Tuberculosis
Most urinary tuberculosis is due to hematogenous spread. At times the primary site is not identified, although active or inactive lung disease is found in a majority. Although initially both kidneys are infected, disease often progresses unilaterally.
Among 57 patients with urogenital tuberculosis, fever, anorexia, and weight loss were evident only in 11%, 16% had an isolated genital lesion, and, surprisingly, 14% presented with renal failure (32); bacilluria was identified only in 5%. These patients have a sterile pyuria, microscopic hematuria, and an acidic urine. The diagnosis is confirmed by urine culture, a procedure taking up to 4 weeks.At times US-guided aspiration is helpful in establishing the diagnosis. A polymerase chain reaction to detect mycobacterial DNA has a high sensitivity and establishes the diagnosis.
Urography was abnormal in 80% of affected individuals, with the most frequent abnormality being a nonfunctioning silent kidney found in 40% (32).
Focal infections, or tuberculomas, develop initially. Tuberculomas tend to be hypointense on both T1and T2-weighted MRI, provided they contain no calcifications, hemorrhage, or fibrosis. These either resolve spontaneously or enlarge, become necrotic, and communicate with the collecting system, spreading infection distally. Imaging at this stage reveals irregular, necrotic, and moth-eaten papilla, at times mimicking papillary necrosis due to other causes. Some calyces become obstructed due to infundibular stenosis. Strictures range in location from calyces to ureters, leading to obstruction and further damage. Cortical scarring, calyceal distortion, and strictures with caliectasis develop. In some, CT simply identifies small hypodense tumors along the renal cortex (33). Ulcerations, abscesses, and fibrosis dominate the late stages of infection. Extension of infection outside the kidney leads to perinephric abscesses. Calcifications vary from curvilinear to diffuse, from homogeneous to granular. If neglected, eventually the small, calcified kidney loses all function.
Ureteral involvement results in a shaggy, irregular lumen. A dilated ureter ensues with ureterovesical junction obstruction. In time, the ureter wall thickens, ulcers develop, and exten-
ADVANCED IMAGING OF THE ABDOMEN
sive fibrosis leads to foreshortening. Ureteral calcifications are uncommon, thus aiding in distinguishing tuberculosis from the more common ureteral calcifications found in schistosomiasis.
Some patients with bladder trigone involvement develop upper tract obstruction and eventually renal function is lost even if the obstruction is relieved by stenting or a percutaneous nephrostomy; a kidney can deteriorate from an acceptable pretherapy glomerular filtration rate to becoming nonfunctional after relief of an obstruction. Predictors of renal recovery after diversion are an adequate residual renal cortex and a glomerular filtration rate of >15mL/min.
At the more advanced stages CT and urography should suggest the diagnosis. In some patients xanthogranulomatous pyelonephritis is in the differential. At times a tuberculous kidney develops a fistula to an adjacent organ.
Schistosomiasis
Schistosomiasis generally affects the lower portion of both ureters. Involvement is usually bilateral and results in stenosis and a thickened ureteral wall. Often multiple strictures are evident and proximal ureteral dilation develops. Early in the course a contrast study often reveals soft tissue polyps. Calcifications develop with chronic infection and have a characteristic linear appearance; a diagnosis of schistosomiasis can be strongly suggested if such calcifications are seen in a young adult from endemic regions.
Curiously, in distinction to bladder involvement, ureteral schistosomiasis is not associated with a high risk of ureter cancer.
Echinococcal Cyst
Although uncommon, hydatid cysts do occur in the kidneys, with Echinococcus granulosus being more common than Echinococcus multilocularis. In rare instances renal cysts develop bilaterally. Ureteral cysts are rare. No age group is immune, including children.
Patients are often asymptomatic until the pressure on an adjacent structure or cyst rupture develops. Rupture into a collecting system leads to hydatiduria and possible renal colic due to cyst debris.