Discussion

The present case describes a 44-year-old woman with a prior history of treated pulmonary TB who was incidentally found to have a nonfunctioning putty kidney with widespread calcified granulomatous lesions involving multiple organ systems. Notably, the patient was completely asymptomatic from a urinary standpoint, emphasizing the silent and insidious progression of GUTB, even years after adequate treatment of the primary pulmonary focus.

A similar atypical presentation was reported by Qadir et al. [7], where a patient presented without classic urinary symptoms but developed acute renal failure requiring dialysis. In contrast to the present case, which was detected incidentally with preserved renal function, their case manifested with severe acute deterioration, highlighting the variable clinical spectrum of GUTB ranging from silent disease to life-threatening renal impairment.

In comparison, Mathur et al. [8] described a patient with previously diagnosed GUTB who remained noncompliant with antitubercular therapy, ultimately progressing to advanced renal failure. That patient developed extensive structural damage, including a “thimble bladder,” ureteric calcification, and a nonfunctioning kidney, with histopathology confirming a putty kidney. While both the present case and Mathur’s case demonstrate end-stage renal TB, the key difference lies in disease course: progression resulted from treatment noncompliance in their case, vs. late sequelae despite prior adequate treatment in the present case.

Similarly, Ranjan et al. [9] reported patients with prolonged symptomatic disease, including flank pain and lower urinary tract symptoms, in whom delayed diagnosis led to irreversible anatomical damage necessitating nephrectomy and reconstructive procedures. Unlike these symptomatic cases, the present patient had no urinary complaints, yet already had complete renal autodestruction, further underscoring the deceptive and subclinical nature of the disease.

Furthermore, Rocco et al. [10] demonstrated that even with timely diagnosis and standard antitubercular therapy, patients may continue to have persistent urological sequelae such as infundibular stenosis and urinary dysfunction. This finding aligns with the present case in highlighting that structural damage caused by TB is often irreversible regardless of treatment, particularly when diagnosis is delayed or the disease remains undetected for prolonged periods.

Overall, the present case is distinctive because of its entirely asymptomatic presentation, incidental diagnosis, and association with multisystem healed tuberculous sequelae many years after treated pulmonary TB. It illustrates that end-stage GUTB may remain clinically silent for years and be detected incidentally despite previous treatment for pulmonary TB. Although renal TB may become clinically apparent long after pulmonary disease, this case cannot determine whether the underlying mechanism represents reactivation of dormant bacilli or progression of previously established latent genitourinary infection. These findings support maintaining a high index of clinical suspicion and performing appropriate imaging when patients with a history of TB develop suggestive clinical or radiological findings, rather than routine imaging surveillance of all patients with previous TB.