A 58-year-old male with known bladder carcinoma (stage T1) on intravesical Bacillus Calmette Guerin (BCG) therapy presented with high fever, weakness for one week and tenderness in lumbar regions. His infectious parameters were elevated while urine examination and blood cultures were negative. Chest x-ray was within normal limits with no other systemic evidence of tuberculosis.
Contrast-enhanced CT examination of the abdomen revealed well defined multiple renal masses bilaterally involving upper and mid pole on the left side and mid pole on the right. No calcification, fat, hemorrhage or necrosis was seen within these lesions. The masses were hypodense relative to the renal parenchyma on contrast-enhanced CT. There was no evidence of perinephric standing (Fig.1). Considering history of intravesical therapy, possibility of BCG granulomas with differential diagnosis of pyelonephritis was raised on imaging. Subsequent CT guided biopsy was performed (Fig. 2) which confirmed BCG granulomas on histopathology (Fig. 3).
Patient was treated with antitubercular regime which lead to gradual decrease in sizes of renal lesions on five months follow-up CT examination (Fig. 4).
Intravesical BCG installation using live attenuated strain of Mycobacterium Bovis is the standard adjuvant therapy in patients with resected superficial bladder tumors. This treatment aims at decreasing the recurrence and progression of disease . Although the therapy is well tolerated in 95% of patients, local and systemic complications are encountered occasionally, including the rare fatal complication of BCGosis . Amongst wide array of complications documented in literature, renal complications are uncommon and can vary from pyelonephritis, abscesses, interstitial nephritis to renal granulomas mimicking renal cell carcinoma [1,3].
Renal granulomas are rare with reported incidence of 0.1% [1,2]. These granulomas can present as either expansile, multifocal renal masses or as a solitary renal lesion [1,2]. They can occur during the BCG therapy or can be detected on surveillance CT years after BCG instillation. The usual clinical presentation is with hematuria, flank pain and fever. Occasionally patients can also be asymptomatic. On contrast enhanced CT, the granulomas appear as hypodense masses- solitary or multifocal, simulating renal neoplasms. To differentiate these from renal cell carcinoma, some authors have described “central unaffected calyx sign” on delayed CT, though not seen in our case. This sign represents a preserved calyx within the granuloma whereas malignant tumours tend to destroy the calyces [4,5]. Granulomas are more commonly seen at upper poles (upper and mid pole in present case) occurring secondary to vesicoureteral reflux or by hematogenous spread [5,6]. On MRI, these granulomas can either have low T2 signal intensity due to fibrosis or high T2 signal due to inflammatory changes. FDG PET in these cases shows avid uptake simulating renal tumors. Imaging is not always able to differentiate these from renal tumour. However, in a patient on or with history of intravesical BCG therapy for bladder cancer, possibility of BCG granulomas should be raised when multiple or solitary renal masses are observed on imaging. Furthermore, it is also imperative to diagnose these lesions as their management is conservative or with antitubercular treatment contrary to a more radical approach for renal cell carcinomas. Final diagnosis is usually established with imaging guided needle biopsy with demonstration of granulomatosis on histopathology [4,5].
In conclusion, in a patient with superficial bladder carcinoma previously treated/or currently receiving intravesical BCG and presenting with solitary or multiple renal masses on imaging, BCG granulomas should always be considered in the differential diagnosis.
Written informed patient consent for publication has been obtained.
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