A patient with myasthenia gravis developed nephrotic syndrome 3 years after thymectomy. The kidney biopsy specimen revealed mesangial proliferative glomerulonephritis with immune deposits. The glomerular mesangial cells and tubular epithelial cells were sensitive to alpha-bungarotoxin (alpha-BT), a ligand for nicotinic acetylcholine receptor (nAChR), and the binding was inhibited by native alpha-BT, as well as other nAChR ligands, nicotine and d-tubocurarine. In addition, FITC-alpha-BT-neuromuscular junction complexes could also bind to the mesangial cells, and preincubation with unlabeled nAChR inhibited the binding. These findings are consistent with the notion that both nAChR-like protein and anti-nAChR antibody are present in t he mesangial cells of the patient. Although the pathogenetic role of anti-nAChR antibody on the development of glomerulonephritis is unclear, the present observations provide an important insight into the autoimmune-mediated pathophysiological relationship between myasthenia gravis and mesangial proliferative glomerulonephritis.
Copyright 2001 Harcourt Publishers Ltd.