Interaction between starch and lipoprotein components.
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Biomedical subjects
Publications and source records attributed to A Pasternack.
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A fine-needle kidney biopsy was performed on eleven patients with dermatitis herpetiformis (DH) who had no previous signs or symptoms of renal disease. Of the eight patients whose biopsy specimens were representative, electron microscopic examination showed mesangial deposits in five. A subsequent conventional renal biopsy was obtained from one of these five, and immunofluorescence microscopy revealed IgA and complement deposits in the glomeruli. Renal involvement was not related either to the degree of jejunal villous atrophy or to the deposition of IgA and complement in the skin. Glomerular deposits, however, were associated with a high frequency of circulating IgA and IgG class immune complexes and IgA class antigliadin and antireticulin antibodies. These results suggest that, in DH, immune complexes or antibodies derived from the gut can be deposited in the kidney.
Recently, we have introduced an atraumatic fine-needle aspiration biopsy method to obtain human glomeruli for morphologic investigation. In the present study, immunofluorescence microscopy of paraffin-embedded, fine-needle specimens is described. The specimens were obtained by aspiration with a 10-mL syringe fitted to the fine-needle prepared from a lumbar puncture needle (Jintan Terumo). Embedding of the specimens into conventional paraffin blocks was carried out after pelleting them by centrifugation between processing steps in conical centrifuge tubes. Sections from the blocks were collected on small pieces of GelBond film (FMC Corporation) instead of objective slides, which prevented the detachment of small sections during enzyme treatment. Localization then was performed on deparaffinized trypsin-digested sections using fluorescein-labeled antibodies. The choice of fixative and digestive enzymes was found to have a marked effect on the localization; periodate-lysine-paraformaldehyde fixative and trypsin digestion gave the most reliable results.
Priapism developed during antihypertensive therapy with prazosin, 3-10 mg daily for 2-4 months, in two young men with severe renal failure. The cases are believed to be associated with alpha-adrenoceptor blocking and/or vasodilatory effects of the drug. Renal failure alone unlikely causes priapism, but may be an exposing factor for the episode.
The effect of furosemide on the lipoprotein profile and the activities of postherapin plasma lipases were studied in 12 patients with chronic renal failure. The concentrations of serum total, VLDL and LDL triglycerides were significantly higher and the concentration of HDL triglyceride was significantly lower in the patients with renal failure than in healthy controls. HDL cholesterol was significantly lower in the patients than in the controls. The activity of postherapin lipoprotein lipase was significantly lower in the patients than in the controls. The introduction of furosemide induced a significant increase in the concentrations of VLDL cholesterol and VLDL triglyceride. These changes were reversed when the drug treatment was discontinued. Postherapin lipase activities were not further altered by furosemide.
The different modes of progression of renal diseases were studied in 73 patients by plotting the reciprocals (1/SCr) and logarithms (logSCr) of their serum creatinine values against time. The regression was linear in the reciprocal plot for 42 patients (57.5%) and in the logarithmic plot for 12 patients (16.4%). The type of renal disease did not predict the mode of progression. The deviations from the linear regression lines were probably most often due to changes in the level of blood pressure and to intensification of treatment for hypertension. The reciprocal plot turned out to be useful for predicting the date when end-stage renal failure was reached. An accuracy of 4 months was reached in 81.5% using the reciprocal plot but only in 25.9% using the logarithmic plot.
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IgA nephropathy was found in three patients with celiac disease; two of them also had dermatitis herpetiformis. These observed associations widen the spectrum of the diseases that have been reported to coexist with IgA nephropathy. This study focused on the possible intestinal origin of the glomerulonephritis.
The nephrotic syndrome was observed in eight out of 170 patients with IgA glomerulonephritis (5%). Three patients had mild glomerular alterations, all of them were normotensive, had normal renal function and responded to treatment with corticosteroids. In five patients moderate to marked mesangial changes associated with segmental sclerosing or proliferative lesions were seen. These patients were hypertensive and four of them had renal insufficiency. Three were treated with corticosteroids without response.
A 34 year old woman is described in whom carditis, arthritis, fever, leukocytosis and a high sedimentation rate developed two weeks after a streptococcal infection. The patient also had the nephrotic syndrome and rapidly progressive renal insufficiency. The renal biopsy specimen showed acute extracapillary (crescentic) glomerulonephritis. The initial response to corticosteroid therapy was good, but later a slowly progressive renal function impairment was seen.
1 Pindolol and propranolol were administered orally in equipotent antihypertensive doses to 14 subjects with mild to moderate hypertension in an open cross-over study. 2 Pindolol caused a smaller decrease in plasma renin activity and heart rate than propranolol. 3 Glomerular filtration rate and effective renal plasma flow remained unchanged during therapy with either agent.
Percutaneous renal biopsy was performed on 15 patients with orthostatic proteinuria and 6 control subjects without proteinuria in order to investigate possible renal alterations. The light-microscopic findings were either normal or showed slight mesangial proliferation in the orthostatic group but were normal in the control subjects, while the immunofluorescence-microscopic study revealed mesangial, capillary or arteriolar deposits of complement C3 and/or immunoglobulins in 10 out of 12 cases with orthostatic proteinuria; complement C3 was seen in only one control subject. The electron-microscopic findings were similar in the two groups, showing slight subepithelial, intramembranous and mesangial alterations. Focal loss of the epithelial foot processes was seen in only one case with orthostatic proteinuria. It is concluded that there are no histological, electron microscopical or immunohistochemical alterations specific for orthostatic proteinuria. A finding of complement in the glomeruli in about half and of immunoglobulin in some of the patients with orthostatic proteinuria is in favour of an association to present or previous glomerulonephritis.
In a series of 374 renal biopsy specimens, 26 from patients with primary glomerulonephritis showed IgM as the main glomerular immunofluorescence finding. By light microscopy 17 of these specimens showed mild mesangial hypercellularity and 9 were normal. Small mesangial electron-dense deposits were seen in 8 specimens. Of the 26 patients, 10 had proteinuria, 6 had the nephrotic syndrome, 6 had hematuria and 4 had both proteinuria and hematuria. The mean serum IgM level was significantly higher in the patients than in healthy controls. Circulating immune complexes were detected by three methods in 39% of the patients.
A study has been made of the fluoride kinetics in man, with a series of 5 healthy subjects and 4 patients with renal insufficiency. The fluoride metabolism was found to conform to nonlinear tissue-binding kinetics. Reanalysis of findings on the rabbit reported in the literature yielded equivalent results. The tissue-binding constants elicited - probably associated with the fluoride metabolism of bone - presented no differences between healthy subjects and uremics. Uremics had a clearly lower fractional fluoride elimination rate (K) compared with the healthy controls. A significant correlation of creatinine clearance on the K value was noted.
Two cases of patients with a bronchial small-cell carcinoma coexisting with IgA nephropathy are reported. The relationship of the bronchial malignancy to IgA nephropathy is discussed.
Eleven patients with amyloidosis were treated for terminal renal failure by transplantation, receiving 12 cadaver allografts. In one patient the amyloidosis was primary and in the remaining 10 it was secondary to a chronic inflammatory disease. All of the patients were subjected to one or two fine-needle aspiration biopsies of the kidney graft during a followup of 11 to 68 months. The biopsies of three patients, one with primary amyloidosis and two with ankylosing spondylitis, revealed amyloid recurrence in the graft. These recurrences were diagnosed at 11, 28, or 37 months, respectively. The risk of amyloid recurrence is thus by no means negligible. The present study revealed no factors determining the development of recurrence. In two additional cases, membranous glomerulonephritis was observed in transplant biopsy. Both of these patients had rheumatoid arthritis as the underlying disease and were treated with gold salts before transplantation. It is suggested that an impaired immune response, related to amyloidosis and/or immunosuppressive therapy, may have favored the formation and deposition of circulating immune complexes.
A series of 40 IgA nephropathy patients is presented. IgA nephropathy was the most common (24%) type of glomerulonephritis in our renal biopsy material. Circulating immune complexes were measured by five methods that gave a positive result in 9-69% of the patients. The platelet aggregation test with heated serum (PAT2) was by far the most commonly positive. The serum concentrations of IgA were measured by two methods, radial immunodiffusion and laser nephelometry. Both tests gave similar results. 58% of the patients had elevated serum IgA. There was no statistically significant association between HLA antigens and IgA nephropathy as compared with the control material.