Pathophysiology

The precise cause of urinary stones is unknown. Theories regarding urinary calculi formation include urinary supersaturation of solute followed by crystal precipitation, or a decrease in the normal urinary proteins that inhibit crystal growth. Urinary stasis from physical anomaly, neurogenic bladder, or catheter placement, and the presence of foreign bodies (e.g., surgical suture) may provide the environment for stone growth.

Approximately 75 percent of calculi are composed of calcium, occurring in conjunction with oxalate, phosphate, or a combination of both.2 These stones may develop as a result of increased urinary excretion of a given solute. Calcium excretion is elevated in conditions such as high dietary calcium intake, immobilization syndrome, or hyperparathyroidism. Oxalate excretion is enhanced in patients with bowel disease (e.g., Crohn's disease or ulcerative colitis) and as a result of small-bowel bypass surgery. Ten percent of stones are magnesium-ammonium-phosphate (struvite).2 These stones are often associated with infection by urea-splitting bacteria and are the most common cause of staghorn calculi. Staghorn calculi are large stones that form a cast of the renal pelvis. Antibiotics are ineffective, since there is poor penetration into the calculus. Uric acid causes 10 percent of uroliths. 2 Cystine and other uncommon minerals comprise the remainder.2

Passage of stones through the urinary tract may be slowed or halted by areas of anatomic narrowing or bending. Progressing proximally to distally, common areas of impaction include the renal calyx, ureteropelvic junction (where the ureter passes over the pelvic brim and arches over the iliac vessels), and the ureterovesical junction (UVJ). The UVJ has the smallest diameter of the urinary tract and is a common location for impacted stones. The posterior pelvis in women, especially where the ureter is crossed anteriorly by the pelvic blood vessels and broad ligament, may slow the passage of a calculus.

If a stone causes acute ureteral obstruction, after an initial rise of renal blood flow and intraureteral pressure, both parameters decline. Concurrently, there is a proportional increase in renal blood flow to the contralateral kidney. These effects are reversible in acute unilateral obstruction if the obstruction is relieved. However, after prolonged obstruction (several weeks), irreversible renal damage occurs. 2 The contralateral kidney is usually able to maintain excretory requirements throughout the course. Therefore, blood urea nitrogen and creatinine levels do not rise even though there is only one functional kidney.

The probability of spontaneous passage of stones is determined by multiple factors, including size, shape, location, and degree of ureteral obstruction. Stones with diameters less than 4 mm will pass in approximately 90 percent of cases, while 50 percent of stones 4 to 6 mm in diameter pass, and only 10 percent of stones exceeding 6 mm pass spontaneously.2 Bizarrely shaped or irregular stones with spicules and sharp edges will have a lower passage rate. Rates of passage based on the location of the stone at first diagnosis are approximately 20, 50, and 70 percent for the proximal, middle, and distal ureter, respectively. 6 Finally, with complete obstruction there is a lower rate of spontaneous passage than if the blockage is partial.

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