Renal calculi
Although they may form anywhere in the urinary tract, renal calculi (sometimes referred to as kidney stones) most commonly develop in the renal pelvis or calyces but may also be found in the bladder. Calculi formation occurs when substances that normally are dissolved in the urine (calcium oxalate, calcium phosphate, magnesium ammonium phosphate [struvite] and, occasionally, uric acid or cystine) precipitate. Renal calculi vary in size and may be solitary or multiple.
About 1 in 1,000 Americans develops renal calculi. They’re more common in males than in females and rare in blacks and children.
Causes
Renal calculi are particularly prevalent in certain geographic areas such as the southeastern United States (called the ‘stone belt’), possibly because a hot climate promotes dehydration and concentrates calculus-forming substances or because of regional dietary habits. Although the exact cause of renal calculi is unknown, predisposing factors include:
dehydration—Decreased water excretion concentrates calculus-forming substances.
infection—Infected, scarred tissue may be a site for calculus development. In addition, infected calculi (usually magnesium ammonium phosphate or staghorn calculi) may develop if bacteria serve as the nucleus in calculus formation. Struvite calculus formation commonly results from Proteus infections, which may lead to the destruction of renal parenchyma.
changes in urine pH—Consistently acidic or alkaline urine may provide a favorable medium for calculus formation, especially for magnesium ammonium phosphate or calcium phosphate calculi.
obstruction—Urinary stasis allows calculus constituents to collect and adhere, forming calculi. Obstruction also encourages infection, which compounds the obstruction.
immobilization—Immobility from spinal cord injury or other disorders allows calcium to be released into the circulation and, eventually, to be filtered by the kidneys.
metabolic factors—Hyperparathyroidism, renal tubular acidosis, elevated uric acid (usually with gout), defective metabolism of oxalate, a genetically caused defect in metabolism of cystine, and excessive intake of vitamin D or dietary calcium may predispose a person to renal calculi.
medications—Some medications known to cause renal calculi include antacids, laxatives, aspirin, and acetazolamide (Diamox). Other possible causes of renal calculi include multiple myeloma, Paget’s disease, bone cancer, Cushing’s disease or syndrome (loss of bone calcium), and milk-alkali syndrome.
Complications
Calculi may either remain in the renal pelvis and damage or destroy renal parenchyma, or they may enter the ureter; large calculi in the kidneys cause pressure necrosis. In certain locations, calculi cause obstruction, with resultant hydronephrosis, and tend to recur. Intractable pain and serious bleeding also can result from calculi and the damage they cause.
Assessment
Assessment findings vary with the size, location, and cause of the calculi. The key symptom of renal calculi is severe pain, which usually results from obstruction: Large, rough calculi occlude the opening to the ureteropelvic junction and increase the frequency and force of peristaltic contractions. The patient usually reports that the pain travels from the costovertebral angle to the flank and then to the suprapubic region and external genitalia (classic renal colic pain). Pain intensity fluctuates and may be excruciating at its peak.
The patient with calculi in the renal pelvis and calyces may complain of more constant, dull pain. He may also report back pain (from calculi causing obstruction within a kidney) and severe abdominal pain (from calculi traveling down a ureter). The patient with severe pain also typically complains of nausea, vomiting and, possibly, fever and chills.
You may note hematuria (when calculi abrade a ureter), abdominal distention and, rarely, anuria (from bilateral obstruction or, in the patient with one kidney, unilateral obstruction).
Diagnostic tests
Diagnosis is based on clinical features and the following tests:
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