PubMed Health⌕ Search

Biomedical subjects

E Grishman

Publications and source records attributed to E Grishman.

At least 37 records · Page 2Linked to original sources

Ultrastructure of transplant glomerulopathy.

Thirty-one specimens of tissue were obtained from 15 renal allografts 3-96 months after transplantation and studied by light, electron and in some cases also by immunofluorescence microscopy. All patients had a degree of renal insufficiency and almost all had proteinuria and moderate hypertension; nephrotic syndrome was present in one and hematuria in two. On histological examination one patient showed cellular proliferation suggestive of glomerulonephritis (recurrent or de novo) and another patient had numerous crescents. The most frequent glomerular lesion was widening of the lamina rara interna with subendothelial accumulation of finely granular material, formation of new subendothelial basement membrane and deposition of microfibrils and fine filaments. The mesangial changes were mainly those of mesangiolysis and mesangial sclerosis with deposition of mesangial matrix and microfibrils, but little cellular proliferation. Fragmented red blood cells were seen in nearly half of the patients. In another seven patients the lesion resembled focal segmental glomerulosclerosis. This combination of changes termed transplant glomerulopathy leads to diffuse glomerular sclerosis. Arterial intimal thickening and occasionally also thrombosis produced ischaemic changes in the kidney and in the glomeruli and contributed significantly to the process of transplant rejection.

Arteries↗

Ultrastructure of hematoxylin bodies in systemic lupus erythematosus.

Two specimens, the first from a percutaneous renal biopsy and the second autopsy tissue of ovary, from two subjects with active systemic lupus erythematosus were found to contain many striking hematoxylin bodies in the walls of several small arteries. The specimens were reprocessed for electron microscopy; in one case, corresponding plastic embedded sections were also stained with hematoxylin-eosin and Feulgen stain. Hematoxylin bodies were easily identified on electron microscopy. They were found to be dense, homogeneous structures, approximately the size of a nucleus. They probably represent mainly altered nuclear material with occasional small chromatin remnants or minor cytoplasmic inclusions.

Adolescent↗

Glomerular injury in malignant nephrosclerosis.

Electron microscopic analysis of subendothelial and mesangial alterations in the glomeruli was performed in 15 cases of malignant nephrosclerosis (MNS). 8 cases showed segmental or diffuse subendothelial accumulation of proteinaceous 'fibrinoid' material associated with thickening of glomerular basement membranes. 2 of these cases also showed similar deposits in the mesangium. When severe, this mesangial insudation resulted in almost complete replacement and destruction of the mesangial matrix. Endothelial injury with alteration of glomerular microcirculation and secondary intravascular coagulation is believed to play a role in the development of the glomerular lesions in MNS.

Basement Membrane↗

Binding of synthetic double-stranded DNA by serum from patients with systemic lupus erythematosus: correlation with renal histology.

Detection of antibody to double-stranded DNA by direct binding assays has proved useful in clinical management of patients with systemic lupus erythematosus (SLE). Recent confusion regarding specificity of these antibodies for SLE appears to be due, at least in part, to contamination of natural DNA preparations with nondouble-stranded DNA antigens. Measurement of binding of a synthetic, self-complementary DNA copolymer (dAT) rather than of natural DNA (KB) has been shown to obviate some of these difficulties, apparently because of freedom of dAT from nondouble-stranded DNA antigens. Among the advantages found in this way was a higher degree of specificity of antibodies to double-stranded DNA for clinically-judged active lupus nephritis than had been suspected. Since activity of nephritis is difficult to assess clinically, histologic data were sought to confirm these observations. Thirty-two kidney specimens were examined by light and/or electron microscopy. The degree of histologic activity and the amount and location of glomerular electron-dense deposits were semiquantitated blindly. The binding of both dAT and KB DNA was measured by the ammonium sulfate method. Correlation with the amount of electron-defense deposits was highly significant for dAT binding and somewhat less so for KB DNA binding as determined by both parametric and nonparametric statistical methods. Significant correlation with histologic activity was found for dAT but not KB DNA binding. These results are consistent with previous data and suggest that dAT binding may provide a useful, noninvasive means of clinically assessing both nephritis activity and the intensity of glomerular immune-complex deposition as reflected by the amount of electron-dense deposits. If it can be confirmed that the latter provides long-term prognostic information, then dAT binding (and perhaps its reponse to therapy) may also prove of value in this regard.

Adenosine Monophosphate↗

Single cutaneous plasmacytoma with crystalloid inclusions.

A patient had a primary cutaneous plasmacytoma of the cheek. Histologic studies showed dense aggregates of plasma cells admixed with occasional histiocytes. The cytoplasm of the histiocytes contained needle-like structures. Electron microscopy showed these structures to be completely enclosed within smooth membranes. They often were rhombic, with occasional broken-off corners. It is hypothesized that these structures represent protein that has been secreted by the plasma cells and subsequently phagocytosed and stored in crystalloid form by the neighboring histiocytes. The patient is asymptomatic 1 1/2 years after removal of the tumor.

Cheek↗

Treatment of idiopathic membranous nephropathy.

In a retrospective study of the effect of treatment in biopsy-proved idiopathic membranous nephropathy, 91 adults and 12 children were followed for periods up to 29 years after clinical onset (mean, 6.5 years). Forty-four were treated with corticosteroids, 15 with corticosteroids and immunosuppressants; 44 had no treatment and served as a control group. Clinical cure and improvement were significantly greater in the treated than in the nontreated group (P less than 0.01). The recurrence rate, occurrence of renal failure and probability of death were significantly greater in the nontreated group, although some of these patients eventually showed improvement. Prognosis was better in patients who responded to therapy. These data strongly suggest that steroid therapy is beneficial in patients with membranous nephropathy.

Adolescent↗

Glomerular morphology in nephrotic heroin addicts.

Renal biopsies of 23 heroin addicts who presented with the nephrotic syndrome were examined by light and electron microscopy. The majority of patients (14) showed focal segmental glomerular sclerosis on light microscopy, four patients showed "minimal change", and two were classified as "focal global sclerosis." In one case focal mesangial proliferation was the outstanding feature; one patient had diabetic glomerulosclerosis; and one had mesangiocapillary glomerulonephritis and dysproteinemia. Visceral epithelial swelling and proliferation were present in 14 patients on light on light microscopy. Electron microscopy showed distinct podocyte changes consisting of loss of foot processes, vacuolization, and cytoplasmic degeneration; focal separation of podocytes from basement membranes was found in 11 of 18 cases. In some instances a few electron-dense deposits were present in the mesangium. Membranous nephropathy was not encountered, although it occurs in 30 to 40% of unselected adult nephrotic individuals. Of 15 patients followed for 2 months to 5 years, one died of heroin overdose, eight went into renal failure, two improved, and four continued to have proteinuria. It is concluded that nephrotic syndrome of heroin addicts is most often associated with focal segmental glomerular sclerosis and occasionally with minimal change disease or focal global sclerosis. Conceivably these three conditions represent different phases of one disease process, although different reactions to heroin or its various vehicles and contaminants cannot be excluded. The morphologic resemblance to experimental aminonucleoside and N,N'-diacetylbenzidine-induced nephrosis suggests a possible toxic origin.

Adolescent↗

Mesangial involvement in hemolytic-uremic syndrome. A light and electron microscopic study.

Electron microscopic analysis of the mesangial injury in the hemolytic-uremic syndrome was performed in 10 patients. Proteinaceous material similar to that found in the subendothelial region was also seen focally in the mesangium altering the matrix and imparting a reticular appearance. This degenerative process was associated with reparative changes in the glomerular tuft. Many of the mesangial cells were hypertrophied and demonstrated phagocytic activity and peripheral extension of their cytoplasmic processes. Mitotic figures in endothelial as well as mesangial cells were regarded as evidence of a reparative process. Severe mesangial insudation of material containing fibrinogen derivatives resulted in segmental tuft necrosis with almost complete replacement and destruction of the mesangial matrix. On some occasions, a break of the glomerular basement membrane was accompanied by the escape of intraluminal contents into the urinary space, leading to crescentic epithelial cell proliferation.

Adolescent↗

Focal glomerular sclerosis in nephrotic patients: an electron microscopic study of glomerular podocytes.

Renal biopsy specimens of 16 adult patients with nephrotic syndrome and focal glomerular sclerosis were examined by light and electron microscopy. Particular attention was paid to alterations of podocytes. Except for loss of foot processes, five patients had no podocyte changes, five had mild changes and six had severe changes. Of the last group (group III), four patients were heroin addicts, the fifth had infectious mononucleosis and the sixth, an apparent idiopathic disease; five patients were males, 16 to 25 yr old. Podocyte changes consisted of cytoplasmic degeneration, detachment of epithelial cells from basement membranes, with filling of resulting space by cell debris and new membranes. Underlying capillaries were often collapsed. Repeat biopsies in three patients in group III revealed progression of lesions, paralleling rapid clinical deterioration. It is concluded that some cases of focal glomerular sclerosis are associated with severe damage to podocytes which may be caused by drugs, infection or unknown factors and may contribute to the development and progression of the glomerular lesions.

Adolescent↗

Intraglomerular fibrin, platelet aggregation, and subendothelial deposits in lipoid nephrosis.

We have investigated the formation of fibrin, platelet aggregates, and subendothelial deposits in lipoid nephrosis. Fibrin formation was found in 10 cases of active lipoid nephrosis. Platelet aggregates were found in eight cases and subendothelial deposits in nine. Fibrin and platelets were also found in cases of nephrotic syndrome due to other causes, and in glomerulonephritis. Fibrin was generally absent in lipoid nephrosis in remission and in benign recurrent hematuria. It is suggested that what seems to be a lower incidence in females is more apparent than real and that fibrin or related material may be present in a less easily identifiable form. Steroid therapy apparently had no effect on the presence or absence of fibrin. Most instances were associated with elevated serum cholesterol and alpha(2)-globulin. It is suggested that elevated serum lipids as well as the disease process in the kidney play a role in this phenomenon. It is further suggested that intraglomerular fibrin formation could lead to irreversible renal damage in lipoid nephrosis.

Adolescent↗