Mesangial proliferative glomerulonephritis with deposits of anti-nicotinic acetylcholine receptor antibody in a patient with myasthenia gravis.
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.
Mitsui
T
T
First Department of Internal Medicine, School of Medicine, The University of Tokushima, Kuramoto-3, Tokushima, 770-8503, Japan.
Okada
K
K
Kuhara
T
T
Hashizume
T
T
Okazaki
S
S
Kawajiri
M
M
Matsumoto
T
T
D000328:Adult; D001323:Autoantibodies / Q000032:analysis*; D001706:Biopsy; D005260:Female; D015432:Glomerulonephritis, Membranoproliferative / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D006801:Humans; D009157:Myasthenia Gravis / Q000150:complications* / Q000276:immunology*; D011978:Receptors, Nicotinic / Q000276:immunology*
D001323:Autoantibodies; D011978:Receptors, Nicotinic