Renal fibrin deposition associated with isoimmune haemolysis in monkeys: observation by light, electron and immunofluorescence microscropy.
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Animals↗
Biomedical subjects
T R Poskitt
Publications and source records attributed to T R Poskitt.
Naturally occurring immune-complex glomerulonephritis in monkeys (Macaca irus). I. Light, immunofluorescence and electron microscopic studies.
Light, immunofluorescence and electron microscopic studies were carried out on renal biopsies from 32 randomly selected adult monkeys (Macaca irus). Histopathology was limited to glomeruli and consisted of mild to moderate segmental increases in mesangial cells, mesangial matrix, and/or glomerular basement membrane (GBM) thickness in 41% of the animals. Granular deposits of IgM were present in the mesangial region and along the GBM in 72% of the monkeys, whereas IgG, C1q, C4 and C3 were detected in approximately 30%. Electrondense deposits were seen predominantly in epithelial foot processes adjacent to the GBM and, to a lesser extent, in the mesangium. Those monkeys with the heaviest IgM deposition were found to have decreased serum levels of C3, IgM and IgA. Follow-up biopsies over a period of 3 to 11 months revealed that the disease process was persistent yet nonprogressive. No correlation with age or sex was noted. All animals examined were clinically healthy and had normal renal function. This is the first documented occurrence of spontaneous immune-complex glomerulonephritis in a large monkey population. It appears to be a persistent disease which does not progress to renal insufficiency and which may serve as an investigative model for mild nonprogressive forms of human glomerulonephritis.
Animals↗
Activation of the alternate complement pathway by autologous red cell stroma.
The present study demonstrates the ability of human autologous RBC stroma to activate the alternate complement pathway (C3-Activator system, properdin system), as evidenced by the generation of C3-Activator (C3A) from C3-Proactivator (C3PA) when RBC ghosts and sonicated ghosts are incubated with autologous serum. Intact RBC's, hemoglobin, and concentrated platelet stroma, on the other hand, are inactive in this regard. We postulate that this in vitro activity of RBC stroma may occur intravascularly when erythrocytes are damaged by immune or nonimmune mechanisms. The ensuing interaction of activated complement components with platelets leading to release of platelet factor three (PF-3) may constitute a mechanism for activation of the coagulation system during acute hemolytic episodes.
Blood Coagulation↗
Immunologic and electron microscopic studies in Goodpasture's syndrome.
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Adult↗
The renal effect of intravenous adenine in humans.
The purine base, adenine, improves the posttransfusion viability of liquid stored blood. However, adenine in high doses may cause kidney damage becuase of the precipitation in renal tubules of its incoluble metabolite, 2,8-dioxyadenine. Adenine is not licensed for use in the United States because it may be nephrotoxic. In a controlled, randomized, double-blind study, eight human subjects received 10 mg/kg of adenine infused intravenously over one hour, four subjects received 5 mg/kg, and four subjects received no adenine. Renal function tests were performed on each subject before adenine infusion and one day and one week following the infusion. Tests included an assessment of glomerular function (serum creatinine, creatinine clearance, protein excretion), proximal tubular function (amino acid and glucose excretion), and distal tubular function (maximal acidifying and concentrating ability). Plasma and urine levels of adenine and 2,8-dioxyadenine were measured. Renal function tests showed no evidence of kidney damage secondary to adenine.
Adenine↗
A study of weak subgroups of blood group A with an antiglobulin-latex test.
The distribution of the blood group A antigen on subgroups A1, A2, A3, Ax, and Ae1 was studied by means of a highly sensitive and specific antiglobulin-latex test. Marked variability in the cell to cell expression of A antigen was observed in A1 and A2 cells. The weaker subgroups (A3, Ax, and Ae1) were characterized by a minor population of cells containing A antigen and a major population with no detectable A sites. Comparison of the antiglobulin-latex test with the fluorescent antibody technique indicates that the former is approximately 10,000 times more sensitive in detecting cell bound antibody, and thereby membrane antigens. The results of this study demonstrate that within each of the A subgroups (with the possible exception of A1) there exist erythrocytes that apparently lack recognizable A antigen sites. The number of such cells is greatest in the weakest subgroups (Ax and Ae1).
ABO Blood-Group System↗