A case of membranoproliferative glomerulonephritis and AA amyloidosis complicated with pulmonary nontuberculous mycobacterial infection

Abstract

A 75-year-old man was diagnosed with pulmonary nontuberculous mycobacterial (NTM) infection in February 2005 and was treated with rifampicin, ethambutol, and clarithromycin. However, the infection was resistant to treatment, and his chest radiograph showed an abnormality that gradually seemed to aggravate. The patient's sputum was positive for Mycobacteria. Moreover, the patient had dyspnea and an underlying chronic inflammation in the lungs. He visited our hospital because of dyspnea and leg edema in June 2011. Laboratory evaluation on admission revealed proteinuria (6 g/day) and decreased serum total protein (5.8 g/dL) and albumin (1.6 g/dL) levels, indicating nephrotic syndrome. Percutaneous renal biopsy revealed membranoproliferative glomerulonephritis (MPGN) in the acute stage and AA amyloidosis of mild degree. AA amyloidosis was also diagnosed histologically on gastric and colonic biopsy, in addition to renal biopsy. His renal function decreased gradually, and therefore, he underwent hemodialysis therapy in January 2012. However, his gastrointestinal-related symptoms persisted, and his appetite diminished, because of which he had become severely malnourished; he died 8 months later. This is a rare case of a patient with two different renal lesions (MPGN and AA amyloidosis) complicated with NTM. Our case suggests that MPGN and amyloidosis should be considered in elderly patients with nephrotic syndrome onset and chronic inflammation.

Keywords: Amyloidosis; Membranoproliferative glomerulonephritis; Nontuberculous mycobacterial infection.

Fig. 1

Chest X-ray and CT findings showing infiltration into the lungs of both sides

Fig. 2

a Light microscopy showing lobulation of glomerular tufts, endocapillary proliferative change, double contour of glomerular basement membrane, increase in mesangial cells and mesangial matrix (PAS staining, ×200). b, c Immunofluorescence microscopy showing deposition of IgG (b) and C3 (c) in mesangium and partly capillary wall

Fig. 3

a Electron microscopy (×3000) showing mesangial interposition and deposits in the subepithelial, subendothelial, and mesangial area. b Electron microscopy (×25000) showing amyloid fibrils

Fig. 4

a, b, c Light microscopy showing the presence of amyloid deposits of glomeruli, gastric mucosa, and intestinal mucosa (congo-red staining, kidney ×200, intestinum ×100). d, e, f The presence of amyloid deposits disappear when treated with potassium permanganate (KMnO₄) was disclosed. g Direct fast scarlet staining, kidney, low-power image

Fig. 5

Clinical course