A Tale of Two Lesions: Tuberculosis Presenting as Granulomatous Interstitial Nephritis with Collapsing Glomerulopathy

Dear Editor,

Collapsing glomerulopathy (CG) is a morphologic variant of focal segmental glomerulosclerosis, with distinctive podocytic hyperplasia and an aggressive clinical course, as outlined in classic pathologic descriptions.¹ Contemporary reviews discuss infection-associated triggers and mechanistic insights relevant to CG.² Granulomatous interstitial nephritis (GIN) is uncommon and often linked to tuberculosis in endemic regions.³ Tuberculosis-associated CG has been described,⁴ and GIN in children has also been reported, underscoring the breadth of infectious-inflammatory renal pathology.⁵

We report the case of a 19-year-old male who presented with anasarca, reduced urine output, and accelerated renal dysfunction over 3 weeks. Blood pressure was 160/100 mmHg, with pallor, ascites, and a healed axillary scar. Laboratory evaluation suggested nephritic-nephrotic syndrome with rapidly progressive renal failure. Renal biopsy demonstrated CG with confluent epithelioid cell granulomas, consistent with GIN [Figure 1]. Direct immunofluorescence showed only minimal mesangial IgM deposition.

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Figure 1:

Composite histopathology panel (a) PAS stain (×200): Segmentally sclerosed glomerulus (red arrow) with hyperplasia of overlying podocytes. (b) H&E stain (×100): Large epithelioid cell granuloma (red arrow) with focal necrosis. (c) Jones methenamine silver stain (×400): Collapse of the glomerular tuft with podocyte hyperplasia (red arrow). (d) H&E stain (×100): Confluent interstitial epithelioid granulomas (red arrow) with chronic inflammatory infiltrate. H&E: Hematoxylin and eosin, PAS: Periodic acid schiff.

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Further evaluation revealed a strongly positive Mantoux test and necrotizing granulomatous inflammation on FNAC of a cervical lymph node. The patient was initiated on renal-dose-modified anti-tubercular therapy, along with a short course of steroids. At the 5-month follow-up, he showed complete remission of proteinuria and normalization of renal function. This case highlights a unique dual pathology, CG and GIN, likely attributable to tuberculosis. The clinical remission following anti-tubercular therapy strongly suggests a common etiologic link. This recognition is important, as CG in the setting of tuberculosis may carry a more favorable prognosis than in idiopathic or HIV-associated forms.