Biopsy-Proven Renal AA Amyloidosis Revealing Underlying Pulmonary Tuberculosis With the Kidney as an Innocent Bystander: A Case Report and Literature Review

When a young patient presents with nephrotic syndrome and no apparent inflammatory history, the underlying diagnosis may be hiding in plain sight, concealed by an incomplete history and an undertreated chronic infection.We report a case in which poor adherence to anti-tubercular therapy silently perpetuated chronic granulomatous inflammation, culminating in biopsy-proven renal amyloid A (AA) amyloidosis presenting as nephrotic syndrome.A 32-year-old woman presented after four months of intermittent lowgrade fever, followed by progressive bilateral lower limb swelling and reduced urinary output; a prior history of pulmonary tuberculosis and documented poor adherence to anti-tubercular therapy was disclosed only on detailed history-taking during subsequent clinical evaluation.Initial laboratory investigations revealed nephrotic-range proteinuria, severe hypoalbuminemia, and preserved renal function.Complement and coagulation profiles were within normal limits, effectively excluding immune-mediated glomerulonephropathies.Abdominal ultrasonography revealed bilaterally normal-sized kidneys with preserved internal architecture, consistent with early-stage renal involvement.Renal biopsy confirmed AA amyloidosis, demonstrating Congo red-positive amyloid deposits with characteristic apple-green birefringence under polarized light and strongly positive immunohistochemical staining for serum amyloid A. Subsequent thoracic evaluation revealed extensive fibrocavitary lung disease with near-complete collapse of the left lung, traction bronchiectasis, and fibrocalcific nodules, consistent with inadequately treated chronic granulomatous pulmonary tuberculosis.Anti-tubercular therapy was reinitiated, and at four-week follow-up the patient demonstrated complete resolution of pedal edema and overall symptomatic improvement.This case makes a compelling argument that non-adherence to anti-tubercular therapy is a direct and preventable cause of secondary AA amyloidosis, a systemic complication that can develop silently before the underlying infection is recognized or adequately managed.Prompt renal biopsy with amyloid subtyping can fundamentally redirect the diagnostic and therapeutic approach, underscoring that the kidney may be the first organ to signal an otherwise inadequately treated chronic infection.