Circulating immune complexes in cutaneous and systemic vasculitis: clinicopathological correlations.

A high incidence of raised levels of circulating immune complexes has found in a group of patients with idiopathic vasculitis. Serial measurements in 8 patients with systemic vasculitis showed a good correlation between clinical status and circulating immune complex levels. Some correlation existed between the constituents of circulating and tissue-bound complexes in 6 patients so studied. However, there was no correlation between apparent organ involvement and hypocomplementaemia and the levels of size of circulating immune complexes. It is concluded that the measurement of circulating immune complexes may be clinically useful in vasculitis, but that no direct evidence is yet available that they are pathogenetically related to those which are tissue-bound.

Infective endocarditis-associated glomerulonephritis in rabbits: evidence of a pathogenetic role for antiglobulins.

Serial studies of circulating immune complexes, serum complement, proteinuria and renal histology and immunofluorescence have been undertaken in infective endocarditis glomerulonephritis in rabbits. Eighteen of 24 rabbits developed evidence of glomerulonephritis and 13 of 18 had circulating immune complexes. Gel filtration studies showed the immune complexes to have a size range of ca 4.10(6)--3.10(5) daltons. Direct immunofluorescence staining of glomeruli showed that IgM was the predominant immunoglobulin present and that antiglobulin activity was associated with IgM deposition. Intraglomerular localization of antiglobulin was closely associated with evidence of glomerulonephritis. Streptococcal antigen(s) were not demonstrable in glomeruli, even after acid elution of sections.

Quantitative assessment of the effects of platelet depletion in the autologous phase of nephrotoxic serum nephritis.

The effects of platelet depletion with antibody have been studied in two models of the autologous phase of nephrotoxic nephritis in the rabbit. In the 'telescoped' model (animals pre-immunized to sheep IgG injected with sheep nephrotoxic antibody), platelet depletion did not alter intraglomerular fibrin deposition or evidence of glomerular damage, but did significantly reduce proteinuria during the first 3 days of the 5 day experiment. In the 'passive' model (animals injected with hyperimmune rabbit antiserum to sheep IgG 48 hr after sheep nephrotoxic antibody and killed 3 hr later), platelet depletion was associated with significantly fewer intraglomerular polymorphonuclear leucocytes (PMN), but again did not alter intraglomerular fibrin deposition. The results indicate that platelets are involved in the initiation of glomerular PMN localization in the autologous phase, but that fibrin-induced glomerular injury is platelet-independent.

The mediation of the localization of polymorphonuclear leucocytes in glomeruli during the autologous phase of nephrotoxic nephritis.

A passive model of the autologous phase of nephrotoxic nephritis (NTN) in rabbits was developed to study the events at the initiation of this stage of the disease. Intravenous injection of sheep anti-rabbit glomerular basement membrane antiserum was followed 48 hr later by 125I trace labelled rabbit anti-sheep IgG. Animals were killed 3 hr after the second antibody injection. Experiments were undertaken to investigate whether or not a reaction between the passive antibody Fc piece and polymorphonuclear leucocyte (PMN) Fc receptor occurred, causing the localization of PMN in glomeruli in the autologous phase of NTN. The results indicate that such a reaction is an important, but not exclusive, factor in glomerular PMN localization. The complement independence of the localization was confirmed. In addition, it appeared that PMN-dependent intraglomerular fibrin deposition was mediated exclusively by a reaction between antibody Fc piece and PMN Fc receptor.