ROLE OF GAMMA GLOBULINS IN PATHOGENESIS OF RENAL LESIONS IN SYSTEMIC LUPUS ERYTHEMATOSUS AND CHRONIC MEMBRANOUS GLOMERULONEPHRITIS, WITH AN OBSERVATION ON THE LUPUS ERYTHEMATOSUS CELL REACTION

Utilizing the fluorescent antibody method for the histologic demonstration of localized γ-globulins, we have made the following observations (in contradistinction to the lack of such findings in a variety of normal and pathologic, control kidneys). In systemic lupus erythematosus (a) γ-globulins were localized in the thickened capillary walls, the "wire-loop" lesions, and the so called "hyaline thrombi" in glomeruli; (b) these sites of localization of γ-globulins were correlated to a considerable degree with the pattern of accentuated eosinophilia of the glomeruli, as seen in hematoxylin-eosin sections, or with the pattern of PAS-positive areas in the glomeruli in sections stained with the periodic acid-Schiff reaction; (c) and γ-globulins were localized rarely in large cytoplasmic granules in tubular epithelium and occasionally in glomerular capsular crescents, tubular protein casts, and inflammatory cells, particularly in the cytoplasm of cells identified as immature and mature plasma cells. In nephrotic glomerulonephritis (a) γ-globulins were localized in the glomerular basement membrane and appertaining structures in chronic membranous glomerulonephritis; (b) γ-globulins were apparently localized in the altered mesangium in chronic lobular glomerulonephritis; and (c) in the tubular protein casts, presumably representing abnormal glomerular filtrates, γ-globulins were present in a lesser concentration and other serum proteins in a greater concentration than found in the glomeruli. In positive lupus erythematosus preparations the nuclei of leukocytes, while undergoing transformation and subsequent phagocytosis to form lupus erythematosus cells, were the sites of localization of γ-globulin (presumably the lupus erythematosus factor) whereas in control preparations no nuclear localization of γ-globulin occurred. These observations are discussed in relation to the pathogenesis of renal lesions in systemic lupus erythematosus, chronic membranous glomerulonephritis, and amyloidosis.