Nephrolithiasis

Kidney stones are concretions of different mineral salts mixed with an organic matrix that form in the upper urinary tract. As a stone moves from the kidney to the ureter, it can present with renal colic symptoms, and may cause urinary tract obstruction and/or infection. In fact, acute passage of a kidney stone is one of the leading reasons for visits to an emergency room. Over the past four decades, the lifetime prevalence of nephrolithiasis has more than doubled in the United States (and several developed countries), afflicting around 11% of men and 7% of women. Unless the underlying etiology of stone formation is adequately addressed, kidney stones can recur at a rate of around 50% ten years after initial presentation. The evaluation of a kidney stone former requires an extensive medical history (to identify environmental, metabolic, and/or genetic factors contributing to stone formation), imaging studies to evaluate and track stone burden, and laboratory studies (serum and urinary chemistries, stone composition analysis) to guide lifestyle and pharmacological therapy. The majority of kidney stones are composed of calcium (calcium oxalate and/or calcium phosphate), either pure or in combination with uric acid. Calcium oxalate stones can be caused by hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, and/or low urine volume. Calcium phosphate stones occur in patients with hypercalciuria, hypocitraturia, an elevated urine pH, and/or low urine volume. In addition to lifestyle changes (increasing fluid intake, reduction in salt intake, moderation of calcium and animal protein intake), pharmacological therapy directed at the underlying metabolic abnormality (thiazides for hypercalciuria, potassium citrate for hypocitraturia, xanthine oxidase inhibitors for hyperuricosuria) can significantly reduce calcium stone recurrence rate. Pure uric acid stones account for 8-10% of all stones, although their prevalence is significantly greater in stone formers with type 2 diabetes and/or the metabolic syndrome. Uric acid stones are primarily caused by an excessively acidic urine, and urinary alkalinization with medications such as potassium citrate can dissolve uric acid stones and prevent recurrent uric acid nephrolithiasis. Cystine stones result from inactivating mutations in genes that encode renal tubular transporters that reabsorb the amino acid cysteine, typically present in childhood, are highly recurrent, and require aggressive control of cystinuria with specific pharmacological therapy. Infection (struvite) stones often present as staghorn, and require careful surgical removal of all of the stone material. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.