Uric acid stones account for less than 10% of all urinary stones in the United States. Their prevalence is slightly higher in some parts of the world, namely some Middle Eastern countries; the cause is not well understood, and seasonal and genetic factors may play a role. The only mammals susceptible to uric acid stone formation are humans and Dalmatian hounds. For most mammals, uric acid, a major end product of purine metabolism, is broken down into its water-soluble form (uric acid is insoluble in water) by the liver enzyme uricase. Humans, however, lack this enzyme. Although Dalmatian hounds contain this enzyme, the low reabsorption of uric acid by the proximal tubule allows a large amount of uric acid to be excreted into the urine. Under normal metabolic conditions, uric acid is filtered by the glomerulus and rapidly absorbed by the epithelium of the proximal tubule. Uric acid is actively secreted in the distal tubule rather than entering recirculation and being further broken down in the liver. It ultimately exists in two forms: a very insoluble non-ionized form and urate, which is almost 20 times more soluble than the former. The proportion of uric acid in its non-ionized form reflects the pKa value of uric acid and the magnitude of the pH of the urine. The pKa value of uric acid is approximately 5.5. This means that when the pH of urine is 5.5, exactly half of the uric acid is present in the insoluble, non-ionized form. In contrast, the urine excreted by humans under normal conditions is acidic compared to serum (normal urine pH is 6-7), which is just above the pKa value of uric acid and therefore does not become supersaturated and crystallized. As the urine becomes more acidic, uric acid becomes more and more present in a non-soluble form and crystallization occurs. For example, when the pH of urine is 5, precipitation can occur with as little as 60 mg of uric acid per liter of urine. However, an average person excretes 400 mg of uric acid per day, which requires a daily urine volume of more than 6 liters to avoid crystallization! Similarly, when the pH is 6, urine saturation can only occur when the urine contains 220mg of uric acid per liter. The remaining ionic form of urate reacts with potassium and sodium to form urates. Potassium urate is more soluble than sodium urate; therefore, elevated sodium concentrations in urine are not conducive to dissolution, while elevated potassium concentrations are conducive to dissolution. Other factors also have an effect on the formation of uric acid stones. It is well established that the pH of urine increases after a meal in normal subjects. There is evidence that people with a tendency to develop uric acid stones are unable to alkalize their urine. Low urine volume does supersaturate the urine, and people with acidic urine and low urine volume have a higher incidence. Such patients include those with severe inflammatory bowel disease or those who have undergone ileostomy, where the normal water and bicarbonate reabsorption mechanisms of the colon do not work. Uric acid stone disease can be divided into four types. The first type is a combination of diseases with elevated blood uric acid, including primary gout and other metabolic diseases such as Lesch-Nyhan syndrome. About one quarter of gout patients have uric acid stones. Patients with an increased rate of cell renewal (such as those with myeloproliferative disorders or those undergoing chemotherapy) are also prone to hyperuricemia due to the release of large amounts of purines during cell collapse. The second category is seen in patients who are prone to dehydration (e.g., patients with chronic diarrhea, ulcerative colitis, severe radiation proctocolitis, or those who have undergone ileostomy). The third category includes patients who have hyperuricuria but do not have elevated blood uric acid. Hyperuricemia is defined as a 24-hour urinary uric acid excretion of more than 800 mg in men and more than 750 mg in women. Certain medications, such as thiazide diuretics, can increase uric acid excretion, which can lead to stone formation. The fourth group of patients has normal serum uric acid and no hyperuricemia despite stone formation. These patients all have typically persistent acidic urine and are referred to as having idiopathic uric acid stone disease. Uric acid stones usually present with the typical symptoms of renal colic. Pure uric acid stones are translucent on x-ray plain films. However, when the stones are covered with a calcium-containing shell or are very large, they may show some degree of turbidity. Uric acid stones appear as translucent filling defects on excretory and retrograde pyelograms and must therefore be differentiated from tumors, blood clots, and necrotic decaying renal papillae. Recently CT has been more commonly used in patients with suspected urolithiasis. In combination with clinical findings, uric acid stones can be considered if a denser shadow is found in the urinary tract that is lower than bone or typical of calcium-containing stones. Therefore CT scan is helpful when there is no calcified shadow on plain film. The combination of typical renal colic, acidic urine and the radiological findings described above fully justify a definitive diagnosis of uric acid stones. Uric acid stones should be treated conservatively, including increasing urine output and alkalinizing the urine. Conservative treatment should be used first in all patients except in cases where early surgery is necessary. Surgery is indicated for those patients for whom drug therapy has failed. Patients should be encouraged to drink large amounts of water (at least 64 ounces per day) to ensure a daily urine output of 3 liters. The urine can be alkalinized by several methods. Giving sodium bicarbonate 50-100 mEq per day is a fairly economical means. The urine pH should be maintained at 7.0-7.5. Potassium citrate 15 mEq is also given three to four times a day. This method is particularly suitable for patients with normal renal function, due to the fact that potassium citrate is more soluble than sodium salts. Transvenous alkalinization of the urine is sometimes necessary, especially if the patient cannot tolerate oral preparations. In addition, patients should be warned to avoid over-alkalizing the urine because overly alkalized urine can lead to calcium phosphate stone precipitation. In patients with hyperuricemia, intake of purine-rich foods (e.g., red meat and chicken) should be limited. In addition, allopurinol should be given. Allopurinol is a xanthine oxidase inhibitor that inhibits the synthesis of uric acid in purine metabolism. Finally, if none of the above methods are effective, the patient may also be advised to use instrumental lithotripsy; these techniques include endoscopic lithotripsy and extracorporeal lithotripsy. These stones are usually a mixture of uric acid and calcium and are therefore not effective against conservative therapies.