You are in: eMedicine Specialties > Radiology > GENITOURINARY Nephrolithiasis/UrolithiasisArticle Last Updated: Feb 21, 2007AUTHOR AND EDITOR INFORMATIONAuthor: J Kevin Smith, MD, PhD, Vice Chairman for Veterans Affairs, Associate Professor, Department of Diagnostic Radiology, University of Alabama at Birmingham Coauthor(s): Mark E Lockhart, MD, Assistant Professor, Department of Radiology, University of Alabama at Birmingham; Nicole W Berland, BA, Outreach Support for Hurricane Relief, Collat Jewish Family Service; Philip Kenney, MD, Chief of GU Section of Diagnostic Radiology, Professor, Department of Diagnostic Radiology, University of Alabama at Birmingham Editors: Steven Perlmutter, MD, FACR, Clinical Associate Professor, Radiology Residency Program Director, Radiology Medical Director, Department of Radiology, University Hospital at Stony Brook; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Joshua A Becker, MD, Professor, Department of Radiology, New York University School of Medicine; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center Author and Editor Disclosure Synonyms and related keywords: urinary lithiasis, upper urinary tract stone disease, renal stones, kidney stones, urinary stones, ureteral stones, renal calculi, urinary calculi, kidney calculi, ureteral calculi, renal calculus disease, urinary calculus disease INTRODUCTIONBackgroundPassage of a urinary stone is the most common cause of acute ureteral obstruction and affects as many as 12% of the population. The pain may be some of the most severe pain that humans experience, and complications of stone disease may result in severe infection; renal failure; or, in rare cases, death. PathophysiologyIn patients with stone disease, more than 1 of 3 general mechanisms is likely to be active. These include the following: (1) the possible presence or abundance of substances that promote crystal and stone formation; (2) a possible relative lack of substances to inhibit crystal formation; and (3) a possible excessive excretion or concentration of salts in the urine, which leads to supersaturation of the crystallizing salt. The greater the degree of supersaturation, the greater the rate of growth of the calculi. Stasis or anatomic factors can also contribute to the development of stone disease. These include ureteropelvic junction (UPJ) obstruction, horseshoe or ectopic kidney, autosomal dominant polycystic kidney disease, and vesicoureteral reflux. Calyceal diverticula, the result of anomalous budding of the calyceal system, is also associated with stone disease. In 10-40% of calyceal diverticula, stones are present. These range from a few large calculi to many tiny seed calculi and to the microscopic "milk of calcium." Medullary sponge kidney is another common anatomic cause of renal calculi. The pathologic process in medullary sponge kidney is renal tubular ectasia. Calculi form in approximately 50% of patients. The calcifications form in the medulla but frequently pass into the collecting system. They are usually bilateral and diffuse, but they may also be unilateral or segmental. On intravenous urography (IVU), pyramidal clusters of calculi within the dilated tubules classically become obscured or appear enlarged after contrast material surrounds them in the dilated tubules. Calcium stones account for 75-85% of urinary stones. Approximately one half of calcium stones are composed of a mixture of calcium oxalate and calcium phosphate. They demonstrate intermediate fragility to extracorporeal shock wave lithotripsy (ESWL). Approximately three eighths of calcium stones are formed of only calcium oxalate dihydrate. These may be spiculated, dotted, mulberry, or jackstone in appearance. Usually, these stones are fragile in response to ESWL. The remaining one eighth of stones are composed of calcium phosphate (apatite) or calcium monohydrate. These stones are the densest and, consequently, the least responsive to ESWL. Calcium stones have numerous causes. Approximately 85% of calcium stones are idiopathic, or primary. Idiopathic hypercalciuria occurs in more than one half of patients with calcium oxalate stones. Most causes of hypercalciuria are absorptive. Increased absorption in individuals after a normal diet causes an elevation of serum calcium levels and a suppression of parathyroid function as an abnormal response to vitamin D. Approximately 10% of cases of primary hypercalciuria are renal in origin. The inability of the kidney to conserve calcium results in low serum calcium concentrations, which stimulate parathormone secretion. The remaining 15% of calcium stones are secondary to some discernible etiology. Most commonly, they result from hyperparathyroidism, which is found in 5-10% of patients with stones. In this situation, hypercalcemia and increased absorption lead to hypercalciuria. Patients with the stones are treated with surgical removal of the parathyroid adenoma or hyperplasia. Calcium stones can also occur in approximately 15% of patients with sarcoidosis in whom the production of activated vitamin D by macrophages is abnormal. Renal tubular acidosis (RTA) is an additional fairly common secondary cause of calcium stones. In type I (distal) RTA, kidneys have a decreased ability to lower urine pH levels, which may be primary or secondary to a variety of renal injuries. The injured distal tubule loses the ability to maintain the hydrogen-ion gradient. This, in turn, causes alkaline urine, hypercalciuria, and hyperphosphaturia. Nephrocalcinosis or urolithiasis is seen in as many as 70% of patients with type I RTA. Conversely, type II (proximal) RTA is associated with increased bicarbonate loss, which helps keep stones from forming. Type IV RTA commonly is seen in medical renal disease and does not predispose patients to stone formation. Immobilization of an individual causes rapid mobilization of the calcium in bones, and this is an important mechanism in patients with spinal cord injury, who may develop stones within weeks to months of immobilization. Hyperoxaluria is another, less common, secondary cause of calcium stone formation and most often results from inflammatory bowel disease, bowel surgery, vitamin C overdose, or renal failure. Primary hyperoxaluria is a rare autosomal recessive disease. Other secondary causes include milk-alkali syndrome, use of steroids, Cushing syndrome, hypervitaminosis D, paraneoplastic phenomenon, and multiple myeloma. Magnesium ammonium phosphate (struvite) stones account for approximately 10-20% of urinary stones. These stones are lucent but complex with calcium phosphate. On occasion, they enlarge and branch (staghorn). Although they fragment easily, patients with these stones usually are treated with percutaneous fragmentation and extraction because of the large size of the stones and, usually, the presence of infection. Struvite stones are caused by urea-splitting bacteria such as Proteus, Klebsiella, and Pseudomonas species. However, as many as one half of patients have an underlying metabolic cause for stone disease; therefore, metabolic evaluation is indicated. Combined obstruction and infection frequently cause renal destruction and, potentially, renal failure if both kidneys are affected. Uric acid stones account for 5-10% of urinary stones. These small smooth stones usually appear radiolucent on conventional radiographs but opaque on CT scans. Predisposing factors include acidic concentrated urine, excess urinary uric acid, small-bowel disease or resection, gout, and cell lysis (eg, resulting from treatment of leukemia or from starvation). Treatment and prevention for these stones is alkalinization and dilution of the urine. Cystine stones account for only approximately 1% of urinary stones. These ground-glass stones, which result from cystinuria (a rare autosomal recessive metabolic disorder), are homogeneous; less opaque; and less fragile than other stones, especially if they are smooth. Several other less common forms of urolithiasis may produce stones that appear relatively lucent, even on CT scans. Inspissation of indinavir, an antiretroviral protease inhibitor used to treat HIV infection, may cause stones that appear lucent on CT scans. Matrix stones formed from inspissated mucoproteins in patients with a chronic Proteus infection may demonstrate soft tissue attenuation on CT scans. Stones can also be caused by metabolic byproducts and drugs (eg, sulfa drugs, salicylates, triamterene ephedrine). FrequencyUnited StatesRenal calculi occur in 5-12% of the American population, and they are bilateral in 10-15% of patients. The prevalence of urinary lithiasis is as high as 2-3% in the general population. InternationalA slightly lower prevalence of urinary stones is found in less developed countries, possibly because of diets lower in protein. Mortality/Morbidity
RaceUrinary stones occur more often in white populations than in black populations. They are also more prevalent in highly developed countries, possibly as a result of a higher protein diet. SexMales are at a greater risk than females, with a male-to-female ratio of 3:1 (except for struvite stones and in black populations). AgeStones are uncommon but not unknown in children. The peak age for development is in persons aged 40-60 years. Clinical DetailsAcute ureteral obstruction by stone causes severe colicky (intermittent) flank pain that can radiate throughout the groin, testicles, back, and periumbilical region. Some patients with renal calculi may have no symptoms at all. Hematuria usually occurs. It can be intermittent or persistent and microscopic or gross. However, as many as 10% of patients with acute stones may not have hematuria. Occasionally, recurrent infection may result in pyelonephritis or abscess. Stones can result in renal scarring, damage, and renal failure. Preferred ExaminationThe goals of imaging are to determine the presence of stones within the urinary tract, evaluate for complications, estimate the likelihood of stone passage, confirm stone passage, assess the stone burden, and evaluate disease activity. When acute flank pain suggests the passage of a urinary stone, many methods of examination can be used. Often, conventional radiography is initially used to screen for stones, bowel abnormalities, or free intra-abdominal air. Radiographs can also be used to monitor the passage of visible stones. IVU (excretory urography) provides important physiologic information regarding the degree of obstruction. Ultrasonography (US) is useful in young or pregnant patients and in patients allergic to iodinated contrast material. US is also helpful in problem solving. All of these methods have become less useful with the advent of more sensitive and specific nonenhanced CT scanning. When CT is available, it is now considered the examination of choice for the detection and localization of urinary stones. Almost all studies conducted to date show that IVU provides no additional clinically important information after nonenhanced CT is performed. As a result of the higher radiation dose of CT, conventional or digital radiography should be used to monitor the passage of stones if radiographic follow-up studies are indicated and if the stone is visible on conventional radiographs. Limitations of TechniquesBecause of the higher radiation dose with CT, conventional or digital radiography should be used to monitor the passage of stones if radiographic follow-up is believed to be indicated and if the stone is visible on conventional radiographs. Pregnant or pediatric patients may be imaged with US first to avoid radiation exposure. The rare false-negative finding is usually due to reader error or a protease-inhibitor CT-lucent stone. False-positive results are usually due to phleboliths adjacent to the ureter. In some cases, intravenous contrast material may be needed to opacify the ureter. US has limited sensitivity for smaller stones, and does not depict the ureters well. It should be used mainly in patients who are young, those who are pregnant, or those undergoing multiple examinations (eg, patients with spine injury). IVU is the traditional examination for the assessment of urinary stone disease, and it does provide physiologic information related to the degree of obstruction. The radiation dose is generally smaller than that of CT, but it is of the same order of magnitude. Intravenous contrast is required, with resultant risks of an allergic reaction or nephrotoxicity. IVU is less sensitive than CT, especially for small or nonobstructing stones. DIFFERENTIALSAppendicitis Cholecystitis, Acute Cholelithiasis Colon, Diverticulitis Congenital Cystic Adenomatoid Malformation Crohn Disease Duodenum, Ulcers Epididymitis Gastric Ulcer Gout Meckel Diverticulum Midgut Volvulus Nephrocalcinosis Obstructive Uropathy, Acute Ovarian Torsion Ovarian Vein Thrombosis Pancreatitis, Acute Pancreatitis, Chronic Papillary Necrosis Pelvic Inflammatory Disease/Tubo-ovarian Abscess Renal Cell Carcinoma Renal Vein Thrombosis Retroperitoneal Fibrosis Testicular Torsion Transitional Cell Carcinoma Tuberculosis, Genitourinary Tract Ureterocele Ureteropelvic Junction Obstruction, Vesicoureteral Reflux Wilms Tumor Xanthogranulomatous Pyelonephritis
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| Media file 1: Magnified scout intravenous urogram shows a large, relatively lucent calculus in the lower pole of the right kidney. | |
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| Media file 2: Scout intravenous urogram shows a smooth, dense, round calculus in the left kidney (same patient as in Image 3). | |
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| Media file 3: Intravenous urogram. After the intravenous injection, contrast material in the collecting system obscures the calculus (same patient as in Image 2). | |
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| Media file 4: Scout intravenous urogram shows a smooth stone in the right kidney (same patient as in Images 5-8). | |
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| Media file 5: Intravenous urogram obtained 5 minutes after the intravenous injection. Contrast material in the collecting system obscures the stone (same patient as in Images 4 and 6-8). | |
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| Media file 6: This intravenous urogram was obtained 10 minutes after the intravenous injection of contrast medium. Additional contrast material is present in the collecting system, and the stone is seen as a relatively lucent filling defect (same patient as in Images 4-5 and 7-8). | |
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| Media file 7: Renal sonogram demonstrates an echogenic shadowing calculus in the renal collecting system with hydronephrosis (same patient as in Images 4-6 and 8). | |
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| Media file 8: Contrast-enhanced CT section reveals a dense calculus in the right kidney, but the hydronephrosis has resolved (same patient as in Images 4-7). | |
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| Media file 9: Abdominal radiograph shows calcification filling the left collecting system. This finding is consistent with a staghorn calculus. For its size, the stone is relatively lucent (same patient as in Image 10). | |
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| Media file 10: Contrast-enhanced CT scan demonstrates an opaque staghorn calculus filling the left renal collecting system (same patient as in Image 9). | |
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| Media file 11: Scout intravenous urogram shows innumerable small calcifications in the region of the renal pyramids in a patient with nephrocalcinosis. | |
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| Media file 12: Scout intravenous urogram demonstrates innumerable calcifications over the medullary region of the left kidney in a patient with nephrocalcinosis (same patient as in Image 13). | |
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| Media file 13: Renal longitudinal sonogram in a patient with nephrocalcinosis shows diffuse echogenic shadowing calcifications in the renal pyramids (same patient as in Image 12). | |
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| Media file 14: Intravenous urogram. Prospectively, no stone was seen on the scout radiograph (same patient as in Images 15-16). In retrospect, a stone in the distal left ureter is projected over the lateral edge of the mid sacrum. | |
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| Media file 15: This intravenous urogram was obtained 5 minutes after the intravenous injection of contrast agent (same patient as in Images 14 and 16). A prolonged hyperintense left nephrogram demonstrates delayed contrast material excretion into the left collecting system due to ureteral obstruction. | |
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| Media file 16: This intravenous urogram was obtained 10 minutes after the intravenous injection of contrast material (same patient as in Images 14-15). Mild left hydronephrosis and hydroureter extend to the level of the stone in the true pelvis. | |
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| Media file 17: Scout intravenous urogram demonstrates a small, focal, almost triangular, radiopaque calculus on the left side of the pelvis (same patient as in Images 18-19). Another pelvic calcification with central lucency is a typical phlebolith. | |
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| Media file 18: Scout intravenous urogram was obtained 5 minutes after the intravenous injection of contrast agent (same patient as in Images 17 and 19). A prolonged hyperintense nephrogram and moderate hydronephrosis are present in the left kidney. The right kidney and collecting system are normal. | |
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| Media file 19: Intravenous urogram was obtained 10 minutes after the intravenous injection of contrast agent (same patient as in Images 17-18). A column of contrast material in the left ureter extends down to the calculus noted on the scout radiograph. The small phlebolith can barely be seen projecting slightly off the ureter. | |
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| Media file 20: Intravenous urogram (30-minute delay image) of the right kidney shows a moderately hydronephrotic collecting system to the level of a proximal ureteral stone (arrow) (same patient as in Image 21). | |
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| Media file 21: Axial nonenhanced CT section at the level of the kidney demonstrates an attenuating proximal ureteral calculus (arrow) (same patient as in Image 20). No significant hydronephrosis is identified. CT can be performed much more rapidly than urography and without the use of intravenous contrast material. | |
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| Media file 22: Scout intravenous urogram demonstrates several calcifications in the left hemipelvis (same patient as in Images 23-25). | |
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| Media file 23: Intravenous urogram was obtained 10 minutes after the intravenous injection of contrast agent (same patient as in Images 22 and 24-25). A prolonged hyperintense nephrogram and mild hydronephrosis are present. | |
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| Media file 24: Intravenous urogram, delayed radiograph, reveals a large amount of contrast material extravasation (likely a fornix rupture with pyelosinus backflow) in the region of the left renal pelvis (same patient as in Images 22-23 and 25). Contrast agent fills the distal ureter. | |
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| Media file 25: Intravenous urogram, magnified view, shows extravasated contrast agent from a fornix rupture and pyelosinus backflow (same patient as in Images 22-24). | |
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| Media file 26: Axial nonenhanced CT image at the level of the kidneys shows bilateral renal calculi, right hydronephrosis, and moderate perinephric fluid (same patient as in Images 27-28). | |
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| Media file 27: Axial nonenhanced CT image of the urinary bladder demonstrates an attenuating calculus at the right ureteropelvic junction (same patient as in Images 26 and 28). | |
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| Media file 28: Axial contrast-enhanced CT scan. The excretory phase image through the kidneys shows extravasation of contrast material in and near the renal pelvis and surrounding the proximal ureter, which is opacified. The finding is consistent with fornix rupture (same patient as in Images 26-27). | |
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| Media file 29: Scout intravenous urogram demonstrates radiopaque left renal calculi in the mid kidney and lower pole (same patient as in Images 30-32). | |
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| Media file 30: Scout intravenous urogram obtained after lithotripsy (same patient as in Images 29 and 31-32) shows absence of the previously seen calcification over the mid kidney and linear group of calcifications in the path of the distal left ureter (steinstrasse, from the German, meaning "stone street"). | |
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| Media file 31: Intravenous urogram, magnified view of the scout image in Image 30, was obtained after lithotripsy and shows a steinstrasse appearance (same patient as in Images 29-30 and 32). | |
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| Media file 32: Intravenous urogram, 10-minute delay image, demonstrates delayed excretion and a slightly hyperopaque left nephrogram due to obstruction by distal ureteral stone fragments (same patient as in Images 29-31). Stents are often placed to prevent obstruction after lithotripsy. | |
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| Media file 33: Intravenous urogram, scout radiograph. Large radiopaque calculus overlies the left hemipelvis near the expected location of the ureterovesical junction (same patient as in Images 34-37). Two adjacent phleboliths are noted lateral and caudal to the stone. | |
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| Media file 34: Intravenous urogram. Magnified view of the scout radiograph in Image 33 reveals faintly lamellated pelvic calcification at the expected location of the left ureterovesical junction (same patient as in Images 33 and 35-37). | |
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| Media file 35: Intravenous urogram (10-min delay). Contrast-enhanced study demonstrates the left ureterocele as a slightly lucent halo around the previously noted pelvic calcification (same patient as in Images 33-34 and 36-37). | |
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| Media file 36: Intravenous urogram (10-min delay) Magnified view of the left ureterocele (see Image 35) with a large stone in it (same patient as in Images 33-35 and 37). | |
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| Media file 37: Axial contrast-enhanced CT image through the ureterovesical junction confirms the stone within a left ureterocele (same patient as in Images 33-36). A Foley catheter balloon is visible in the bladder. | |
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| Media file 38: Intravenous urogram (tomogram) shows enlarged relatively lucent right kidney with no excretion of contrast material (same patient as in Images 39-41). | |
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| Media file 39: Intravenous urogram (5-min renal view) shows enlarged relatively lucent right kidney with no excretion of contrast (same patient as in Images 38 and 40-41). | |
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| Media file 40: Longitudinal sonogram of the right kidney demonstrates marked dilatation of the calyces. No calculi are apparent (same patient as in Images 38-39 and 41). | |
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| Media file 41: Sonogram shows marked dilatation of the calyces and communication with the renal pelvis, which confirms severe hydronephrosis (same patient as in Images 38-40). | |
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| Media file 42: Nonenhanced CT image of the kidneys demonstrates left hydronephrosis and strands of perinephric fluid but no dense calculus (same patient as in Images 43-44). | |
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| Media file 43: Nonenhanced CT image of the pelvis shows dilatation of the distal left ureter and mild periureteral fluid near the left ureterovesical junction (same patient as in Images 42 and 44). | |
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| Media file 44: Nonenhanced CT image of the pelvis shows a small attenuating stone at the left ureterovesical junction (same patient as in Images 42-43). | |
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| Media file 45: Nonenhanced CT image shows slightly hyperattenuating renal pyramids, most notably on the left. This is a secondary sign and indicates a lack of obstruction of the collecting system (same patient as in Image 46). | |
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| Media file 46: Nonenhanced CT image shows a nonobstructing calculus just above the left ureterovesical junction (same patient as in Image 45). | |
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| Media file 47: Contrast-enhanced CT image of the kidneys shows mild hydronephrosis, perinephric fluid, and delayed enhancement. The perinephric fluid indicates obstruction and correlates with the likelihood of the passage of the stone (same patient as in Image 48). | |
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| Media file 48: Contrast-enhanced CT image of the lower abdomen shows a tiny, obstructing, left ureteral calculus (same patient as in Image 47). | |
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| Media file 49: Magnified nonenhanced CT image of the right kidney shows slightly hyperattenuating renal pyramids in the right kidney despite the mild hydronephrosis (same patient as in Image 50). | |
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