A Pathogen’s Whisper: Reactivation of Quiescent Membranous Nephropathy by Disseminated Tuberculosis

TL;DR

A case study shows that tuberculosis can trigger a relapse of membranous nephropathy, suggesting that treating the infection may prevent unnecessary immunosuppressive therapy.

Contribution

This is the first documented case linking tuberculosis to a relapse of primary PLA2R-positive membranous nephropathy.

Findings

A patient with quiescent membranous nephropathy experienced a relapse following a disseminated tuberculosis infection.

The nephropathy resolved completely with anti-TB treatment alone, without additional immunosuppression.

The case suggests that TB may trigger MN relapse through immune activation or molecular mimicry.

Abstract

Primary membranous nephropathy (MN) is an autoimmune glomerular disease commonly associated with anti-PLA2R antibodies, with relapses typically attributed to spontaneous immune reactivation. We report the first documented case of a relapse of primary, PLA2R-positive MN that was temporally and immunologically linked to disseminated tuberculosis (TB) infection. A 42-year-old man, previously in complete remission, developed severe nephrotic syndrome and acute kidney injury unresponsive to standard immunosuppressive regimens. Concomitant diagnosis of miliary TB was confirmed by culture and imaging. Remarkably, the MN relapse resolved completely with anti-TB therapy alone, without further immunosuppression, and remission has been sustained for over two years. This case highlights infection, specifically TB, as a modifiable and overlooked trigger of MN relapse, potentially via molecular mimicry or system immune activation. In TB-endemic regions, identifying infectious triggers early in relapsing MN may spare patients from unnecessary immunosuppression and facilitate long-term remission through targeted antimicrobial therapy.

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