Renal amyloidosis: immunofluorescence and electron microscopy studies.

Renal biopsy specimens of 15 patients with renal amyloidosis were studied by immunofluorescence microscopy. The amyloidosis was associated with chronic pulmonary disease in five, rheumatoid arthritis in one, chronic lymphocytic leukemia in one, and familial Mediterranean fever in five patients. In three patients no associated condition could be determined although the pattern of organ involvement resembled that of secondary amyloidosis. IgG and complement (C3) were demonstrated in the glomerular capillary walls and in the mesangium in all patients. The pattern of the deposits was neither granular nor linear. Ig and C3 appeared as large confluent masses or broad ribbon-like segments. In the six patients studied by electron microscopy the fibrillary formation of amyloid was seen in the mesangium and the glomerular capillary walls corresponding to the Ig deposits. No immunofluorescence or ultrastructural differences were observed among the patients with secondary, inherited and leukemia-associated amyloidosis included in this study.

Acute glomerulonephritis. Immunofluorescent and electron-microscopic observations in sporadic cases.

The authors studied by immunofluorescent and electron microscopy renal biopsy specimens from 29 patients with various glomerular diseases. Poststreptococcal glomerulonephritis was characterized by the presence of complement (beta1C) in the mesangium and/or on the basement membrane in all cases. Immunoglobulin G (IgG) was also present in less than half of the cases in the same distribution. Electron microscopy, carried out in six cases, revealed no uniform ultrastructural change: minimal subepi helial deposits were observed in three cases, intramembranous deposits were seen in two cases, and the basement membrane was normal in one case. Glomerular abnormalities during the courses of some systemic diseases were similar. Mild renal involvement was characterized by only beta1C deposition. This finding raises the question whether a mechanism other than or in addition to that involving immune complexes is operative in the pathogenesis of acute glomerulonephritis. There is circumstantial experimental evidence that an alternate pathway of complement activation and deposition may be operative in acute glomerulonephritis.