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Biomedical subjects

I J Simpson

Publications and source records attributed to I J Simpson.

At least 37 records · Page 2Linked to original sources
PubMed1983

Lupus nephritis: clinicopathological correlations.

We have reviewed our experience of lupus nephropathy in Auckland over a 15 year period during which time 70 biopsies were obtained from 56 patients with systemic lupus erythematosus. Based on appearances by light microscopy, the biopsies were categorised as mesangial, focal, diffuse or membranous lupus nephritis. Immunofluorescence, where performed, was positive in all instances, including those biopsies showing only mesangial disease by light microscopy. By electronmicroscopy, biopsies with mesangial disease by light microscopy usually had deposits confined to the mesangium, while more severe forms of disease usually had deposits present both around the loops and in the mesangium. Clinical renal abnormalities were uncommon in the mesangial group, usual in the focal group and ubiquitous in the diffuse group. Notably, four of the 18 patients who had no clinical renal or urinary abnormalities, had focal or diffuse disease, indicating a small but definite risk of missing significant renal disease if a biopsy is not performed.

Adult↗
PubMed1983

Immune complexes in normal subjects.

Immune complex (IC) levels were measured in normal subjects using the C1q solid phase, C1q deviation, C1q binding and polyethylene glycol precipitation assays. Significant changes in IC levels were seen in normals with each of the assays but the pattern of variation was not consistent between assays or subjects or in the same subject from day-to-day. There were no consistent changes with meals, time of day, exercise or the prior administration of prednisone. Low levels of IC appear to be normal in plasma but the variation in IC levels is not explained. Normal IC may well comprise mixtures of non-specific immunoglobulin aggregates, rheumatoid factor-immunoglobulin complexes, idiotype-anti-idiotype complexes as well as specific antibody complexes with antigens from food, infective agents and other sources.

Adult↗
PubMed1983

Circulating immune complexes in myocardial infarction.

Thirty-one patients with proven acute myocardial infarction (MI) were studied prospectively at the time of admission to hospital and at 3, 7 and 18 days using 4 immune complex (IC) assays. Each assay showed an increased incidence of IC activity in MI with 76% of patients being positive in at least 1 assay on one or more of the sampling days. A positive IC assay did not show a significant correlation with cardiac failure, pericarditis, post MI syndrome or previous infarction. The presence of IC was found to correlate with serum C-reactive protein (CRP), serum enzymes and ESR and suggested that complexed CRP or other acute phase proteins may account for some of the IC activity found with less specific assays. The measurement of IC levels in MI has not proved helpful in the diagnosis, management or prediction of outcome in this disorder.

Antigen-Antibody Complex↗
PubMed1982

Plasma exchange in Goodpasture's syndrome.

The clinical course and levels of anti-glomerular basement membrane (GBM) antibody were compared in 20 patients with Goodpasture's syndrome treated with plasma exchange and immunosuppression (8 patients), immunosuppression alone (4 patients) or no specific therapy (8 patients). There was a more rapid fall in the level of anti-GBM antibody and pulmonary hemorrhage was less protracted in the 8 patients treated with plasma exchange and immunosuppression. In this group, 1 patient who presented with severe renal failure showed a marked improvement of renal function and there was no progression of disease in the 4 with milder renal involvement. 2 of the 4 patients treated with immunosuppression alone, and only 2 of the 8 patients who received no specific therapy, maintained normal renal function. In the group which received no specific therapy, 1 of the 6 patients who progressed to renal failure had mild renal involvement initially. There was a significant correlation between the level of anti-GBM antibody and the severity of the morphological changes seen at renal biopsy but not between the level of anti-GBM antibody and the severity of lung hemorrhage. The course and outcome of the disease in those patients not treated, or treated with immunosuppression alone, was better than that described in early reports of this disease, while those patients with plasma exchange and immunosuppression fared even better. An adequately stratified controlled trial of immunosuppression and plasma exchange versus immunosuppression alone is in order.

Adolescent↗
PubMed1982

Immune complex-like activity associated with abnormal serum lipoproteins in systemic erythematosus.

Sera from four patients with systemic lupus erythematosus (SLE) were shown to contain abnormal lipoproteins which behaved as immune complexes (IC). One IC lipoprotein (IC VLDL) had the density in ultracentrifugation of very low density lipoprotein, but a markedly altered electrophoretic mobility. A second IC lipoprotein (IC LDL) had the electrophoretic mobility of very low density lipoprotein but was slightly denser than low density lipoprotein on ultracentrifugation. Both the IC VLDL and IC LDL contained IgG and behaved as IC in the Clq deviation test, platelet aggregation and rheumatoid factor inhibition assays, but not in the conglutinin and Clq binding assays and the Clq solid phase assay. These differences could be due to the low densities of the IC VLDL and IC LDL. The abnormal lipoprotein IC disappeared with clinical remission in two patients and were not present in the sera of other patients with inactive or mild SLE, Type IV hyperlipidaemia, or during prednisone therapy or plasma exchange for other conditions. These IC appeared to be markers of severe and active SLE.

Adolescent↗
PubMed1981

The clinical significance of right ventricular infarction.

Three patients with inferior myocardial infarction complicated by predominant right ventricular (RV) dysfunction are described. Two patients had clinical and haemodynamic evidence of RV infraction associated with pump failure and improved with infusion of plasma expanders and inotropic agents. A third patient presenting with severe RV failure without left ventricular (LV) dysfunction illustrated the haemodynamic similarities between RV infarction and pericardial tamponade.

Aged↗
PubMed1981

Goodpasture's syndrome with normal renal function.

Two young men with anti-glomerular basement membrane (anti-GBM) antibody-induced Goodpasture's syndrome are described. Despite the characteristic renal morphological features and high titers of anti-GBM antibody, they had normal renal function. Both patients recovered spontaneously without treatment and remain well with normal renal function more than four years after presentation. The use of more sensitive diagnostic techniques has demonstrated that there is a broad spectrum of clinical severity in this disease and that mild cases can be expected to have a good outcome.

Adolescent↗
PubMed1980

Therapeutic plasmapheresis by continuous flow cnetrifugation.

This report reviews the experience at Auckland Hospital with continuous flow centrifugation as a mean of carrying out therapeutic plasmapheresis. Over a three year period from August 1975, 26 patients, most with dysproteinaemias or Goodpasture's syndrome, were treated with a total of 260 therapeutic procedures.

Adolescent↗
PubMed1978

Prolonged complement activation in mice.

Because antibody responses to the alternative complement pathway activator, cobra venom factor, are T-dependent and B mice therefore do not develop resistance to its action, it was possible to examine whether renal injury occurs under circumstances of protracted third-phase alternative pathway activation. After periods of up to three months, no evidence from measurements of blood urea or proteinuria or from examinations with light microscopy immunofluorescence or electron microscopy was obtained to indicate a directly nephrotoxic effect of this type of complement activation.

Animals↗
PubMed1978

Goodpasture's syndrome: an analysis of 29 cases.

The pathologic features of 29 cases of Goodpasture's syndrome occurring during a 13-yr period in Auckland have been reviewed and correlated with clinical findings. There were 20 males and nine females in the series; two of the males and three of the females were Maoris. Age at the time of onset of symptoms ranged from 17 to 75 yr, with about 76% of the patients being from 17 to 27 yr of age. Sixteen (55%) of the patients died from less than a week up to about two years following the onset of symptoms, and the remaining 13 are live from 30 weeks to 14 yr after initial presentation. Underlying renal disease varied from mild focal glomerulitis to end-stage glomerulonephritis by light microscopy, but characteristic glomerular changes were seen in all specimens examined by electron and immunofluorescent microscopy. The lungs of 13 of the patients examined at autopsy showed typical abnormalities. The syndrome pursues a notably variable clinical course, affects a considerable proportion of females, occurs over a wide age range, and appears to be disporportionately common among Maoris.

Adolescent↗
PubMed1978

Complement-mediated immune mechanisms in renal infection. II. Effect of decomplementation.

Animals were depleted of complement using cobra venom factor and the influence of complement depletion on the course of renal infection was studied. Complement depletion markedly increased the susceptibility of renal tissue to a challenge with an E. coli strain sensitive to the bactericidal activity of normal serum, but did not influence the outcome of a challenge with a serum-resistant strain of E. coli. These observations are consistent with the hypothesis that complement-mediated host immune mechanisms do play a role in the biology of renal infection and are an important component of the host's immune response in pyelonephritis.

Animals↗
PubMed1977

Guinea-pig nephrotoxic nephritis II. Autologous phase: complement activation without detectable injury.

In the autologous phase of nephrotoxic induced by sheep antibody to glomerular basement membrane (GBM) in Dunkin-Hartley and C4 deficient strain guinea-pigs, less than 50% of animals developed proteinuria at the height of the autologous antibody response despite high anti-sheep immunolglobulin tetres and fixation of guinea-pig IgG and complement in the kidney. tonly two of thirty-sdven animals (5-4%) developed progressive. In a passive model of autologous phase injury using high titres rabbit antibody to sheep IgG, proteinuria failed to occur despite fixation of up to 95 microng rabbit antibody per kidney. Repeated injection of sheep nephrotoxic antibody (NTab) caused a persisting nephrotic syndrome but not the characteristic proliferative lesion of anti GBM diseases in other species.

Animals↗
PubMed1976

Defibrination with ancrod in nephrotoxic nephritis in rabbits.

Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. When further glomerular fibrin deposition was prevented by defibrination, deposited fibrin was rapidly removed, indicating that glomerular fibrin-clearing mechanisms are retained in crescentic nephritis. Defibrination had no effect on the extent of glomerular C3 deposition or on the amount of proteinuria.

Ancrod↗
PubMed1976

The role of C3 in the autologous phase of nephrotoxic nephritis.

The role of complement has been studied in the autologous phase of nephrotoxic nephritis (NTN) in rabbits. No reduction in glomerular fibrin deposition, crescent formation or protection from renal failure was observed in either the standard model of NTN when decomplementing doses of cobra venom factor (CVF) were given before the autologous phase or in a telescoped model when CVF was administered before the nephrotoxic antibody. In the latter situation glomerular fibrin deposition and crescent formation were found in the absence of detectable deposition of C3. However, substantial protection was observed when circulating polymorphonuclear leucocytes (PMN) were depleted by antipolymorph serum. These observations establish the existence of a system of allergic glomerular injury mediated by PMN but independent of C3. It is postulated that this system may account for the glomerular injury seen in patients with Goodpasture's syndrome in whom glomerular C3 deposition is not found.

Animals↗
PubMed1975

Recovery from Goodpasture's syndrome after immunosuppressive treatment and plasmapheresis.

A patient with Goodpasture's syndrome has recovered after treatment with immunosuppressive drugs (cyclophosphamide and prednisolone) and removal of circulating antibodies by plasma exchange. This was performed on seven occasions and seems to have hastened the decline in circulating antibody levels. Undertaken early in the course of the disease plasmapheresis could prove a useful addition to its therapy.

Adult↗
PubMed1975

Guinea-pig nephrotoxic nephritis. I. The role of complement and polymorphonuclear leucocytes and the effect of antibody subclass and fragments in the heterologous phase.

In guinea-pig nephrotoxic nephritis induced by a sheep antibody there was minimal glomerular capillary deposition of C3 and accumulation of polymorphonuclear leucocytes (PMN) in the heterologous phase. The C4-deficient strain developed the same injury as normal Duncan-Hartley animals. Complement depletion with cobra venom factor, polymorph depletion with nitrogen mustard or anti-PMN serum and treatment with antihistamines provided no protection. The relationship between the dose of nephrotoxic antibody and the proteinuria was similar for gamma1 and gamma2 subclasses and the F(ab')2 fragment of gamma1 antibody. However, the F(ab') and F(ab) antibody fragments, though fixing on the glomerular basement membrane, did not cause proteinuria. It is concluded that the development of proteinuria in this system: is largely independent of the complement-polymorph system; is due to the fixation of the F(ab')2 fragment of the antibody molecule; and does not depend on an intact Fc piece.

Animals↗