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Nephrolithiasis specifically refers to calculi in the kidneys, but this article discusses both renal calculi, shown below, and ureteral calculi (ureterolithiasis). Ureteral calculi almost always originate in the kidneys, although they may continue to grow once they lodge in the ureter.
Patients with urinary calculi may report pain, infection, or hematuria. Small nonobstructing stones in the kidneys only occasionally cause symptoms. If present, symptoms are usually moderate and easily controlled.
The passage of stones into the ureter with subsequent acute obstruction, proximal urinary tract dilation, and spasm is associated with classic renal colic.
Renal colic is characterized by undulating cramps and severe pain and is often associated with nausea and vomiting.
As the stone travels through the ureter, the pain moves from the flank to the lower abdomen, down to the groin, and eventually to the scrotal or labial areas.
Associated irritative bladder symptoms are common when the stone is located in the distal or intramural ureter.
Staghorn refers to the presence of a branched kidney stone occupying the renal pelvis and at least one calyceal system. Such calculi usually manifest as infection and hematuria rather than as acute pain.
Asymptomatic bilateral obstruction, which is uncommon, manifests as symptoms of renal failure.
Important historical features are as follows:
Duration, characteristics, and location of pain
History of urinary calculi
Prior complications related to stone manipulation
Urinary tract infections
Loss of renal function
Family history of calculi
Solitary or transplanted kidney
Chemical composition of previously passed stones
Physical
Dramatic costovertebral angle tenderness is common; this pain can move to the upper or lower abdominal quadrant as a ureteral stone migrates distally.
Peritoneal signs are usually absent-an important consideration in distinguishing renal colic from other sources of flank or abdominal pain.
Findings should correlate with the reports of pain, so that complicating factors (eg, urinary extravasation, abscess formation) can be detected.
Beyond this, the specific location of tenderness does not always correlate with the exact location of the stone, although the calculus is often in the general area of maximum discomfort.
Causes
Most research on the etiology and prevention of urinary tract stone disease has been directed toward the role of elevated urinary levels of calcium, oxalate, and uric acid in stone formation, as well as reduced urinary citrate levels.
Hypercalciuria is the most common metabolic abnormality. Some cases of hypercalciuria are related to increased intestinal absorption of calcium (associated with excess dietary calcium and/or overactive calcium absorption mechanisms), some are related to excess resorption of calcium from bone (ie, hyperparathyroidism), and some are related to an inability of the renal tubules to properly reclaim calcium in the glomerular filtrate (renal-leak hypercalciuria).
Magnesium and especially citrate are important inhibitors of stone formation in the urinary tract. Decreased levels of these in the urine predispose to stone formation.
A low fluid intake, with a subsequent low volume of urine production, produces high concentrations of stone-forming solutes in the urine. This is an important, if not the most important, environmental factor in kidney stone formation.
The exact nature of the tubular damage or dysfunction that leads to stone formation has not been characterized.
The most common findings on 24-hour urine studies include hypercalciuria, hyperoxaluria,hyperuricosuria, hypocitraturia, and low urinary volume. Other factors, such as high urinary sodium and low urinary magnesium concentrations, may also play a role. To identify these risk factors, a 24-hour urine profile, including appropriate serum tests of renal function, uric acid, and calcium, is needed. Such testing is available from various commercial laboratories. A finding of hypercalcemia should prompt follow-up with an intact parathyroid hormone study to evaluate for primary and secondary hyperparathyroidism.