symptom of kidney stones : First Stone Episode
Approximately 80 percent of kidney stones contain calcium. The majority of these stones are composed of calcium oxalate, with a minority containing calcium phosphate or admixtures of oxalate and phosphate salts. About 10 percent of stones are composed of uric acid (sometimes associated with a history of gout) or mixed uric acid and calcium. Another 10 percent are struvite stones, which develop exclusively in patients with urinary tract infections caused by urease-producing organisms, most typically Proteus species. Cystine accounts for no more than 1 percent of all stones. Cystine stones arise only in patients with cystinuria, an autosomal recessive disorder.1
Stone analysis is inexpensive (about $25) and is worth performing for first stones, those formed during preventive treatment and those occurring in conjunction with infection. If no stone is available for analysis, qualitative screening for urinary cystine should be performed at least once in younger patients.
Risk factors for nephrolithiasis are summarized in Table 2. Identifying a familial incidence of stones is useful because it indicates an increased risk of recurrence. Environmental or occupational factors and bowel surgeries such as ileostomy may be predisposing factors because of low urine volumes. Residents of the "stone belt" in the southeastern part of the United States also appear to be at higher risk for stone formation.3 In the stone belt, two mechanisms have been implicated: the hot climate causes increased perspiration and reduced urine volume, and exposure to sunlight activates vitamin D, stimulating the absorption of dietary calcium.
Drugs associated with stone formation include triamterene (Dyrenium) and the sulfonamides, which have low solubility. Calcium and vitamin D supplements cause hypercalciuria, and carbonic anhydrase inhibitors, which are used to treat glaucoma, increase the urinary pH and precipitate calcium phosphate. Indinavir (Crixivan), a protease inhibitor, can also crystallize and form stones in the urinary tract.4
Other important risk factors for calcium stones include hypercalciuria, hyperoxaluria and hypocitraturia. The major risk factors for uric acid stones are a low urinary pH and hyperuricosuria. Several dietary factors may contribute to these abnormalities and should be sought in the history.5,6
Animal protein is a major dietary constituent responsible for the relatively high prevalence of stones in populations of developed countries. Several mechanisms have been identified. Protein ingestion increases renal acid excretion. This, in turn, increases renal reabsorption of potential base, such as citrate, which is an endogenous inhibitor of calcium stone formation. Acid loads may be buffered in part by bone, which releases calcium to be excreted by the kidney. Finally, acid loading directly inhibits renal calcium reabsorption.5
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