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Biomedical subjects

A F Michael

Publications and source records attributed to A F Michael.

At least 217 records · Page 12Linked to original sources
PubMed1973

Properdin anc C3 proactivator: alternate pathway components in human glomerulonephritis.

Serological and immunopathological studies of human glomerulonephritis have suggested that alternate pathways of activation of the third component of complement may be important in some forms of glomerulonephritis. We have investigated the role of two alternate pathway proteins, properdin and C3 proactivator, in 22 patients with chronic membranoproliferative glomerulonephritis, 21 patients with systemic lupus erythematosus, 20 patients with acute poststreptococcal glomerulonephritis, and 19 patients with other forms of renal disease. C3 (measured at beta(1)A), properdin, and C3 proactivator were assayed by single radial immunodiffusion. In sera with low beta(1)A (< 2 SD), mean properdin was most significantly decreased in patients with acute poststreptococcal glomerulonephritis but was also significantly decreased in chronic membranoproliferative glomerulonephritis and in untreated systemic lupus erythematosus. Properdin levels in other renal disease, acute glomerulonephritis, and chronic membranoproliferative glomerulonephritis with normal beta(1)A levels were not significantly different from normal. A positive correlation between beta(1)A and properdin levels in individual sera was present in all diseases except systemic lupus erythematosus. Serum C3 proactivator was markedly decreased in active systemic lupus erythematosus and there was a positive correlation between beta(1)A and C3 proactivator levels in systemic lupus erythematosus and other renal diseases but not acute poststreptococcal glomerulonephritis. Properdin in fresh sera from four patients with systemic lupus erythematosus and five with chronic membranoproliferative glomerulonephritis showed increased migration toward the cathode on immunoelectrophoresis, suggesting in vivo change of the properdin molecule. The observation of reduced serum levels of properdin and C3 proactivator and altered electrophoretic migration of properdin in some patients with glomerulonephritis provide new evidence for participation of these alternate pathway proteins in glomerulonephritis.

Adolescent↗
PubMed1973

The effect of thorotrast and cortisone on renal cortical fibrinolytic activity in the rabbit.

Previous studies have shown that a single injection of endotoxin inhibits renal cortical fibrinolytic activity in the rabbit. This suggests that the initial injection of endotoxin may prepare for the generalized Shwartzman reaction by depletion of cortical fibrinolytic activity. A fibrin slide technic was used to determine whether Thorotrast(R) and cortisone prepare for the generalized Schwartzman reaction by a similar mechanism. Renal cortical fibrinolytic activity was inhibited following Thorotrast injection, but no inhibition could be detected following cortisone injection. This suggests that Thorotrast, like endotoxin, prepares for the generalized Shwartzman reaction by depletion of cortical fibrinolytic activity. Failure to demonstrate inhibition of lytic activity following cortisone injection may indicate that cortisone prepares for the generalized Shwartzman reaction by another mechanism, or that the fibrin slide technic was unable to detect quantitative changes in lytic activity.

Animals↗
PubMed1972

The glomerular mesangium. I. Kinetic studies of macromolecular uptake in normal and nephrotic rats.

This study was designed to define quantitatively the function of the rat glomerular mesangium in the uptake and processing of intravenously administered protein macromolecules (radiolabeled aggregated human IgG, AHIgG-(125)I), to relate this function to that of the general reticuloendothelial system, and to examine the effects of increased glomerular permeability to protein on the mesangial cell system.Mesangial localization of human IgG as demonstrated by immunofluorescent microscopy showed good correlation with concentrations of AHIgG-(125)I in preparations of isolated glomeruli. In normal rats the concentrations of AHIgG-(125)I in glomeruli were similar to those of lung, liver, and spleen and demonstrated a rapid decrease with increasing time intervals after aggregate administration. In rats given aminonucleoside of puromycin a marked increase in mesangial uptake of aggregates was found while studies of nephrotic lungs, liver, spleen, and blood showed no such differences. Glomerular levels of AHIgG-(125)I in aminonucleoside animals could not be correlated with the quantity of proteinuria. Nephrotic and control animals given unaggregated human IgG showed little glomerular localization by immunofluorescent microscopy; no difference in the concentration of this protein in nephrotic as compared to control glomerular isolates was found.Thus, the mesangium in normal animals functions in a manner analogous to that of the general reticuloendothelial system. In nephrotic rats the mesangial uptake of macromolecules is makedly increased, a finding not observed in other tissues.

Animals↗
PubMed1972

Transfer of aminonucleoside nephrosis by renal transplantation.

The pathogenesis of aminonucleoside of puromycin (PA) nephrotic syndrome in rats was studied using renal transplantation to separate systemic from renal factors. The nephrotic syndrome was transferred by transplantation of kidneys from rats with established proteinuria. Bilaterally nephrectomized normal rats receiving kidneys removed as early as 15 min after intravenous PA injection (100 mg/kg) of donors also developed proteinuria (602+/-125 mg/24 hr) and a nephrotic syndrome after the usual induction period of 4-7 days observed in this disease. Arterial perfusion of isolated kidneys with PA (50 mg/kg) followed by perfusion with isotonic saline 3 min later and then transplantation to normal bilaterally nephrectomized rats led to a nephrotic syndrome. Urine protein excretion was 494+/-42 mg on the 7th day after transplantation. In contrast, urine protein excretion after transplantation of normal kidneys to normal bilaterally nephrectomized rats was 40+/-20 mg on the 7th day. Exposure of a normal kidney to a nephrotic host environment by transplantation of a normal kidney to a unilaterally nephrectomized PA-injected rat did not transfer the disease to the normal kidney. After removal of the nephrotic kidney 11-13 days after transplantation, proteinuria of the donor kidney was normal (21+/-13 mg on day 15). These studies indicate that pathogenesis of aminonucleoside nephrosis involves programming of the kidney directly by PA within minutes after exposure although increased urinary protein excretion does not occur until several days later.

Animals↗