Tuberculosis (TB) is caused by Mycobacterium tuberculosis when the bacilli laden droplets are inhaled, ingested or enters the human body through the skin (aberration or local trauma) or the mucous membranes, with the most common pathway being the respiratory tract (70%-80% cases) [3,4].

The course of the disease is mainly directed by the interaction between the host response and the virulence of the bacilli. In an immunocompetent host, the organism is initially subjected to fierce resistance from the body’s immune system, making the TB bacilli dormant, also known as latent TB. The vital host defence mechanism against the organism is cell-mediated immunity that is influenced primarily by means of macrophages and T-lymphocytes [3-5]. Once the organism overpowers the defence mechanism of the host, usually in an immunocompromised state, TB can reactivate causing widespread damage either locally or affect other parts of the body after spreading via lymphatics or bloodstream [6-8].

The incidence of isolated tuberculous mediastinal lymphadenopathy declines with increasing age and is scarcely seen in adults [9]. Ayed et al. also reported the occurrence rate of intrathoracic tuberculous lymphadenitis to be as 2% out of 1700 new cases of TB over a period of 4 years. [10] The differential diagnoses of anterior mediastinal mass include thymoma, lymphoma, teratomatous neoplasms, thyroid mass, vascular masses, lymphadenopathy due to metastasis or TB, and pleuropericardial and bronchogenic cysts. Nevertheless, in younger individuals like our patient, lymphoma and germ cell tumours are more common [11].

Genitourinary TB (GUTB) is the second most common form of extrapulmonary TB after lymphadenopathy and accounts for almost 27% of nonpulmonary cases worldwide [12]. The few reported types of glomerulonephritis due to TB include immune complex glomerulonephritis complication of miliary TB and pulmonary TB, membranoproliferative glomerulonephritis in the course of disseminated TB, membranous nephropathy associated with TB, IgA nephropathy associated with pulmonary TB and collapsing glomerulopathy with pulmonary TB. [13-20] In all these reports, there was some degree of lung lesions and clinical and radiological evidence of pulmonary infection unlike in our patient who remained asymptomatic.

Moreover, data on GIN as the only manifestation of renal TB is limited in the literature. GIN is an infrequent diagnosis encountered in less than 1% of all renal biopsies performed. [21,22] Recently, Colvin et al. reported only 34 cases of GIN from a total of 10,383 renal biopsies, with the commonest aetiology of GIN as drug allergy closely followed by sarcoidosis and only one case of TB [21]. On the contrary, reports from Southeast Asia reveal TB as an important cause of GIN [23]

Another interesting consideration is the clinical presentation of hypertension, facial oedema and subnephrotic range of proteinuria mimicking a glomerular disease. Similar presentation of GIN with membranous nephropathy has been reported only twice in the literature [24,25]. In our case, detailed evaluation of other aetiologies like infection, autoimmune disorders and systemic conditions such as sarcoidosis revealed negative results.

Previously, a few cases of GIN associated with pulmonary or peritoneal foci have been reported, albeit rare, but active cervical adenitis with GIN due to TB has been reported only once to the best of our knowledge. [26] It can be hypothesized that our patient had a primary infection involving the cervical and mediastinal lymph nodes and kidneys.

As a part of the initial evaluation, a detailed history along with physical examination is pertinent to look for any thyroid pathologies, testicular/ovarian masses, or evidence of immunosuppression. Usually, patients with a mediastinal mass would remain asymptomatic unless they develop mass effects like chest pain, dyspnoea or cough. It can be very perplexing to diagnose a mediastinal mass radiologically. [3] Gene Xpert analysis is another well-recognized modality in rapid diagnosis of tuberculosis and should be considered in the work up of a mediastinal mass. Contrast enhanced CT of the thorax is useful to further characterize a mediastinal mass [27]. Since TB tends to mimic malignancy mainly radiologically, it is imperative to confirm the diagnosis by histopathology before any therapeutic interventions [27].

In our case a lymphoproliferative disorder was suspected initially along with systemic severe hypertension leading to hypertensive nephropathy. The final diagnosis was of TB was only made after the histopathological examination of mediastinal lymph node biopsy which was finally confirmed by a positive response to ATT. Furthermore, renal survival in GIN is determined by the degree of renal dysfunction at presentation. [28] It is often difficult to diagnose, and non-specific symptoms of genitourinary TB can lead to a delayed diagnosis and rapid progression to a non-functioning kidney.