Teaching Case

An elderly male presented with chronic kidney disease and recurrent urinary infections for a few years. He was recently hospitalized elsewhere because of severe lumbar pain radiating to both legs.
The patient was transferred to our hospital with diagnosis of infectious spondylo-diskitis, physically found afebrile, and unable to walk. Laboratory changes: elevated acute phase reactants, 2mg/dL serum creatinine.

Lumbosacral imaging (Fig.1) showed MR signal changes affecting the L4-L5 vertebral bodies and liquefied intervertebral disk, plus bilateral paravertebral abscesses. Incidental findings included moderate left-sided hydronephrosis, parenchymal thinning of right kidney with dilated distorted calyces, non-dilated pelvis with mild mural thickening.
Chest radiographs (Fig.2) excluded active pleuropulmonary changes and mediastinal abnormalities. A peripheral calcified nodule was noted in the left lung.
At multidetector CT-urography (Figs.3, 4) the atrophied right kidney showed uneven calyceal dilatation, delayed nephrogram and no collecting system opacification; the mild mural thickening along the ispilateral renal pelvis and ureter showed positive contrast enhancement. Calcifications were absent. The left kidney showed normal size and function, despite hydronephrosis secondary to short stricture of the distal ureter. Additional findings included septated hip effusion, small-sized hypodense lesion of the right seminal vesicle.
Multifocal urinary and spinal tuberculosis was diagnosed on the basis of positive Quantiferon, vertebral biopsy, clinical and biochemical improvement after antitubercular therapy.

Despite effective therapies, tuberculosis is having a resurgence due to drug-resistant Mycobacteria and increased migrations, particularly in Eastern Europe, parts of Africa and Asia. Albeit rare compared to lung disease, urogenital tuberculosis (UGTB) is the second most common (27%-35%) form of extrapulmonary involvement. Increasingly encountered in non-endemic Western countries, UGTB should be suspected in unexplained haematuria or resistant urinary infection, particularly in immigrants, HIV or medication-related immunosuppressed patients. Pathogenesis involves haematogenous dissemination from the lungs, followed by granulomatous inactivation and by late reactivation in the kidneys when the host’s immunity decreases after a median 20 years after primary pulmonary infection. Afterwards, dissemination into urine causes involvement of collecting systems, ureter and bladder with mucosal inflammation, thickening and ultimately fibrosis [1-4].
The manifestations vary according to the disease stage and are often subtle, without active lung infection in 50% of patients. Renal, collecting system and unilateral ureteral involvement are generally asymptomatic. The commonest clinical pattern is represented by unexplained resistant urinary tract infection, accompanied by irritative voiding symptoms and micro- or macroscopic haematuria. Back or flank pain, fever and malaise are common. Frequently delayed, diagnosis of UGTB relies on lengthy cultures or nuclei acid amplification tests. Unfortunately, untreated disease progresses causing ureteral strictures and ultimately loss of kidney function. The prostate, epididymis, seminal vesicles and fallopian tubes are commonly affected. Alternatively, signs of UGTB are detected in patients with lung or disseminated tuberculosis. UGTB is effectively cured by usual anti-tuberculous drug combinations, but ablative or reconstructive urologic surgery is often required [2, 4-7].
Compared to the abandoned intravenous urography, nowadays multidetector CT depicts parenchymal abnormalities even in nonfunctioning kidneys and is most sensitive for calcifications, renal cavities, mural thickening. Acute renal changes closely mimic those of acute pyelonephritis. More suggestive signs include calyceal deformity, uneven caliectasis from infundibular strictures, mild enhancing urothelial thickening. Advanced disease is indicated by variably shaped renal calcifications which ultimately partially or completely replace the kidney. In almost 50% of patients, ureteral strictures develop, usually at the distal third or pyeloureteral junction. Long-standing hydronephrosis leads to parenchymal atrophy with thinned, poorly functioning parenchyma. Bladder involvement progressively causes reduced capacity, mural thickening and irregularities. As this case exemplifies multidetector CT may support the diagnosis of UGTB particularly when combined consistent findings are observed. Urinary changes which should alert the radiologist to the possibility of tuberculosis are summarized in Figure 5 [8-14].