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J L Olson

Publications and source records attributed to J L Olson.

At least 37 records · Page 2Linked to original sources
PubMed1998

Contribution of tubular injury to loss of remnant kidney function.

BACKGROUND: The remnant kidney model has been widely used to identify mechanisms responsible for the progression of renal disease. However, the structural changes associated with progressive loss of function in this model have not been well characterized. METHODS: Kidney function and structure were assessed at 10 weeks (REM 10) and 25 weeks (REM 25) after five-sixths renal ablation and in control rats (Control). Serial sections were examined to relate glomerular and tubular structure in individual nephrons. RESULTS: Remnant kidney function declined between 10 and 25 weeks after ablation (GFR 0.90 +/- 0.34 vs. 0.23 +/- 0.07 ml/min, REM 10 vs. REM 25, P < 0.05). This decline in function was associated with an increase in the prevalence of globally sclerotic glomeruli (14 +/- 10 vs. 0 +/- 0 vs. 0 +/- 0%, REM 25 vs. REM 10 vs. Control, P < 0.05 REM 25 vs. REM 10 and Control). The decline in remnant kidney function between 10 and 25 weeks was also associated with the appearance of glomeruli that were atubular (48 +/- 14 vs. 9 +/- 8 vs. 3 +/- 5%, REM 25 vs. REM 10 vs. Control, P < 0.05 REM 25 vs. REM 10 and Control) or connected to atrophic proximal tubule segments (26 +/- 10 vs. 11 +/- 6 vs. 1 +/- 2%, REM 25 vs. REM 10 vs. Control, P < 0.05 all comparisons). Atubular glomeruli, which usually had open capillary loops available for filtration, were more numerous than globally sclerotic glomeruli at 25 weeks after ablation. CONCLUSIONS: These findings indicate that tubular injury contributes to progressive loss of renal function following reduction in nephron number.

Animals↗
PubMed1998

Digital imaging of black and white photomicrographs: impact of file size.

The publication of black and white photomicrographs has a long tradition in pathology. High-resolution film and quality objectives have been the backbone of generating quality photomicrographs suitable for publication. However, the digital imaging revolution has changed the way we view and capture images. As the quality of image capture devices increases and as their price decreases, more and more investigators are using digital imaging, and the use of color digital imaging for teleconferencing, telediagnosis, and reproduction is now well established. The purpose of this study was to determine the file sizes needed to obtain publication-quality black and white images using digital imaging technology. In this study, four experts in renal pathology reviewed 70 black and white images of various file sizes obtained from specimens representing a variety of renal histopathology. Without knowledge of the file size, the four renal pathologists graded the degree of pixelation, and the overall diagnostic and publication quality of the images. In all cases, digital imaging was capable of obtaining publication quality images equal to those achieved using film. The file size needed to achieve publication quality black and white images depended on magnification, with lower magnification images requiring larger file sizes.

Computer Communication Networks↗
PubMed1997

Retinal function abnormalities in membranoproliferative glomerulonephritis type II.

PURPOSE: To characterize retinal electrophysiologic and psychophysical abnormalities associated with membranoproliferative glomerulonephritis type II. METHODS: Three adults with membranoproliferative glomerulonephritis type II were studied. Retinal function was measured psychophysically (automated perimetry, Farnsworth D-15 color vision testing, and dark adaptometry) and electrophysiologically (full-field flash electroretinography and electro-oculography). RESULTS: Two symptomatic individuals had prominent drusenlike deposits and retinal pigment epithelial disturbances, findings characteristic of membranoproliferative glomerulonephritis type II retinopathy. These individuals had mild visual field and color vision abnormalities, prolonged dark adaptation, and delayed electroretinographic dark-adapted dim and bright flash responses of normal amplitude. The electro-oculogram of the most severely affected individual was abnormal. The third individual who was asymptomatic had the mildest fundus abnormalities and exhibited normal psychophysical and electrophysiologic responses. CONCLUSIONS: Membranoproliferative glomerulonephritis type II retinopathy may be associated with symptomatic and measurable psychophysical and electrophysiologic abnormalities of retinal function.

Adult↗
PubMed1997

In utero hematopoietic stem cell transplants prolong survival of postnatal kidney transplantation in monkeys.

The authors hypothesized that in utero transplantation of T-cell-depleted paternal marrow into rhesus monkey fetuses would induce tolerance to postnatal kidney grafts from the marrow donor. T-cell-depleted paternal bone marrow was transplanted intraperitoneally into two female fetal rhesus monkeys at 61 +/- 1 days' gestation. Chimeric monkeys (n = 2) received kidney transplants from paternal donors. Control monkeys (n = 2) underwent kidney transplants without prior in utero stem cell transplants. Both chimeric monkeys demonstrated low level (<0.1% donor cells) engraftment in the bone marrow and peripheral blood using the polymerase chain reaction assay for the Y chromosome. The mixed lymphocyte reaction demonstrated hyporeactivity to the donor. Control animals demonstrated severe acute rejection and graft failure 1 week posttransplant. The first chimeric monkey had no significant clinical or sonographic evidence of renal failure until 7 weeks after the transplant. Biopsy findings showed mild rejection 1 week postoperatively, but rejection did not significantly progress until 5 weeks later. The second chimeric monkey had no significant clinical or sonographic changes for 4 weeks, but evidence of moderate rejection was seen on biopsy results. This monkey was given a 10-week course of immunosuppression, and had no clinical or sonographic renal deterioration, although biopsy results showed chronic rejection that was confirmed when electively euthanized 8 months later. Our data suggest that in utero transplantation of hematopoietic stem cells can increase the survival of a kidney allograft in the rhesus monkey.

Animals↗
PubMed1997

Polyomavirus-induced interstitial nephritis in two renal transplant recipients: case reports and review of the literature.

We present two case reports of renal polyomavirus infection leading to renal allograft dysfunction, review the literature of this entity, and discuss the role of specific immunosupressives. Histologically, the virus caused an interstitial infiltrate composed of plasma cells and lymphocytes, interstitial fibrosis, and tubular atrophy. Viral inclusions were seen within tubular cells on light microscopy. Electron microscopy showed viral particles of 40 to 50 nm in a characteristic paracrystalline array. Both patients had been on FK-506-based immunosuppression. In both patients, the virus appeared to clear histologically and renal function stabilized when the patients were converted to cyclosporine-based immunosuppression. Contrary to prior reports, our patients have not lost their grafts and continue to have stable, albeit reduced, graft function at 2.5 years and 4.5 years following the initial diagnosis of renal polyomavirus infection.

Acute Disease↗
PubMed1996

Atubular glomeruli in patients with chronic allograft rejection.

Morphometric studies were performed in 15 patients with chronic renal allograft rejection. Biopsy cores were serially sectioned so that atubular glomeruli could be identified and volumes of individual glomeruli could be measured. Control tissue was obtained from 9 cadaver donors and 8 living donors. Serial sectioning revealed that atubular glomeruli were as common as sclerotic glomeruli in chronic rejection. The prevalence of atubular glomeruli averaged 18 +/- 15% (mean +/- SD) in recipients with chronic rejection, 2 +/- 2% in cadaver donors, and 1 +/- 3% in living donors (P<0.05, recipients vs. donor groups). In comparison, the prevalence of sclerotic glomeruli averaged 19 +/- 13%, 4 +/- 7%, and 7 +/- 10% in the three groups (P<0.05 recipients vs. donor groups). Atubular glomeruli exhibited reduced mean volume (3.1 +/- 0.9 x 10(6)micron(3) vs. 4.5 +/- 1.5 x lO(6)micron(3), atubular vs. open glomeruli in recipients, P < 0.05) but could not be distinguished from open glomeruli by their appearance on single sections. Recipients with chronic rejection exhibited tubular atrophy and interstitial fibrosis with an increase in the interstitial volume fraction to 51 +/- 14% as compared with 29 +/- 6% in cadaver donors and 17 +/- 2% in living donors (P<0.05 recipients vs. donor groups). Similar interstitial expansion was observed in recipients with a high prevalence of atubular glomeruli, recipients with a high prevalence of sclerotic glomeruli, and also in four recipients in whom the predominant form of glomerular injury was transplant glomerulopathy. These results suggest that mechanisms responsible for development of atubular glomeruli are among the processes that contribute to loss of graft function in patients with chronic rejection.

Adult↗
PubMed1995

Histopathological concordance of paired renal allograft biopsy cores. Effect on the diagnosis and management of acute rejection.

To assess the effect of sampling error on renal allograft biopsies, we determined the concordance of diagnoses between 2 biopsy samples from the same renal allograft and the frequency with which 1 biopsy sample would underdiagnose or lead to the undertreatment of acute rejection. Two core samples from the same allograft biopsy procedure were labeled as core A and core B and presented to both unblinded and blinded pathologists, and each pathologist independently assigned an acute and a chronic rejection grade. A set of clinical data with pertinent prebiopsy information was combined with either the core A or core B histopathological diagnosis and presented to 3 transplant nephrologists who made treatment recommendations for each combination. Two cores were obtained in 79 allograft biopsies. Core pairs differed by > or = 1 grade of acute rejection in 30% and 50% of cases for unblinded and blinded pathologist readings, respectively. Moderate or severe acute rejection would have been missed with a 1 core in 9.5% of cases, increasing to 25.6% if only biopsy pairs containing at least 1 reading of moderate or severe acute rejection are included. Therapy would have failed to be increased with a single core in 7.5% of cases, increasing to 10.5% if only pairs containing at least one recommendation of an increase in therapy are included. The use of 2 cores of renal allograft tissue provides better diagnostic information and thereby leads to appropriate increases in antirejection therapy without increasing the complication rate of the procedure.

Adult↗
PubMed1995

Epithelioid hemangioendothelioma of the lung: pleural effusion cytology, ultrastructure, and brief literature review.

Epithelioid hemangioendothelioma (EHE) of the lung is a low-grade malignant tumor of vascular origin initially described under the name intravascular bronchioloalveolar tumor (IVBAT). We present a case of a 44-yr-old Caucasian female with severe radiating back pain, shortness of breath, recurrent malignant pleural effusions, and a negative malignancy workup. Cytopathologic examination of the four pleural fluid specimens revealed large undifferentiated plasmacytoid malignant cells with abundant pink and finely granular cytoplasm, round nuclei, and prominent nucleoli. The differential diagnosis based on the cytologic findings included hepatocellular, adrenal, and renal carcinomas, melanoma, mesothelioma, and neuroendocrine tumors. Electron microscopy performed on a pleural fluid specimen and subsequent histologic examination of pleural and lung biopsies established the diagnosis of EHE.

Adult↗
PubMed1995

Detailed characterization of experimental acute alcoholic pancreatitis.

BACKGROUND: With the ex vivo perfused canine pancreas preparation, the infusion of acetaldehyde, the primary metabolite of ethanol oxidation, plus a short period of ischemia to convert xanthine dehydrogenase to xanthine oxidase, results in the physiologic injury response of acute pancreatitis (edema, weight gain, hyperamylasemia). The free radical scavengers superoxide dismutase and catalase and a xanthine oxidase inhibitor, allopurinol, ameliorate this injury response, suggesting that toxic oxygen metabolites generated by xanthine oxidase play an intermediary role. METHODS: The isolated ex vivo canine pancreas preparation was perfused for 4 hours, and weight gain of the preparation and amylase activity in the perfusate were monitored. Changes in pancreatic acinar cell architecture were characterized by light and electron microscopy, and intracellular phosphate metabolism was followed by magnetic resonance spectroscopy in control preparations and in glands simulating alcoholic pancreatitis. RESULTS: Control preparations and preparations with a 1-hour period of ischemia before perfusion gained little weight (7 +/- 3 gm and 8 +/- 1 gm), amylase activity in the perfusate remained normal (933 +/- 513 units/dl and 1537 +/- 553 units/dl), and no changes in architecture were observed. Weight gain (5 +/- 6 gm) and amylase activity (1188 +/- 173 units/dl) were also normal in the preparations receiving acetaldehyde without preceding ischemia, but mild vascular and islet cell injury were observed on electron microscopy. One hour of ischemia followed by acetaldehyde infusion resulted in edema, increased weight gain (21 +/- 12 gm [p < 0.05]), and amylase activity (2487 +/- 1484 units/dl [p < 0.05]). Microscopy showed mild acinar cell damage and greater injury to the capillaries and the islets. The capillary and islet cell changes were reduced by superoxide dismutase and catalase. Intracellular adenosine triphosphate levels remained at baseline levels in the control preparations. Adenosine triphosphate decreased during ischemia but quickly recovered during perfusion without a significant difference whether acetaldehyde was infused after ischemia. An iron chelator desferoxamine ameliorated the injury response in the preparations simulating acute pancreatitis (weight gain, 13 +/- 6 gm [p = 0.09] and amylase activity, 1198 +/- 471 units/dl [p = 0.08]), but a cholecystokinin receptor antagonist L364,718 did not have an effect. A sulfhydryl group protector, dithiothreitol, decreased weight gain (10 +/- 7 gm [p = 0.06]), and amylase activity was not significantly increased over that of the control group (1582 +/- 641 units/dl), but a serine protease inhibitor phenylmethylsulphonylfluoride was ineffective. CONCLUSIONS: In this model simulating acute alcoholic pancreatitis, both the early physiologic injury response and the early morphologic changes are mediated at least in part by free radicals, which are generated by xanthine oxidase converted reversibly from xanthine dehydrogenase. In addition to the superoxide radical, the hydroxyl radical may also be an important early intermediate step, but the cholecystokinin receptor is not.

Acetaldehyde↗
PubMed1995

Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase.

The Sod2 gene for Mn-superoxide dismutase (MnSOD), an intramitochondrial free radical scavenging enzyme that is the first line of defense against superoxide produced as a byproduct of oxidative phosphorylation, was inactivated by homologous recombination. Homozygous mutant mice die within the first 10 days of life with a dilated cardiomyopathy, accumulation of lipid in liver and skeletal muscle, and metabolic acidosis. Cytochemical analysis revealed a severe reduction in succinate dehydrogenase (complex II) and aconitase (a TCA cycle enzyme) activities in the heart and, to a lesser extent, in other organs. These findings indicate that MnSOD is required for normal biological function of tissues by maintaining the integrity of mitochondrial enzymes susceptible to direct inactivation by superoxide.

Acidosis↗
PubMed1995

Intimate association of eosinophils to collagen bundles in eosinophilic myocarditis and ranitidine-induced hypersensitivity myocarditis.

BACKGROUND: Eosinophilic myocarditis is an inflammatory condition of the heart in which the infiltrate is composed predominately of eosinophils. DESIGN: We identified three cases of eosinophilic myocarditis in which the infiltrating eosinophils showed a remarkable intimate association with bundles of collagen. Two of the hearts examined were explants from heart transplant recipients with hypersensitivity myocarditis at the time of transplant and the third was from an autopsied patient with Churg-Strauss syndrome. These hearts were examined using light and electron microscopy. The cellular infiltrate in all three cases was characterized using immunoperoxidase stains with a panel including antibodies against myeloperoxidase, common leukocyte antigen (CD45), B lymphocytes (CD20), T lymphocytes (CD3), active-memory T lymphocytes (CD45RO), inactive T lymphocytes (CD45RA), and macrophages (CD68). RESULTS: Ultrastructural examination in all three cases confirmed the apposition of eosinophils to both large bundles of collagen and smaller aggregates of collagen fibrils. The eosinophils and the bundles of collagen stained strongly for myeloperoxidase, suggesting at least partial degranulation of the eosinophils. A KP-1 stain (CD68) revealed macrophages admixed with the eosinophils adjacent to the collagen bundles, and stains for CD45RA (naive lymphocytes) and CD45RO (memory T cells) showed an interstitial infiltrate of predominantly CD45RO-positive cells. Clinically, the cardiac decompensation of one of the transplant patients was most likely due to ranitidine-induced hypersensitivity myocarditis. CONCLUSIONS: These results suggest that some cases of eosinophilic myocarditis may be caused by the expression of novel antigens bound to collagen bundles. In one of the patients awaiting cardiac transplant, cardiac decompensation was temporally associated with ranitidine therapy, an agent not previously implicated as a cause of hypersensitivity myocarditis.

Adult↗
PubMed1994

Palmaz stent in the treatment of central venous stenosis: safety and efficacy of redilation.

PURPOSE: To assess the safety and efficacy of redilation of central venous stents in a growing animal model. MATERIALS AND METHODS: Palmaz stents were placed in the inferior vena cava (IVC) in 18 newborn lambs. After 5 months, vena cavography was performed. Those animals in which growth of the IVC adjacent to the stent and/or neointimal hyperplasia had resulted in a stenosis were considered candidates for redilation. Repeat vena cavography, intravascular ultrasound, and histologic examination were performed at 2 or 6 months. RESULTS: A stenosis of > 20% was demonstrated in 13 animals. Redilation was performed, and a 50% mean increase in stent diameter was achieved. There were no immediate complications. Late complications included nonocclusive laminar clot (n = 2), and a bar of tissue dividing but not occluding the caval lumen (n = 1). Moderate neointimal hyperplasia occurred in all stents. Stent compression (unrelated to redilation) occurred in seven animals. CONCLUSION: Palmaz stents can be redilated safely and effectively in an animal model of growing central veins.

Animals↗
PubMed1993

Myocarditis associated with doxorubicin cardiotoxicity.

In contrast to previous reports, the authors were impressed by the frequency of myocarditis in the endomyocardial biopsy specimens of patients treated with anthracyclines. To examine this, they reviewed the histologic and electron microscopic results and immunoperoxidase stains of myocardial biopsy specimens from 11 patients with doxorubicin cardiotoxicity grades 1.0-3.0. Immunoperoxidase stains for lymphocytes, macrophages, and endothelial cells and induced expression of Class II antigen were performed using the avidin-biotin complex procedure. A full panel of monoclonal antibodies was employed on fresh-frozen tissue; a smaller panel was used with formaldehyde-fixed paraffin-embedded material. Four of the 11 endomyocardial biopsy specimens showed myocarditis, and 2 showed borderline myocarditis by the Dallas criteria. The infiltrating lymphocytes were generally characterized as T lymphocytes and were associated with induced Class II antigen expression by arterial endothelial cells. In addition, foci of replacement fibrosis, suggesting a chronic process, were identified. Although this association does not prove a causal relationship, these results suggest that myocarditis can be a component of doxorubicin-induced myocardial injury.

Adult↗
PubMed1993

Progressive hemochromatotic cardiomyopathy despite reversal of iron deposition after liver transplantation.

Dilated cardiomyopathy is a frequent and serious complication of idiopathic hemochromatosis. The mechanism by which disordered iron metabolism induces heart failure is not entirely understood, but myocardial dysfunction appears to be intimately related to the deposition of iron in myocytes. Cardiac function characteristically worsens or improves in proportion to the degree of iron accumulation in cardiac myocytes. The authors report the case of a 47-year-old man with idiopathic hemochromatosis and cirrhosis who developed symptoms of congestive heart failure and was found to have dilated cardiomyopathy 7 months after receiving a liver transplant. An initial endomyocardial heart biopsy demonstrated severe iron deposition in myocytes. The patient's heart failure worsened in the next 3 years and he eventually required a heart transplant. Examination of the explanted heart revealed dilated cardiomyopathy, but the previously demonstrated iron deposits in the cardiac myocytes were depleted. This "uncoupling" of cardiac function and cardiac iron load suggests that a threshold may be reached at which point the metabolic and ultrastructural derangements of iron deposition are no longer reversible, even with the removal of the inciting agent. Furthermore, displacement of myocyte iron stores after liver transplantation implicates altered hepatic iron metabolism as a primary or contributing mechanism in the pathophysiology of idiopathic hemochromatosis.

Cardiomyopathy, Dilated↗
PubMed1992

Indian childhood cirrhosis in an American child.

Indian childhood cirrhosis is a fatal liver disease characterized by a striking accumulation of copper-containing granules within hepatocytes. A two-year-old American boy, the product of a third-cousin marriage, with clinical, biochemical, and histological signs of Indian childhood cirrhosis was studied. Liver biopsies at 22 and 30 months of age revealed a rapid progression from fibrosis to micronodular cirrhosis, with many of the remaining hepatocytes staining strongly for copper and copper-binding proteins. Electron microscopy showed characteristic dense granules containing copper and sulfur by electron probe analysis. Hepatic copper content was 1500 micrograms/g dry weight (normal, 20-50). Urinary copper was 3.6 mumol/d (229 micrograms/24 hours; normal, 15-20), and serum ceruloplasmin was 352 mg/L (normal, 150-320). The case suggests that both genetic and environmental components contribute to the manifestations of Indian childhood cirrhosis, and that the diagnosis of Indian childhood cirrhosis should be considered even in non-Indian infants with progressive liver disease.

Copper↗