Introduction

Tuberculosis (TB) remains a major global health burden and continues to be one of the leading causes of death from infectious disease worldwide. Extrapulmonary TB accounts for a substantial proportion of cases, and genitourinary tuberculosis (GUTB) represents one of the most common forms, particularly in endemic regions such as India [1,2]. GUTB typically arises from hematogenous dissemination of Mycobacterium tuberculosis from a primary pulmonary focus, often years after the initial infection, reflecting its indolent and latent nature [2].

Renal involvement is the most frequent manifestation of GUTB, and the disease often progresses silently, with minimal or nonspecific clinical symptoms despite significant parenchymal destruction [3]. The pathogenesis involves granuloma formation, caseous necrosis, cavitation, and progressive fibrosis, ultimately leading to strictures, obstruction, and loss of renal function [4]. Over time, chronic inflammation and dystrophic calcification may replace the entire renal parenchyma, producing the characteristic radiological appearance known as a “putty kidney,” which represents an end-stage, nonfunctioning, autonephrectomized kidney [4].

The term “putty kidney” describes dense, homogeneous calcification within a shrunken kidney caused by longstanding TB and is now rarely encountered because of earlier diagnosis and treatment. However, delayed or missed diagnosis remains a significant clinical challenge, as GUTB can mimic other urological conditions and may remain clinically occult for years [5]. In many cases, patients present late with complications such as obstructive uropathy, hydronephrosis, or chronic kidney disease, sometimes discovered incidentally during imaging performed for unrelated conditions [6].

Renal TB may become clinically apparent years after successful treatment of pulmonary TB. This delayed presentation may result from reactivation of dormant bacilli or progression of previously established latent genitourinary infection; however, the exact mechanism cannot usually be determined in an individual patient. Consequently, clinicians should maintain awareness of the possibility of delayed genitourinary involvement in patients with a history of TB who develop compatible clinical or radiological findings. The occurrence of silent renal autodestruction culminating in a putty kidney years after treated pulmonary TB is rare and underscores the insidious progression of the disease.

Here, we report a case of incidental discovery of end-stage GUTB presenting as a putty kidney 14 years after treated pulmonary TB, associated with multisystem sequelae. This case emphasizes the importance of maintaining clinical suspicion and performing appropriate imaging when patients with a history of TB present with suggestive clinical or radiological findings.