Kidney stones are one of the most common urologic problems. In the United States, ~13% of men and 7% of women will develop a kidney stone during their lifetimes, and the prevalence is increasing throughout the industrialized world.
Calcium salts, uric acid, cystine, and struvite are the constituents of most kidney stones in the western hemisphere (Chap. e14). Calcium oxalate and calcium phosphate stones make up 75–85% of the total (Table 287-1) and those constituents may be admixed in the same stone. Calcium phosphate in stones is usually hydroxyapatite [Ca5(PO4)3OH] or, less commonly, brushite (CaHPO4H2O), although the incidence of brushite stones is increasing.
Table 287-1 Major Causes of Renal Stones
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Table 287-1 Major Causes of Renal Stones
|Stone Type and Causes||Percent of all Stonesa||Percent Occurrence of Specific Causesa||Ratio of Males to Females||Etiology||Diagnosis||Treatment|
|Calcium stones||75–85||2:1 to 3:1|
|Idiopathic hypercalciuria||50–55||2:1||? Hereditary||Normocalcemia, unexplained hypercalciuriab||Low-sodium, low-protein diet; thiazide diuretics|
|Hyperuricosuria||20||4:1||Diet||Urine uric acid >750 mg per 24 h (women), >800 mg per 24 h (men)||Allopurinol or low-purine diet|
|Primary hyperparathyroidism||3–5||3:10||Neoplasia||Hypercalcemia with nonsuppressed parathyroid hormone||Surgery|
|Distal renal tubular acidosis||Rare||1:1||Hereditary or acquired||Hyperchloremic acidosis, minimum urine pH >5.5||Alkali replacement|
|Dietary hyperoxaluria||10–30||1:1||High-oxalate diet or low-calcium diet||Urine oxalate >40 mg per 24 h||Low-oxalate, normal-calcium diet|
|Enteric hyperoxaluria||∼1–2||1:1||Bowel surgery||Urine oxalate >75 mg per 24 h||Low-oxalate diet and oral calcium pills|
|Primary hyperoxaluria||Rare||1:1||Hereditary||Urine oxalate and glycolic or l-glyceric acid increased||Fluids, pyridoxine, citrate and neutral phosphate|
|Hypocitraturia||20–40||1:1 to 2:1||? Hereditary, diet||Urine citrate <320 mg per 24 h||Alkali supplements|
|Idiopathic stone disease||20||2:1||Unknown||None of the above present||Oral phosphate, fluids|
|Uric acid stones||5–10|
|Metabolic syndrome||∼30||1:1||Diet||Glucose intolerance, obesity, hyperlipidemia||Alkali and allopurinol if daily urine uric acid >1000 mg|
|Gout||∼30||3:1 to 4:1||Hereditary||Clinical diagnosis||Alkali and allopurinol|
|Idiopathic||∼30||1:1||? Hereditary||Uric acid stones, no gout||Alkali and allopurinol if daily urine uric acid >1000 mg|
|Dehydration||?||1:1||Intestinal, habit||History, intestinal fluid loss||Alkali, fluids, reversal of cause|
|Rare||Males only||Hereditary||Reduced hypoxanthine-guanine phosphoribosyltrans ferase level||Allopurinol|
|Cystine stones||1||1:1||Hereditary||Stone type; elevated cystine excretion||Massive fluids, alkali, D-penicillamine if needed|
|Struvite stones||5||1:3||Infection||Stone type||Antimicrobial agents and judicious surgery|
Calcium stones are more common in men; the average age of onset is the third to fourth decade. Approximately 50% of people who form a single calcium stone form another within the next 10 years, and some form multiple recurrent stones. The average rate of new stone formation in recurrent stone formers is about one stone every 3 years. Uric acid stones account for 5–10% of kidney stones and are also more common in men. Five percent of stones are struvite, whereas cystine stones are uncommon, accounting for ~1% of cases in most series of nephrolithiasis.
As stones grow on the surfaces of the renal papillae or within the collecting system, they do not necessarily produce symptoms. Asymptomatic stones may be discovered during the course of radiographic studies undertaken for unrelated reasons. Stones are a common cause of isolated hematuria. Stones become symptomatic when they enter the ureter or occlude the ureteropelvic junction, causing pain and obstruction.
A stone can traverse the ureter without symptoms, but passage usually produces pain and bleeding. The pain begins gradually, usually in the flank, but increases over the next 20–60 min to become so severe that narcotics may be needed for its control. The pain may remain in the flank or spread downward and anteriorly toward the ipsilateral loin, testis, or vulva. A stone in the portion of the ureter within the bladder wall causes frequency, urgency, and dysuria that may be confused with urinary tract infection. The vast majority of ureteral stones <0.5 cm in diameter pass spontaneously.
Helical computed tomography (CT) scanning without radiocontrast enhancement is now the standard radiologic procedure for diagnosis of nephrolithiasis. The advantages of CT include detection of uric acid stones in addition to the traditional radiopaque stones, no exposure to the risk of radiocontrast agents, and possible diagnosis of other causes of abdominal pain in a patient suspected of having renal colic from stones. Ultrasound is not as sensitive as CT in detecting renal or ureteral stones. Standard abdominal x-rays may be used to monitor patients for formation and growth of kidney stones, as they are less expensive and provide less radiation exposure than CT scans. Calcium, cystine, and struvite stones are all radiopaque on standard x-rays, whereas uric acid stones are radiolucent.
Struvite, cystine, and uric acid stones often grow too large to enter the ureter. They gradually fill the renal pelvis and may extend outward through the infundibula to the calyces themselves. Very large staghorn stones can have surprisingly few symptoms and may lead to the eventual loss of kidney function.
Calcium stones grow on the papillae. Most break loose and cause colic, but they may remain ...