Title : A sticky scenario: An unusual cause of nephrotic syndrome in a young male
Abstract:
Background:
Amyloidosis is a heterogeneous group of disorders characterised by extracellular deposition of misfolded protein fibrils in various organs, leading to progressive dysfunction. The two most clinically important forms are AL amyloidosis, associated with monoclonal plasma cell disorders, and AA amyloidosis, secondary to chronic inflammatory or infectious states such as tuberculosis (TB). While AA amyloidosis is a recognized complication of TB, AL amyloidosis in the context of Tuberculosis is exceptionally rare, particularly in young individuals without known plasma cell dyscrasias.
Case Presentation:
My presentation will be on a diagnostically challenging case of AL amyloidosis in a 19-year-old male with a history of non-compliant pulmonary TB. He presented with facial puffiness, pedal edema, and systemic symptoms including fever and cough. These symptoms were initially misattributed to antibiotic hypersensitivity, delaying appropriate evaluation. Laboratory findings revealed nephrotic-range proteinuria (3.8 g/day), hypoalbuminemia (1.3 g/dL), and preserved renal function (creatinine 0.3 mg/dL). Autoimmune serologies were negative (ANA, c-ANCA, p-ANCA), and complement levels were within normal limits.
A renal biopsy revealed Congo red–positive deposits with apple-green birefringence under polarized light, confirming amyloidosis. Immunofluorescence was negative for immunoglobulins and complement, while immunohistochemistry confirmed AL-type amyloid. On further history taking, it was clear that the patient had a history of poorly managed tuberculosis (TB). A CT scan revealed pulmonary consolidation, and a cervical lymph node biopsy confirmed the presence of caseating granulomas, indicative of TB. Despite receiving supportive care and antitubercular therapy, the patient's condition deteriorated rapidly, leading to death within three months of presentation.
Conclusion:
This case illustrates an exceedingly rare occurrence of AL amyloidosis in a young patient with pulmonary TB, without any evidence of a monoclonal gammopathy. It challenges the conventional paradigm associating TB primarily with AA amyloidosis and raises the possibility that chronic antigenic stimulation from untreated infection may rarely trigger clonal B-cell proliferation and light chain production, even in the absence of plasma cell disorders. The clinical presentation mimicked common causes of nephrotic syndrome, and the initial misdiagnosis underscores the importance of considering amyloidosis in the differential when systemic features accompany renal involvement.
Early renal biopsy with Congo red staining and accurate fibril subtyping is critical, as therapeutic approaches and prognosis differ significantly between AL and AA amyloidosis. This case also highlights the need for heightened clinical suspicion in endemic regions, especially when TB coexists with unexplained proteinuria and systemic symptoms. Prompt diagnosis and access to targeted therapies such as proteasome inhibitors could potentially alter outcomes in such cases. This case contributes to the limited literature on infection-associated AL amyloidosis in young individuals and calls for further research into its pathophysiology.
