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Biomedical subjects

J M Bergstein

Publications and source records attributed to J M Bergstein.

At least 55 records · Page 3Linked to original sources
PubMed1983

Basement membrane nephropathy: a new classification for Alport's syndrome and asymptomatic hematuria based on ultrastructural findings.

Renal biopsy specimens from 19 patients with asymptomatic hematuria, normal glomeruli on light microscopic examination, and negative immunofluorescence were studied to characterize the ultrastructural changes of the glomerular basement membrane. Three groups of patients were identified. Four patients (group 1) had type I basement membrane nephropathy, characterized by marked thickening and lamellation of the basement membrane in a pattern resembling that of Alport's syndrome. Seven patients (group 2) had type II basement membrane nephropathy, which was characterized by extensive attenuation of the basement membrane with only occasional small areas of lamellation or fragmentation. Eight patients (group 3) had moderate variability in basement membrane thickness with no other structural alterations. The authors propose that this pathologic classification be used in patients with asymptomatic hematuria as a basis for long-term clinical investigations, in hopes of distinguishing the natural history of each group.

Adolescent↗
PubMed1982

Development of insulin-dependent diabetes mellitus during the hemolytic-uremic syndrome.

Three children developed hyperglycemia and ketoacidosis three, eight, and 60 days after the onset of hemolytic-uremic syndrome. During hyperglycemia, the two patients studied had dramatically low insulin concentrations. Circulating islet-cell and insulin antibodies were not detected. These studies suggest that pancreatic beta cell dysfunction may occur during hemolytic-uremic syndrome, and that the serum glucose concentration should be closely monitored during this disease.

Blood Glucose↗
PubMed1982

Plasma inhibitor of glomerular fibrinolysis in the hemolytic-uremic syndrome.

To detect an inhibitor of glomerular fibrinolysis, dilutions of human plasma were incubated on microscope slides with two frozen sections of normal human kidney. The slides were studied by the fibrin slide technique. The lysis inhibitory titer was defined as the highest dilution completely inhibiting glomerular fibrinolysis. Of 27 children without renal disease, none had a lysis inhibitory titer greater than 1:2. Defining an elevated lysis inhibitory titer as 1:8 or greater, we found an elevated lysis inhibitory titer in plasma from all 17 children with hemolytic-uremic syndrome. No correlation was found between the lysis inhibitory titer and the hematocrit, white blood cell or platelet counts, serum creatinine level, or levels of the antiplasmins alpha 1-antitrypsin, alpha 2-macroglobulin, C1-esterase inhibitor, or alpha 2-antiplasmin. The inhibitor was found to have a molecular weight of less than 12,000. A close correlation was discovered between the duration of lysis inhibitory titer elevation and the clinical course; removal of the inhibitor from the plasma by peritoneal dialysis was associated with improvement in renal function. Results suggest that the inhibitor may play an important role in the pathogenesis and persistence of glomerular fibrin deposition.

Child↗
PubMed1981

Hypokalemia, normal blood pressure, and hyperreninemia with hypoaldosteronism.

The etiology of persistent hypokalemia and renal potassium loss was investigated in three children. Each had normal blood pressure but low plasma aldosterone values in relation to elevated plasma renin activity. None had a history of licorice abuse, laxative or diuretic use, persistent vomiting or diarrhea, pyelonephritis, or diabetes insipidus. Additional studies in one patient showed low prostaglandin E excretion and a normal platelet aggregation response to epinephrine and ADP. Although certain aspects of this condition resemble Bartter syndrome, the low concentrations of aldosterone and the absence of evidence for mineralocorticoid excess suggest a previously undescribed syndrome.

Aldosterone↗
PubMed1978

Immune complex glomerulonephritis mediated by thyroid antigens.

Hypothyroidism, microscopic hematuria, and proteinuria developed in an 11-year-old girl. A renal biopsy specimen showed increased mesangial cells and matrix with focal glomerular basement membrane thickening. Three years later, a pronounced increase in proteinuria was detected. Elevated levels of antibody to thyroid microsomal antigen and thyroglobulin were found in the serum. A renal biopsy specimen showed a pronounced increase in mesangial cells and matrix with generalized glomerular basement membrane thickening. Electron microscopic studies demonstrated granular deposits in the capillary walls and mesangium. Immunofluorescent studies revealed granular deposits of IgG, IgM, and C3, primarily on the glomerular basement membrane. By indirect immunofluorescence, granular glomerular basement membrane and mesangial staining were detected with antibody specific for thyroglobulin and thyroid microsomal antigen. These observations suggest development of immune complex glomerulonephritis mediated by thyroid antigens.

Antigen-Antibody Complex↗
PubMed1977

Development of a lesion resembling diabetic nephropathy in a renal homograft.

One month following a cadaver renal transplant for obstructive uropathy, a 27-year-old man developed diabetes mellitus. Two years later, marked proteinuria and decreased renal function were detected. Eight months later, a second decline in function occurred. Light microscopy of graft biopsy specimens obtained after each decline in renal function showed increased mesangial cells and matrix, thickening of Bowman capsule, and tubular atrophy with basement membrane thickening. Vascular changes, interstitial infiltrate, and fibrosis were not prominent. Electron microscopic studies of the second biopsy specimen confirmed the light microscopic changes; subepithelial dense deposits were also detected. Immunofluorescent studies of both biopsy specimens demonstrated linear staining of glomerular and tubular basement membranes and Bowman capsule for IgG and albumin. Antikidney antibodies were not detected in the patient's serum. These observations suggest development of the diffuse form of diabetic nephropathy in a renal homograft following steroid-induced diabetes mellitus.

Adult↗
PubMed1977

Cutaneous vascular fibrinolytic activity in the local Shwartzman reaction.

A fibrin slide test was utilized to study cutaneous vascular plasminogen activator activity in normal rabbit, rat, monkey, and human skin and in rabbit skin following development of the local Shwartzman reaction and after substituting epsilon-aminocaproic acid for the preparatory injection of endotoxin in the local Shwartzman reaction. Cutaneous vascular plasminogen activator activity was also studied in rats after attempted induction of the local Shwartzman reaction following inhibition of fibrinolysis with epsilon-aminocaproic acid and/or pregnancy. Plasminogen activator activity was detected in vessels of normal rat, monkey, and human skin but was absent in skin from normal rabbits and rabbits with the local Shwartzman reaction. Intradermal injection of epsilon-aminocaproic acid failed to prepare for the local Shwartzman reaction. In the rat, which has greater cutaneous vascular plasminogen activator activity than the rabbit, inhibition of vascular activator with epsilon-aminocaproic acid and/or pregnancy failed to prepare for the local Shwartzman reaction. These studies indicate that although the markedly diminished level of cutaneous vascular plasminogen activator in the rabbit may be important in the pathogenesis of the local Shwatzman reaction, factors other than inhibition of fibrinolysis are also necessary for preparation of the reaction.

Aminocaproic Acid↗
PubMed1977

The local Shwartzman reaction in the rabbit. Immunopathologic findings in the skin.

Four albino rabbits received two intradermal injections of endotoxin followed in 24 hours by an intravenous injection of endotoxin. All animals developed the local Shwartzman reaction, characterized by hemorrhagic necrosis over each intradermal injection site. Light microscopy of the Shwartzman lesion showed intense inflammation and vascular thrombosis. Frozen sections of the skin lesion revealed marked vascular deposition of fibrin with lesser amounts of IgG, IgM, C3, and albumin. Light microscopy was normal and immunofluorescence was negative in skin obtained prior to the initial injection of endotoxin and skin adjacent to the Shwartzman lesion. These findings suggest nonspecific trapping of serum proteins within vascular thrombi and indicate that immune mechanisms may not play a role in the pathogenesis of the local Shwartzman reaction.

Albumins↗
PubMed1976

Platelet inhibition of renal cortical fibrinolytic activity in the rabbit.

A fibrin slide test was utilized to study the effect of platelets and endotoxin on renal cortical fibrinolysis in rabbits. Cortical lysis was absent in kidney from animals made markedly thrombocytopenic with goat antirabbit platelet serum or endotoxin; light microscopy was normal and immunofluorescent microscopy for fibrin was negative. No loss of lysis was detected in kidney of animals given goat anti-rabbit albumin or isotonic saline. Plasma from animals with endotoxin or antiplatelet antibody-induced thrombocytopenia demonstrated an increased capacity to inhibit cortical fibrinolytic activity of normal rabbit kidney. Antiplatelet antibody could be substituted for the preparatory injection of endotoxin in the generalized Shwartzman reaction; a parallel rise in lysis inhibitory titer was detected in plasma from animals prepared with antibody or endotoxin. Although lysis was absent following incubation of normal renal cortex with washed platelets, no inhibition of lysis was found after incubation of normal cortex with endotoxin, histamine, serotonin, platelet membranes, or granules. Using a modified fibrin slide technique, a diffusable platelet inhibitor of lysis could be demonstrated. These studies indicate that platelets contain an inhibitor to renal cortical fibrinolysis which is released into the circulation upon platelet destruction. The findings also suggest that platelet destruction is the mechanism through which endotoxin inhibits cortical lysis.

Animals↗