The patient’s pain and accompanying nausea and vomiting symptoms are consistent with renal colic. Microscopic hematuria is thought to be consistent with urolithiasis. These manifestations should be highly suspicious of obstruction due to urinary tract stones. Abdominal plain radiographs fail to show pathologic dense calcified shadows. However, only 90% of urinary tract stones are X-ray impermeable. Pure uric acid stones are translucent and will not show up on abdominal plain films. Further imaging is required to confirm the diagnosis. Intravenous urography has been done as a traditional test to evaluate low back pain and suspected obstructive stones. This patient did not undergo intravenous urography, which can confirm specific filling defects with delayed contrast excretion and formation of uric acid stones with or without light transmission.CT non-enhanced scans are better able to demonstrate uric acid stones. All urinary stones show significant attenuation images on CT scans, and CT attenuation values for uric acid stones are in the 300-400 range. In many research institutions, spiral non-enhanced CT scans are replacing venography as the first imaging test to evaluate the cause of low back pain. CT scans and intravenous urography have the same value in determining the presence of obstruction, but CT is better at confirming the presence of stones. The pH of the urine is also a key indicator when diagnosing uric acid stones. Uric acid is the main end metabolite of purine. The formation of uric acid stones is associated with the supersaturation of undissociated uric acid in the urine. Urine PH and uric acid concentration are the main determinants of urinary supersaturation. At urine pH below 5.5, most uric acid is insoluble and in a non-dissociated state, leading to uric acid crystals and stone formation. The concentration of uric acid depends on the volume of urine and the amount of uric acid excreted. A chronic state of dehydration can lead to a decrease in urine output and an increase in uric acid excretion caused by endogenous production and a diet rich in purine foods (e.g. meat, poultry, fish, etc.). Unlike other more common stones, uric acid stones can be successfully treated with medications. Increasing urine pH and reducing uric acid concentrations by increasing urine output and decreasing uric acid excretion are the main goals of treatment. Alkalinization of the urine to achieve a urinary pH of 6.5-7 can be accomplished exclusively with oral medications such as potassium citrate or sodium bicarbonate, or with an intravenous infusion of 1/6 molar lactate. Urine output needs to reach 2 liters throughout the day, and lower uric acid excretion is achieved by consuming foods low in purines or by using allopurinol (a xanthine oxidase inhibitor). Occasionally, surgical intervention is required. Severe obstruction, intractable renal colic, co-infection and renal insufficiency are all indications for surgical intervention to drain the urine. A CT scan of this patient revealed a high-density shadow in the distal part of the right ureter, a ureteral stone (see figure, arrow). The second sign of obstruction was increased ipsilateral renal cortical thickness. He was accompanied by infection, which manifested as fever, elevated white blood cells and pusuria. Therefore, retrograde insertion of a ureteral stent tube was required to lower the pressure in the obstructed kidney. While the symptoms were relieved, the stone was treated with drug lysis.