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Biomedical subjects

J Klassen

Publications and source records attributed to J Klassen.

At least 55 records · Page 3Linked to original sources
PubMed1982

An improved solid-phase immunoassay for anti-GBM antibodies.

A solid-phase immunoassay has been developed for the detection of anti-glomerular basement membrane (GBM) antibodies in the circulation of patients with Goodpasture's syndrome and one form of rapidly progressive glomerulonephritis. The procedure involves the formation of a covalent linkage between the antigen and a solid support disc. Antibodies bound to the antigen are then detected on a fluorometer using fluorescein-labeled antisera to human immunoglobulins. The assay is easy to perform, fast, inexpensive and has been optimized with respect to sensitivity, range and reproducibility.

Antibodies↗
PubMed1980

Irreversible attachment of immunoglobulins and F(ab')2 fragments to their specific cell membrane antigens.

Antiserum was raised in sheep against rat kidney glomerular basement membrane, and the antibodies and their F(ab')2 fragments were prepared. These were reacted with one arm of the bifunctional reagent toluene diisocyanate at pH 7.5 and injected into the tail vein of rats. Kidney sections were taken from the rats and, after washing, incubated at pH 8.5 to permit the other arm of the toluene diisocyanate to become reactive. This procedure resulted in the specific irreversible attachment of the antibodies and their F(ab')2 fragments to their corresponding glomerular basement membrane antigens.

Animals↗
PubMed1979

Study of serum beta-2 microglobulin levels in breast cancer patients.

Serum beta-2 microglobulin levels were measured in normal individuals and in breast cancer patients. It was observed that there was a significant rise in levels especially in advanced stages of the disease. It was concluded that patients with a beta-2 microglobulin/creatinine ratio of greater than 3.8 were likely to have metastatic breast cancer.

Beta-Globulins↗
PubMed1979

Autoimmune myocarditis: a clinical entity.

In a case of myocarditis electron microscopic and immunoflourescent studies of a transmural myocardial biopsy specimen indicated an autoimmune process. Extensive inflammatory cell infiltration, immunoglobulin and complement deposition along the sarcolemma and in the interstitium, and capillary endothelial injury were found. After a short course of immunosuppressive therapy the inflammatory process was replaced by collagenous scarring and lymphocytic depletion; the blood vessels were then normal. Earlier therapy in such cases may be lifesaving.

Adult↗
PubMed1979

Late hypertension following renal allotransplantation.

Post-transplant hypertension has been observed in 98 renal allograft recipients who had good renal function and whose follow-up was more than 15 months. The role of the original diseased kidneys as well as the role of the renal pressor system was studied with emphasis on late hypertension. Post-transplant hypertension was found to be a multifactorial phenomenon with frequency decreasing as a function of prolonged graft survival. Renal artery stenosis was an infrequent but significant cause of hypertension and was found in 10 of 29 arteriograms performed. Renin studies performed in 34 hypertensive patients and in a control group of 11 recipients showed that elevation of plasma renin activity and of plasma aldosterone level is frequent but difficult to interpret, particularly when a renal artery stenosis is observed. These investigations may be useful in recognizing the role of retained diseased kidneys in sustaining hypertension. Plasma aldosterone was found elevated in nearly all of the patients. The role of corticosteroids and the similarity of post-transplant hypertension, in some cases, with the one kidney model of experimental hypertension are discussed.

Adolescent↗
PubMed1978

Donor pretreatment in an unselected series of cadaver renal allografts.

In a single center, an unselected non-exclusion series of 78 consecutive cadaver renal allografts in 76 recipients was studied. Since 1971, using kidneys obtained from donors pretreated with large doses of cyclophosphamide and methylprednisolone, excellent clinical results with 2-year graft-survival of 70% 5-year graft survival of 66% have been obtained. The improvement in results is believed to be aided by the reduction in allograft immunogenicity due to short-term donor pretreatment. In this series, poor tissue-matching grades are notable, heavily transfused patients are few, 33 patients were high risk, and 43 patients were presensitized. In spite of these negative selection factors, the results obtained in this pretreated series, with 18% of graft losses due to rejection, are superior to those obtained in patients who did not receive pretreated allografts during the same time period, with 34% of graft losses due to rejection, and 2-year and 5-year graft survivals of 57% and 53%, respectively.

Adolescent↗
PubMed1977

Studies of the antigens involved in an immunologic renal tubular lesion in rabbits.

Rabbits injected with nonglomerular components of rabbit kidney incorporated in Freund's complete adjuvant develop a lesion characterized a) extensive interstitial fibrosis, tubular degenerative changes, and sparse focal lymphocytic infiltrates; b) the deposition of IgG and C3 in a granular pattern along the basement membranes of proximal convoluted tubules; and c) functional tubular defects if the lesions are severe. The antibodies were eluted from kidneys with such lesions and labeled with fluorescein isothiocyanate. It was shown that these fluorescein-labeled eluates reacted with the corresponding antigens in the tubular deposits and also with the antigens present in the brush border and/or cytoplasm of the proximal tubules. The antigens are found in proximal tubules of the kidney but not in brain, lung, heart, liver, spleen, bowel, muscles, or urine. They appear to be soluble but may also be present in the plasma membrane.

Animals↗
PubMed1976

Filtration of protein in the anti-glomerular basement membrane nephritic rat: a micropuncture study.

Production on an anti-glomerular basement membrane (anti-GBM) nephritis in the rat results in a 30-fold increase in glomerular membrane permeability to albumin. The concentration of albumin in glomerular filtrate, estimated from proximal tubular fluid samples, is ten times the normal value. Tubular reabsorption of albumin is not enhanced so that essentially the filtered load is excreted. A nephrotic syndrome develops rapidly. Total kidney glomerular filtration rate (GFR) is reduced to 40% of normal with a proportional reduction in filtration fraction. Glomerulo-tubular balance is maintained since proximal fractional reabsorption remains constant near control levels. Calculated efferent arteriolar plasma colloid osmotic pressure (COP) is about one-third normal. Sodium excretion, sharply curtailed in the first days of anti-GBM nephritis, returns to control values after the fourth postinjection day. Restoration of sodium balance despite reduced filtered load and constant proximal fractional reabsorption must be accomplished by adjustments at a distal site in the nephron.

Albuminuria↗
PubMed1976

Glomerular injury in patients with neoplasia.

There is considerable circumstantial evidence relating neoplasia to glomerular injury. Recently, more convincing evidence has been derived from the demonstration of tumor-associated antigen or antibody to such antigen, in relation to glomerular basement membranes in four patients with glomerular injury and cancer. The most common form of glomerulopathy reported in patients with carcinoma has been membranous glomerulonephritis. However, increased mesangial cells and matrix have also been found in some patients with hematuria and progressive renal failure. In contrast, most patients with Hodgkin's disease and glomerulopathy have had the minimal lesion-type nephrotic syndrome, which has usually responded to successful treatment of the Hodgkin's disease. Glomerular abnormalities have also been reported with chronic lymphocytic leukemia, lymphosarcoma, Waldenstrom's macroglobulinemia, and benign tumors. When there is no apparent cause, proteinuria with or without hematuria or impaired renal function should suggest the possibility of associated neoplasia, particularly in elderly patients.

Adolescent↗
PubMed1976

Nonessential role of neutrophils as mediators of hyperacute cardiac allograft rejection in the rat.

The presence of neutrophils within the graft has been widely emphasized as a characteristic feature of hyperacute rejection, and analogies have been drawn to the Arthus reaction, in which neutrophils are essential mediators of tissue damage. To evaluate the role of neutrophils as mediators of graft destruction in hyperacute rejection, we studied a series of 16 heterotopic ACT strain rat cardiac allografts in skin-presenitized Lewis strain recipients, all of which recieved prior treatment with cyclophosphamide and methotrexate or heterologous rabbit antirat polymorphonuclear globulin. Fourteen recipients showed significant depression in levels of circulating neutrophils prior to transplant, and neutrophils were not detected in 13 allogrates at the time of functional rejection. There was no abrogation of hyperacute rejection in this series and the characteristic pattern of vacular and myocardial damage was not altered by the absence of neutrophils from the graft. Although the possibility that neutrophil-derived agents may contribute to late graft destruction cannot be excluded, this study has shown that neutrophils are neither essential nor specific participants in hyperacute allograft rejection in this model.

Animals↗
PubMed1975

Antilymphocyte globulin in renal transplantation: Nephrotic syndrome and infection as possible complications.

During a two-year period, nine patients received equine antilymphocyte globulin (ALG) as part of their immunosuppressive therapy following cadaver renal transplantation. Of these, three patients (33%) developed nephrotic syndrome. A fourth patient had proteinuria greater than 3 gm/24 hr not attributable to recurrent disease or rejection. Of 32 other patients with cadaver renal allografts done during the same time, none had nephrotic syndrome and two (6%) had proteinuria greater than 3 gm/24 hr, both with biopsy evidence of rejection. This suggests an association between ALG therapy and risk for developing nephrotic syndrome, but the mechanism is not clear and deserves further investigation. During the first three months following transplantation, the nine patients treated with ALG had 20 infections, which seems to be more per patient than in our other transplant recipients.

Adolescent↗
PubMed1975

A controlled sequential morphologic study of hyperacute cardiac allograft rejection in the rat.

A series of heterotopic cardiac allografts from ACI strain rat donors to ACI skin-presensitized Lewis strain recipients was examined by light and electron microscopy at intervals from 1 minute to 24 hours for a sequential morphologic study of hyperacute rejection. Syngeneic Lewis hearts grafts in ACI skin-presensitized Lewis recipients provided controls. Extensive platelet aggregation throughout the vasculature of the allografts in the presence of a largely intact endothelium was the initial morphologic event, which was present by 1 minute posttransplant and absent in all syngeneic controls. This was followed by widespread endothelial damage. Endothelial damage preceded neutrophil margination and emigration in the graft. Neutrophil degranulation or evidence of phagocytosis was not observed within the 1st hour. At 6 and 24 hours, degranulated forms were common and apparent extrusion of granule contents with progressive ischemic injury. Segmental occlusion of the vasculature by platelet plugs and progressive disruption and loss of capillaries combined with an increase in permeability may result in myocardial ischemia. Neutrophil-derived agents do not appear to be of major significance in hyperacute rejection during the early posttransplant phase, but may play a role in mediating myocardial injury if the allograft survives for alonger period. However, on morphologic grounds, it is suggested that microcirculatory hypoperfusion with resultant ischemia is a major determinant of myocardial damage and graft function. No significant change was noted over the observation period in peripheral neutrophil or platelet counts when compared to syngeneic controls, and a slight reudction in specific cytotoxic antibody titer in the allografts was immediate but very transient.

Animals↗