104
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Histological Criteria for Encapsulating Peritoneal Sclerosis – A Standardized Approach

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          The two most relevant pathologies of long-term peritoneal dialysis (PD) are simple sclerosis and encapsulating peritoneal sclerosis (EPS). The histological differentiation of those two entities is difficult. The Aim of the study was to establish a method to standardize and facilitate the differentiation between simple sclerosis and EPS

          Methods

          We investigated 58 peritoneal biopsies - 31 EPS patients and 27 PD patients. Two blinded investigators analyzed 20 histological characteristics in EPS and PD patients.

          Results

          The following findings were significantly more common in EPS than in patients on PD without EPS: fibroblast like cells (FLC) (p<0.0001), mesothelial denudation (p<0.0001), decreased cellularity (p = 0.008), fibrin deposits (p<0.03), Fe deposits (p = 0.05), podoplanin vascular (p<0.0001), podoplanin avascular (p<0.0001). Using all predictor variables we trained the classification method Random Forest to categorize future cases. Podoplanin vascular and avascular were taken together (p<0.0001), FLC (p<0.0001), mesothelial denudation (p = 0.0005), calcification (p = 0.0026), acellular areas (p = 0.0094), and fibrin deposits (p = 0.0336) showed up as significantly important predictor variables. Estimated misclassification error rate when classifying new cases turned out to be 14%.

          Conclusion

          The introduced statistical method allows discriminating between simple sclerosis and EPS. The misclassification error will likely improve with every new case added to the database.

          Related collections

          Most cited references28

          • Record: found
          • Abstract: found
          • Article: not found

          Lymphatic neoangiogenesis in human kidney transplants is associated with immunologically active lymphocytic infiltrates.

          Renal transplant rejection is caused by a lymphocyte-rich inflammatory infiltrate that attacks cortical tubules and endothelial cells. Immunosuppressive therapy reduces the number of infiltrating cells; however, their exit routes are not known. Here a >50-fold increase of lymphatic vessel density over normal kidneys in grafts with nodular mononuclear infiltrates is demonstrated by immunohistochemistry on human renal transplant biopsies using antibodies to the lymphatic endothelial marker protein podoplanin. Nodular infiltrates are constantly associated with newly formed, Ki-67-expressing lymphatic vessels and contain the entire repertoire of T and B lymphocytes to provide specific cellular and humoral alloantigenic immune responses, including Ki-67(+) CD4(+) and CD8(+) T lymphocytes, S100(+) dendritic cells, and Ki-67(+)CD20(+) B lymphocytes and lambda- and kappa-chain-expressing plasmacytoid cells. Numerous chemokine receptor CCR7(+) cells within the nodular infiltrates seemed to be attracted by secondary lymphatic chemokine (SLC/CCL21) that is produced and released by lymphatic endothelial cells in a complex with podoplanin. From these results, it is speculated that lymphatic neoangiogenesis not only contributes to the export of the rejection infiltrate but also is involved in the maintenance of a potentially detrimental alloreactive immune response in renal transplants and provides a novel therapeutic target.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Transient overexpression of TGF-{beta}1 induces epithelial mesenchymal transition in the rodent peritoneum.

            Epithelial mesenchymal transition (EMT), a process involved in many growth and repair functions, has been identified in the peritoneal tissues of patients who undergo peritoneal dialysis. The sequence of changes in gene regulation and cellular events associated with EMT after TGF-beta1-induced peritoneal fibrosis is reported. Sprague-Dawley rats received an intraperitoneal injection of an adenovirus vector that transfers active TGF-beta1 (AdTGF-beta1) or control adenovirus, AdDL. Animals were killed 0 to 21 days after infection. Peritoneal effluent and tissue were analyzed for markers of EMT. In the animals that were treated with AdTGF-beta1, an increase in expression of genes associated with EMT and fibrosis, such as type I collagen A2, alpha-smooth muscle actin, and the zinc finger regulatory protein Snail, was identified. Transition of mesothelial cells 4 to 7 d after infection, with appearance of epithelial cells in the submesothelial zone 7 to 14 d after exposure to AdTGF-beta1, was demonstrated. This phase was associated with disruption of the basement membrane and increased expression of matrix metalloproteinase 2. By 14 to 21 d after infection, there was evidence of restoration of normal submesothelial architecture. These findings suggest that EMT occurs in vivo after TGF-beta1 overexpression in the peritoneum. Cellular changes and gene regulation associated with EMT are evident throughout the fibrogenic process and are not limited to early time points. This further supports the central role of TGF-beta1 in peritoneal fibrosis and provides an important model to study the sequence of events involved in TGF-beta1-induced EMT.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Encapsulating peritoneal sclerosis: incidence, predictors, and outcomes.

              Encapsulating peritoneal sclerosis is a complication of peritoneal dialysis characterized by persistent, intermittent, or recurrent adhesive bowel obstruction. Here we examined the incidence, predictors, and outcomes of encapsulating peritoneal sclerosis (peritoneal fibrosis) by multivariate logistic regression in incident peritoneal dialysis patients in Australia and New Zealand. Matched case-control analysis compared the survival of patients with controls equivalent for age, gender, diabetes, and time on peritoneal dialysis. Of 7618 patients measured over a 13-year period, encapsulating peritoneal sclerosis was diagnosed in 33, giving an incidence rate of 1.8/1000 patient-years. The respective cumulative incidences of peritoneal sclerosis at 3, 5, and 8 years were 0.3, 0.8, and 3.9%. This condition was independently predicted by younger age and the duration of peritoneal dialysis, but not the rate of peritonitis. Twenty-six patients were diagnosed while still on peritoneal dialysis. Median survival following diagnosis was 4 years and not statistically different from that of 132 matched controls. Of the 18 patients who died, only 7 were attributed directly to peritoneal sclerosis. Our study shows that encapsulating peritoneal sclerosis is a rare condition, predicted by younger age and the duration of peritoneal dialysis. The risk of death is relatively low and not appreciably different from that of competing risks for mortality in matched dialysis control patients.
                Bookmark

                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2012
                7 November 2012
                : 7
                : 11
                : e48647
                Affiliations
                [1 ]Department of Internal Medicine, Division of Nephrology, Robert Bosch Hospital, Stuttgart, Germany
                [2 ]Margarete Fischer–Bosch Institute of Clinical Pharmacology, University of Tuebingen, Tuebingen, Germany
                [3 ]Department of Surgery, Robert Bosch Hospital, Stuttgart, Germany
                [4 ]Department of Diagnostic Medicine, Division of Pathology, Robert Bosch Hospital, Stuttgart, Germany
                [5 ]Department of Internal Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States of America
                [6 ]Department of Mathematics, University of Stuttgart, Stuttgart, Germany
                [7 ]Division of Nephrology, University Hospital, Zurich, Switzerland
                Queensland Institute of Medical Research, Australia
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: JL NB CU MDA SS MK. Performed the experiments: DB KPT GO JL NB CU FR PF. Analyzed the data: JL NB CU PF DB SS FR GO JD. Contributed reagents/materials/analysis tools: CU PF DB SS FR GO JL. Wrote the paper: JL NB PF MDA.

                Article
                PONE-D-12-17362
                10.1371/journal.pone.0048647
                3492493
                23144917
                c32ccbaa-0d82-48a1-b42c-cd7eee5dc376
                Copyright @ 2012

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 14 June 2012
                : 27 September 2012
                Page count
                Pages: 8
                Funding
                This work was supported by the Robert-Bosch Foundation and the Sabine- Dörges- Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Biology
                Population Biology
                Epidemiology
                Medicine
                Clinical Research Design
                Epidemiology
                Diagnostic Medicine
                Pathology
                General Pathology
                Biomarkers
                Epidemiology
                Biomarker Epidemiology
                Nephrology
                Dialysis

                Uncategorized
                Uncategorized

                Comments

                Comment on this article