Adult nephrotic syndrome: Clinicopathological correlation and results of treatment.
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Biomedical subjects
Publications and source records attributed to V Boonpucknavig.
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We undertook a correlative study between the frequency and patterns of immunoglobulin deposits at the dermoepidermal junction of clinically normal skin and the morphologic features (histopathologic and immunopathologic) of the glomerular lesions and various immunologic measurements in 38 patients with systemic lupus erythematosus. Thirty-five (92.1%) showed a positive immunoglobulin band at the skin. A statistically significant (P less than .001) correlation was observed between the pattern of deposit and the duration of disease. The stippled pattern was found to be more common in those cases of less than one year's duration, while the thready pattern was more common in those cases lasting longer than one year. There seemed to be no significant relationship between either the frequency (P greater than .100) and pattern (P greater than 0.25) of the immunoglobulin band and the glomerular pathologic or other immunologic measurements.
Renal pathological changes were studied by renal biopsy in 31 patients bitten by tropical poisonous snakes which included seasnake (2 cases), cobra (11 cases), green-pit viper (8 cases) and Russell's viper (10 cases). Renal failure was present only in patients bitten by seasnake and Russell's viper. Glomerular mesangial proliferation was noted in the victims of cobra, green-pit viper and Russell's viper. There was deposition of IgM AND C3 in the glomerular mesangium with extension along the capillary walls. Fibrin deposition was seen in green-pit viper cases. By electron microscopy electron dense deposits were observed in the glomerular basement membrane-like matrix. Irregular thickening of the basement membrane was found in cobra cases. Vascular changes included arteritis of the interlobular artery with C3 deposition in the arterial walls in Russell's viper cases and thrombophlebitis in both green-pit viper's and Russell's viper's victims. Dense deposits of C3 in the arteriolar walls were noted in viper-bite and cobra-bite. Tubular necrosis was demonstrated in patients envenomated by green-pit viper and Russell's viper. Necrosis was severe in seasnake and Russell's viper poisoning, but was mild in green-pit viper cases.
Swiss albino mice infected with Plasmodium berghei berghi showed the serum-soluble malarial antigen and antibody on day 10 of infection onward. Immune complex nephritis in these mice developed on the seventh day after inoculation. The infected kidneys revealed the deposition of mouse gamma globulin, mouse beta1C globulin and malaria antigen along the capillary wall of the glomeruli. Proteinuria was detected on seventh day of infection. Serum-soluble malaria antigen in probably responsible for forming the soluble immune complex which causes glomerulonephritis in infected mice.
Percutaneous needle biopsies were performed on the kidneys of 20 patients who had dengue hemorrhagic fever with some clinical manifestation of renal impairment. In ten cases IgG or IgM, or both, and C3 could be localized in the glomeruli, using the fluorescent antibody technique. In those cases in which immune complex was found, the biopsy had been done in the second week after the onset of fever. Electron microscopy showed focal thickening of the glomerular basement membrane, with hypertrophy of mesangial cells at the sites where the immune complex was shown. Dense, spherical particles, 40 to 50 nm in diameter, were found in 12 cases. Those particles were carried into the glomeruli by monocyte-like cells.
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Renal glomeruli of Plasmodium berghei infected mice were studied electron microscopically. The endothelial cell proliferation and endothelial cytoplasmic changes were greatly stimulated on day 7, at the time when there were collections of dense granular aggregates in the glomerular capillary lumens and electron-dense deposits in the mesangial areas. The basement membrane lesion developed with the infiltration of polymorphonuclear leucocytes on day 14 with more electron-dense deposits in the mesangial areas and in the basement membrane. On the basis of these ultrastructural alterations and on previous findings of immune complex (P berghei antigen, mouse globulin and mouse beta1C globulin) deposits by immunofluorescent study, we concluded that glomerular lesions in P berghei infected mice are induced by immune mechanism.
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