Rationale: Anti-phospholipase A2 receptor (PLA2R) antibody is a highly specific serological marker for primary membranous nephropathy, with a detection rate of <2% in minimal change disease (MCD). This case represents the first report of PLA2R-positive adult MCD complicated by active pulmonary tuberculosis (TB) and systemic osteoarthropathy, highlighting the potential for chronic infection to induce PLA2R antibodies through inflammatory activation or molecular mimicry. Patient concerns: A 73-year-old male with 7-year steroid-dependent nephrotic syndrome developed pulmonary TB and systemic osteoarthropathy during immunosuppressive therapy. Diagnoses: Serial renal biopsies confirmed MCD/focal segmental glomerulosclerosis (FSGS) without membranous nephropathy features. PLA2R antibody was transiently positive (16.6 RU/mL) during active TB but turned negative after anti-TB treatment. TB was confirmed by next-generation sequencing. Interventions: A multidisciplinary strategy was implemented: rifapentine replaced rifampicin to maintain tacrolimus levels; rituximab was administered for refractory proteinuria; and TB was treated with a 9-month regimen. Osteoarthropathy was managed with Tripterygium glycosides and joint injections. Outcomes: Following rituximab administration, 24-hour urinary protein decreased from 6.32 g to 1.5 g. TB was controlled with sputum conversion within 2 months. PLA2R antibody became negative post anti-TB therapy, supporting the hypothesis of infection-induced seropositivity. No renal function decline or TB dissemination occurred. Lessons: This case suggests that chronic infections like TB may transiently induce PLA2R antibodies via inflammatory activation, highlighting the need for dynamic serologic and histopathologic correlation to avoid misdiagnosis in PLA2R-positive non-MN patients. Multidisciplinary management is critical to balance immunosuppression and infection control.