Urinary calcuria (stones) can be formed from several materials, including calcium (the most common form), uric acid, magnesium ammonium phosphate (struvite), and cystine stones.
Calcium stones can be caused by several mechanisms, including primary parathyroidism, sarcoidosis, vitamin D intoxication, hyperthyroidism, renal tubular acidosis, multiple myeloma, metastatic cancer, and primary hyperoxaluria. Idiopathic hypercalciuria is a hereditary condition, is present in 50% of men and 75% of women who form calcium stones. Several conditions predispose to forming calcium stones.
Decreased urinary citrate (hypocitricuria) promotes calcium stones because citrate normally binds 50% of urinary calcium as a soluble calcium citrate salt.
Excessive urinary oxylate (hyperoxaluria) is caused by excess ingestion of oxalate-containing foods (e.g., rhubarb, spinach, cocoa, nuts, pepper, and tea) or excess oxalate absorption due to a variety of enteric diseases (e.g., bacterial overgrowth syndromes, chronic pancreatic or biliary disease, or ileojejunal surgery).
Excess urinary uric acid (hyperuricosuria) promotes urinary stone formation because uric acid crystals provide a nidus on which calcium oxalate crystals can orient themselves and grow. These patients can form what appear to be pure calcium stones or mixed calcium and uric acid stones, because the uric acid nidus is not measurable by commercial laboratories. The cause of hyperuricosuria is usually excess consumption of purine, in the form of meat, fish, and poultry. Uric acid stones occur because of increased urine acidity in which undissociated uric acid crystallizes. Increasing the urine pH to between 6 and 6.5 with oral alkalinizing agents (such as sodium bicarbonate, or sodium or potassium citrate) or reducing purine intake and increasing water intake, are usually effective.
Magnesium ammonium phosphate stones (struvite) indicates the presence of urinary tract infection, with urea-splitting bacteria, usually of the Proteus species. The stones are loci of infection and must be treated as infected foreign bodies. In contrast to the other types of stones, infection stones occur mostly in women. Fastidious attention to even small numbers of urea-splitting bacteria as well as treatment of any metabolic causes of stone may delay the need for surgery.
Cystine stones are associated with defects in the transport of the amino acids cystine, lysine, arginine, and ornithine. Clinical disease is due solely to the insolubility of cystine, which forms stones. Three types of inheritance have been described. Conventional medical consists of a high fluid intake, even at night. Daily urine volume should exceed 3 Liters. Raising urine pH with alkali is helpful, provided the urine pH exceeds 7.5. A low-salt diet can reduce cystine excretion up to 40 percent. Captopril, which has a free sulfhydryl group to bind cysteine, has been used in a limited number of patients with some success. Low-methionine diets have not proved to be practical for clinical use, but patients should avoid protein gluttony.
Urinalysis (hematuria nearly 100%; if pH < 5.5 means uric acid, if pH > 7.5 means struvite); Chemistries (Calcium, phosphorus, electrolytes, uric acid, creatinine); Parathyroid hormone if serum calcium is high; Urine cystine if stone is not visible on plain x-ray; Urine culture if pyuria or fever is present.
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