A Possible Clue for the Production of Anti-Glomerular Basement Membrane Antibody Associated with Ureteral Obstruction and Hydronephrosis

Abstract

Background: Anti-glomerular basement membrane (anti-GBM) antibody-mediated glomerulonephritis (anti-GBM GN) is an autoimmune disease with rapidly progressive glomerulonephritis. Based on a case report of anti-GBM GN following hydronephrosis, we hypothesized that hydronephrosis may act as a trigger for the development of anti-GBM antibodies. Patients and Methods: We evaluated 11 patients who were diagnosed with hydronephrosis. It was measured with serum anti-GBM antibody. These patients' medical histories as well as risk factors for the development of anti-GBM antibodies and causes of hydronephrosis were reviewed. Renal function and hematuria were also considered. The serum anti-GBM antibody was measured with enzyme-linked immunosorbent assays (ELISA) or chemiluminescent enzyme immunoassays (CLEIA). Histopathological findings of renal biopsy specimens were also evaluated. Results: No patient had a medical history of renal disease. Five patients had a history of smoking. Ten of the 11 patients had renal dysfunction as evidenced by serum creatinine levels of 0.85-13.8 mg/dl, while 8 patients had RBCs in their urinary sediment at the time of diagnosis for hydronephrosis. Two of the patients assessed by ELISA and CLEIA were positive for anti-GBM antibodies. In 1 of these 3 patients, anti-GBM antibodies and renal dysfunction improved upon treatment for hydronephrosis. Another of the 3 patients developed anti-GBM GN, but anti-GBM antibodies and renal dysfunction improved dramatically upon treatment. In the 3rd patient without improved hydronephrosis, anti-GBM antibodies and renal dysfunction remained unchanged. Conclusion: Our results provide insights into the development of anti-GBM antibodies in patients with ureteral obstruction and hydronephrosis.