A 40-year-old male was admitted to our hospital with a 3-month history of recurrent respiratory infections and persistent pitting pedal edema. His past history revealed 3 to 5 episodes of recurrent respiratory tract infections and diarrhoea each year since last 20 years. He had been successfully treated for sputum positive pulmonary tuberculosis 8 years back for which he was prescribed isoniazid (300 mg/day), rifampicin (600 mg/day), ethambutol (1.5 g/day) and pyrazinamide (2 g/day) for 3 months, followed by isoniazid and rifampicin for 6 more months. Sputum smear examination for acid fast bacillus (AFB) was negative at 3 and 9 months of treatment. Physical examination revealed a malnourished afebrile male with blood pressure 100/60 mm Hg; and a heart rate of 96/min with pitting pedal edema in both lower limbs. Laboratory studies disclosed; hemoglobin level of 12 g/dl, white blood cells (WBC); 17270/mul, platelets; 641000/mul, erythrocyte sedimentation rate (ESR); 110 mm/h, C-reactive protein (CRP); 32 mg/dl (normal 0-5), total protein; 2.4 g/dl; and serum albumin of 1.4 g/dl. Liver function tests were normal. Urinalysis revealed 3+ proteinuria. Twenty four-hour urine protein was 3.4 g/day. Serum immunoglobulins were as follows: IgG; 1.28 g/l (normal 7-16), IgM ; <0.4 g/l (normal 0.4-2.3); IgA ; <0.6 g/l (normal 0.7-4). CD4/CD8 ratio and CD3 level was normal. C3 and C4 complement levels were normal. The abdominal and pelvic ultrasonography (USG) revealed that the liver was normal in size with a homogenous parenchyma. The spleen was also of normal size, and the parenchymal echotexture was homogenous. Both kidneys were enlarged (right kidney; 120 mm and left kidney; 130 mm) with normal corticomedullary differentiation. Chest x-ray and Electrocardiography (ECG) were normal. Cultures of blood and urine were negative. Serologies for HIV, hepatitis B virus (HBV), and hepatitis C virus (HCV) were negative. Thoracic computed tomography (CT) scan revealed fibrotic scars with bronchiectatic changes in both upper lobes of lungs, suggestive of old healed tuberculosis. Since the patient had recurrent infections, hypogammaglobulinemia, nephrotic level proteinuria, and enlarged kidneys in the renal USG we conducted a renal biopsy. Biopsy revealed, AA positive secondary renal amyloidosis. Glomeruli showed variable widening of mesangial regions with deposition of periodic schiff stain (PAS) pale positive pink matrix showing apple green birefringence on Congo-red staining under polarizer. Immunohistochemistry was AA stain positive (Figure 1). Immunofluorescence microscopy revealed no staining with anti-human IgG, IgM, IgA, C3, C1q, kappa and lambda light chains antisera. Patient was treated symptomatically for respiratory tract infection and was discharged with low dose angiotensin receptor blocker.