Neutropenia with each standard antituberculosis drug in the same patient.

The finding of deposits embedded in the basement membrane and electron-lucent lacunae may be characteristic of many cases of idiopathic membranous glomerulonephritis. Successive exposures to hydrocarbons, however, are thought to be followed by a corresponding sudden rise in deposits or in situ formation of immunocomplexes at glomerular level. The immunocomplexes may consist of renal tubular epithelial components or plasma proteins that become antigenic on contact with the hydrocarbon, and the antibodies would be directed against these antigens. Each period of contact with the hydrocarbons was quickly followed in our patient by an increase in proteinuria, which quickly disappeared when he was no longer exposed. We cannot therefore exclude the hypothesis of Lagrue et all that the inhaled toxin may alter the pulmonary alveolar macrophages. These changes would lead to the later release of enzymes or proinflammatory substances which, after a time, act on capillary permeability. Although the mechanism of glomerular injury induced by hydrocarbons may be unknown, our case gives further evidence of a cause-and-effect relation between hydrocarbon exposure and glomerulonephritis.