Biomedical subjects
A F Gohara
Publications and source records attributed to A F Gohara.
Crescentic fibrillary glomerulonephritis associated with intermittent rifampin therapy for pulmonary tuberculosis.
This case study reveals an unusual finding of rapidly proliferative crescentic glomerulonephritis in a patient treated with rifampin who had no other identifiable causes for developing this disease. This patient underwent a 10-month regimen of rifampin and isoniazid for pulmonary tuberculosis and was discovered to have developed signs of severe renal failure five weeks after completion of therapy. Renal biopsy revealed severe glomerulonephritis with crescents, electron dense fibrillar deposits and moderate lymphocytic interstitial infiltrate. Other possible causes of rapidly progressive glomerulonephritis were investigated and ruled out. This report documents the unusual occurrence of rapidly progressive glomerulonephritis with crescents and fibrillar glomerulonephritis in a patient treated with rifampin.
Adherence to exercise interventions in the treatment of hypercholesterolemia.
The goals of this study were to determine the rate of adherence to exercise treatment of hypercholesterolemia and to identify personality and demographic factors associated with adherence. Of the 31 subjects entering the 26-week program, 12 attended 80% or more of the scheduled sessions. Adherence was positively associated with the perceived seriousness of hypercholesterolemia, the expectation of benefit from treatment, and depressed feelings of helplessness and hopelessness. Negative associations were identified between adherence and the perception of health status being under the control of chance or of powerful others. Older subjects were more likely to be adherers at 8 and 16 weeks but not at 26 weeks.
The Toledo Exercise and Diet Study. Results at 26 weeks.
This study was designed to test whether an exercise program is additive to diet counseling in lowering elevated blood cholesterol levels. From a screened population of 1024 subjects, we randomized 66 predominantly female subjects to two intervention groups: diet counseling and diet counseling with exercise. Subjects were selected who had elevated levels of serum low-density lipoprotein cholesterol, an average or low fitness level, and a diet high in saturated fat and cholesterol. After 26 weeks of intervention, 51 subjects exhibited significant decreases in serum levels of cholesterol, high-density lipoprotein cholesterol, triglycerides, and low-density lipoprotein cholesterol. The addition of exercise to diet counseling resulted in improved aerobic capacity, losses of body fat and weight, and further nonsignificant decreases in serum cholesterol and low-density lipoprotein cholesterol levels. Since these results differ from data acquired in individuals with normal to borderline serum cholesterol levels, further studies appear indicated in hypercholesterolemic subjects, especially in women.
Malignant islet cell tumor of the pancreas associated with high plasma calcitonin and somatostatin levels.
In this case report we describe a 41-year-old man, without a recognizable preexisting syndrome, who had ascites of massive proportions and died. A malignant tumor of the endocrine pancreas was identified and associated with an extremely high plasma calcitonin level. The plasma somatostatin level was also significantly elevated. Only one previous case report of a tumor with comparable secretory characteristics has been identified.
Morphometric evaluation of the renal arterial system of Dahl salt-sensitive and salt-resistant rats on a high salt diet. II. Interlobular arteries and intralobular arterioles.
The progression of small vessel renal vascular disease was studied in inbred Dahl salt-sensitive (SS/Jr) and salt-resistant rats with acute hypertension induced by a high salt diet. Corrected cross-sectional areas of wall (WAC) and lumen were measured by planimetry and histologic staining for fibrin, hyalin deposition, and elastic lamellae was performed. In SS/Jr rats on the high salt diet, the hallmarks of malignant hypertension (fibrinoid necrosis, hyperplastic and necrotizing arteritis) appeared by week 2 and were intensified after 4 weeks on the high salt diet. Renal vascular lesions from SS/Jr rats were characterized by: hyperplasia and/or hypertrophy of medial smooth muscle cells; intimal proliferation; fibrin, basophilic mucoid, and hyalin deposition within the the subendothelial space and media; variable adventitial fibrosis; and accumulation of mononuclear inflammatory cells in the adventitia and media. Interlobular arteries from both rat strains exhibited significantly increased cross-sectional areas over time for all measured parameters. Intralobular arterioles from both rat strains exhibited significantly increased cross-sectional areas over time for all measured parameters except lumen from SS/Jr rats. For SS/Jr rats, increased WAC from both arterial divisions correlated positively with systolic blood pressure, but not body weight. In salt-resistant rats, increased WAC from both arterial divisions correlated positively with body weight, but not systolic blood pressure. We concluded that the rapid increase in WAC from SS/Jr rats could not be attributed solely to the normal growth of the rat. With the development of acute hypertension in the SS/Jr rat, these results demonstrate the potential usefulness of this model to investigate the pathogenesis of similar renal vascular alterations which are observed in man.
Morphometric evaluation of the renal arterial system of Dahl salt-sensitive and salt-resistant rats on a high salt diet. I. Interlobar and arcuate arteries.
Structural changes in intrarenal arteries of inbred Dahl salt-sensitive and salt-resistant rats with acute hypertension were studied morphometrically. After a week on a normal salt diet (1% NaCl), animals were placed on a high salt diet (8% NaCl) for 4 weeks. Systolic blood pressure (BP) and body weights (BW) were recorded, and six salt-sensitive and six salt-resistant animals were sacrificed weekly for a total of five sampling periods. Corrected cross-sectional (C/S) areas of adventitia, media (MAC), intima, wall (WAC), and lumen (LAC) were measured by planimetry. Although significant increases (p less than 0.01) in both BW and systolic BP were observed over time in both strains, salt-sensitive rats became hypertensive (systolic BP greater than 150 mm Hg) by week 2 on a high salt diet, while salt-resistant rats remained normotensive. In interlobar arteries, significant increases over time were observed for the WAC, MAC, and LAC in salt-resistant rats and in the WAC, adventitia, MAC, and LAC for salt-sensitive rats. Significant increases over time were observed for the WAC, adventitia, MAC, and LAC in arcuate arteries from salt-sensitive rats only. Increased C/S areas observed over time in both strains were observed by week 3 on the high salt diet, after the elevated systolic BP. Analysis of covariance indicated that increased C/S areas observed over time in salt-sensitive rats paralleled elevated systolic BP but did not follow an increase in BW. On the other hand, in salt-resistant rats, increased C/S areas observed over time correlated with BW but not systolic BP. The documented rapid development of vascular changes in salt-sensitive rats in conjunction with the development of acute hypertension demonstrates the potential usefulness of this model for investigating the pathogenesis of hypertensive renal vascular alterations.
Effects of chrysotile asbestos on coho salmon and green sunfish: evidence of behavioral and pathological stress.
The effects of chrysotile asbestos on larval coho salmon (Oncorhynchus kisutch) and juvenile green sunfish (Lepomis cyanellus) were investigated at levels approximating those reported in the Great Lakes basin (10(6) fibers/liter). Behavioral stress effects, such as loss of rheotaxic position and balance, were observed in salmon exposed at 3.0 X 10(6) fibers/liter and in sunfish exposed at 1.5 and 3.0 X 10(6) fibers/liter. Coho larvae at 1.5 X 10(6) fibers/liter were significantly more susceptible to an anesthetic stress test, becoming ataxic and losing equilibrium faster than control cohorts (P less than 0.001). Two of 106 larvae exposed at 3.0 X 10(6) fibers/liter developed tumorous swellings and three additional fish developed coelomic distentions. Cytological examination of ventral epidermal tissue revealed cellular histolysis, and evidence by transmission electron microscopy confirmed the presence of asbestos in the salmon larvae. Distortion of the lateral line region in asbestos-treated coho salmon was linked to behavioral and orientational aberrations. Differential mortality was not observed between control and treated groups of either test species.
Variable susceptibility to immune complex glomerulonephritis among mice sharing the same major histocompatibility complex.
Three inbred strains of mice were identified which demonstrated different susceptibilities to induction of immune complex glomerulonephritis (ICGN) despite sharing the same major histocompatibility complex haplotype (H-2k). Groups of mice from each of these three strains, B10.BR, CBA and C3H/HeJ, were injected with one of two different dose schedules of horse apoferritin (HAF) for 4 weeks, after which glomerular morphology, immunoglobulin deposition, and serum anti-HAF antibody levels were examined. With either dose schedule, only those mice which demonstrated a high level antibody response developed ICGN and glomerular immunoglobulin deposition. These results suggest that susceptibility to ICGN in this model is related to the level of antigen exposure and to the magnitude of the antibody response, which is not under strict control of the major histocompatibility complex.
Primary mediastinal hemangiopericytoma: computed tomography correlation.
A case of primary mediastinal hemangiopericytoma with computed tomography correlation is presented. Although this is rare cause of mediastinal mass, the diagnosis should be considered when computed tomography of the mass shows contrast medium enhancement, particularly if there is a curvilinear encircling structure suggesting a large feeder vessel.
Mesangial proliferative glomerulonephritis associated with multiple myeloma.
IgA lambda multiple myeloma was diagnosed in a 58-year-old white woman after the onset of nephrotic syndrome. Serial renal histology demonstrated progressive mesangial proliferative glomerulonephritis. Electron microscopy revealed subepithelial electron dense deposits. Immunofluorescence microscopy demonstrated granular staining of peripheral capillary loops with IgG and C3. No IgA was present. No evidence of deposition of the myeloma protein in the glomeruli was found. The temporal relationship of occurrence of the two diseases and the progression of glomerular disease suggest that multiple myeloma be added to the list of malignancies causing immune complex glomerulonephritis.
Non-Hodgkin's lymphoma and membranous nephropathy in mixed connective tissue disease.
A 60-year-old woman with a diagnosis of poorly differentiated lymphocytic lymphoma presented with nephrotic syndrome. Her clinical picture and serological studies were consistent with the diagnosis of mixed connective tissue disease (MCTD). Renal biopsy demonstrated the changes of membranous nephropathy by light, immunofluorescence and electron microscopy. Treatment with corticosteroids and cyclophosphamide had no effect on the proteinuria, and she demonstrated progression of renal failure. This patient demonstrates that the lymphadenopathy associated with MCTD may be of a separate malignant origin. The treatment of MCTD may not alter the course of renal disease, and renal failure may ensue in patients with MCTD.
Treatment of murine immune complex glomerulonephritis with prostaglandin E2: dose--response of immune complex deposition, antibody synthesis, and glomerular damage.
A model of immune complex glomerulonephritis (ICGN) produced in mice by the daily injection of apoferritin was employed to study the effect of treatment with various doses of prostaglandin E2 (PGE2) on glomerular damage, immune complex deposition, proteinuria, and serum anti-apoferritin antibody. Administration of PGE2, 200 micrograms twice daily, resulted in a significant decrease in glomerular damage and immune complex deposition, prevented the development of proteinuria, and significantly reduced serum levels of anti-apoferritin antibody. PGE2, 100 micrograms twice daily, resulted in a decrease in immune complex deposition as assessed by immunofluorescence microscopy, but this dosage did not significantly alter glomerular damage, proteinuria, or antibody levels. PGE2 dosages of 50 and 25 micrograms twice daily had no effect on any of these parameters. The protective effect of PGE2 on the development of ICGN occurred only at dosages that were associated with decreased anti-apoferritin antibody.
Alteration in immune complex glomerulonephritis by arachidonic acid.
We employed a model of immune complex glomerulonephritis produced in mice by the daily injection of apoferritin to study the effect of treatment with arachidonic acid (AA). Apoferritin injections produced demonstrable glomerular damage by light microscopy associated with deposition of immunoglobulin along peripheral capillary loops. Treatment with AA 100 micrograms daily resulted in significantly less glomerular damage and a shift inthe location of immune complex deposition to the mesangium. The amount of anti-apoferritin antibody was determined by hemagglutination and found to be significantly decreased in mice treated with AA. Separate studies employing this dose of AA revealed that the number of IgM antibody producing cells to SRBC was not altered by AA.
DNA binding and adduct formation of aflatoxin B1 in cultured human and animal tracheobronchial and bladder tissues.
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Chronic serum sickness in the mouse. Relationship of antigen dose to glomerular pathology.
We studied the effect of the administration of different doses of antigen in a model of chronic glomerulonephritis produced in mice by the daily injection of apoferritin. Four groups of mice received intraperitoneal injections of 4 mg apoferritin (group 1), 2 mg apoferritin (group 2), 1 mg apoferritin (group 3), or saline (group 4) daily. Significant proteinuria and the presence of antiapoferritin antibody were demonstrated in mice immunized with apoferritin. The severity of histologic damage and the extent of staining for IgG significantly increased with larger doses of apoferritin. Electron microscopy revealed subepithelial and mesangial electron-dense deposits. Administration of large daily doses of apoferritin to mice results in a reliable model of immune complex glomerulonephritis and crescent formation.
Suppression of antibody synthesis by prostaglandin E as a mechanism for preventing murine immune complex glomerulonephritis.
A model of immune complex glomerulonephritis induced in mice by the daily injection of 4 mg. of apoferritin was used to examine the effect of administration of two prostaglandins, PGE1 and PGE2. The twice daily administration of either PGE1 or PGE2 in pharmacologic doses resulted in significantly less glomerular damage and a shift in the primary location of immune complex deposition from the capillary loops to the mesangium, as demonstrated by immunofluorescence and electron microscopy. The beneficial effect of the prostaglandins was associated with a significant decrease in antiapoferritin antibody levels. A separate study was performed to determine whether the mechanism of decreased antibody levels produced by PGE administration was related to a decrease in the number of plaque-forming cells (PFC). Mice received injections of saline, apoferritin, or apoferritin plus PGE2 for 9 days, and spleen cells were used to determine the number of direct and indirect PFC. No direct PFC were detected in any of the groups. There was no difference in the number of indirect PFC between mice receiving apoferritin and those receiving apoferritin plus PGE2 (98 +/- 13 versus 108 +/- 30), whereas mice receiving saline had no indirect PFC. The prevention of glomerular damage in immune complex glomerulomephritis and the shift in the site of complex deposition induced by PGE1 and PGE2 appear to be caused by reduction in specific antibody synthesis. This reduced synthesis is not related to an alteration in the number of antibody-producing cells.
Massive post-transplant proteinuria with minimal histological changes.
Three patients developed massive proteinuria, hypoalbuminemia, and edema after transplantation. These findings occurred in the immediate post-transplant period in two patients, and renal failure developed. The third patient developed proteinuria 4 months post-transplantation. There was complete remission of proteinuria in two patients and recovery of renal function in one. Renal histology was similar in all. Light microscopy demonstrated that the glomeruli contained a mild increase in mesangial matrix, but were otherwise normal. No significant interstitial cellular infiltration or fibrosis was present. Immunofluorescence microscopy revealed no staining for immunoglobulins or complement. Electron microscopy demonstrated fusion of foot processes, but the glomerular basement membrane was normal. No electron-dense deposits were found. The usual causes of post-transplant nephrotic syndrome were ruled out. We believe these three patients represent a unique disorder of the transplanted kidney.