone formation, such as bladder outlet obstruction or bladder infection.