UNLABELLED: The pathogenesis of an immune complex-mediated membranoproliferative glomerulonephritis (IMPGN) involves persistent deposition of circulating immune complexes in the glomeruli caused by persistent antigenemia. We have previously reported relatively high incidence of IMPGN in Lithuania. The objective of our study was to evaluate potential causes of persistent antigenemia in the patients with IMPGN. MATERIAL AND METHODS: Forty-five patients with IMPGN diagnosed on renal biopsy during 2000-2002 were retrospectively evaluated for the presence of persistent bacterial or viral infections, autoimmune diseases and other associated medical conditions. Patients with established diagnosis of systemic lupus erythematosus (SLE) before the biopsy were not included in the study. RESULTS: A great majority (20; 44%) of the patients were found to have persistent bacterial infections of various localization. Four patients (9%) were infected with hepatitis B virus (HBV). Three (7%) patients were eventually diagnosed with SLE and another 3 (7%) had other associated pathology. In the remaining 15 (33%) patients, IMPGN remained idiopathic. Testing for hepatitis C virus (HCV) antibody was performed in 36 patients (12 of them with idiopathic IMPGN) and was negative in all patients. Testing for HCV RNA was not performed. Patients with bacterial infections were significantly younger compared to the group of idiopathic IMPGN (36.5+/-19.1 and 53.8+/-16.4, respectively, p=0.01). We conclude that persistent bacterial infection was a major potential source of antigenemia in our patients with IMPGN, particularly in the younger patients, while HBV and HCV infection was rarely detected.
UNLABELLED: The pathogenesis of an immune complex-mediated membranoproliferative glomerulonephritis (IMPGN) involves persistent deposition of circulating immune complexes in the glomeruli caused by persistent antigenemia. We have previously reported relatively high incidence of IMPGN in Lithuania. The objective of our study was to evaluate potential causes of persistent antigenemia in the patients with IMPGN. MATERIAL AND METHODS: Forty-five patients with IMPGN diagnosed on renal biopsy during 2000-2002 were retrospectively evaluated for the presence of persistent bacterial or viral infections, autoimmune diseases and other associated medical conditions. Patients with established diagnosis of systemic lupus erythematosus (SLE) before the biopsy were not included in the study. RESULTS: A great majority (20; 44%) of the patients were found to have persistent bacterial infections of various localization. Four patients (9%) were infected with hepatitis B virus (HBV). Three (7%) patients were eventually diagnosed with SLE and another 3 (7%) had other associated pathology. In the remaining 15 (33%) patients, IMPGN remained idiopathic. Testing for hepatitis C virus (HCV) antibody was performed in 36 patients (12 of them with idiopathic IMPGN) and was negative in all patients. Testing for HCV RNA was not performed. Patients with bacterial infections were significantly younger compared to the group of idiopathic IMPGN (36.5+/-19.1 and 53.8+/-16.4, respectively, p=0.01). We conclude that persistent bacterial infection was a major potential source of antigenemia in our patients with IMPGN, particularly in the younger patients, while HBV and HCV infection was rarely detected.