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      Early Graft Loss after Kidney Transplantation: Endothelial Dysfunction of Renal Microvasculature

      research-article
      Author(s): 1 , 2 , 1 , 3 ,
      Publication date (Electronic):
      Journal: BioMed Research International
      Publisher: Hindawi

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          Abstract

          Decision process about the acceptance of the deceased donor kidney for transplantation might be challenging. Although histological evaluation of pretransplant donor kidney biopsy provides reliable information regarding cortical necrosis, vascular thrombosis, extensive global glomerulosclerosis, and interstitial fibrosis/tubular atrophy, only electron microscopy enables thorough and reliable insights into microvasculature changes of kidney graft. The aim of the present paper is to briefly present two cases of early kidney graft loss. In one case, the donor was exposed to long-term extracorporeal membrane oxygenation (ECMO); in the other case, the donor experienced Takotsubo cardiomyopathy. In both cases, light microscopy of pretransplant biopsy found no pathology or significant discrepancy in morphology of kidney graft, while electron microscopy revealed severe endothelial dysfunction of renal microvasculature. Our results suggest that severe injury of renal microvasculature with relatively preserved tubular epithelium may be associated with some conditions of deceased kidney donors leading to early kidney graft nonfunction and loss. Further studies are needed to determine prognostic significance of severe ultrastructural microvasculature lesions and to evaluate disease states and conditions that could be associated with severe endothelial dysfunction of kidney graft.

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          The inflammatory response to extracorporeal membrane oxygenation (ECMO): a review of the pathophysiology

          Jonathan Millar, Jonathon P Fanning, Charles Mcdonald … (2016)
          Extracorporeal membrane oxygenation (ECMO) is a technology capable of providing short-term mechanical support to the heart, lungs or both. Over the last decade, the number of centres offering ECMO has grown rapidly. At the same time, the indications for its use have also been broadened. In part, this trend has been supported by advances in circuit design and in cannulation techniques. Despite the widespread adoption of extracorporeal life support techniques, the use of ECMO remains associated with significant morbidity and mortality. A complication witnessed during ECMO is the inflammatory response to extracorporeal circulation. This reaction shares similarities with the systemic inflammatory response syndrome (SIRS) and has been well-documented in relation to cardiopulmonary bypass. The exposure of a patient’s blood to the non-endothelialised surface of the ECMO circuit results in the widespread activation of the innate immune system; if unchecked this may result in inflammation and organ injury. Here, we review the pathophysiology of the inflammatory response to ECMO, highlighting the complex interactions between arms of the innate immune response, the endothelium and coagulation. An understanding of the processes involved may guide the design of therapies and strategies aimed at ameliorating inflammation during ECMO. Likewise, an appreciation of the potentially deleterious inflammatory effects of ECMO may assist those weighing the risks and benefits of therapy.
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            The stunned myocardium: prolonged, postischemic ventricular dysfunction.

            R Kloner, E Braunwald (1982)
            Myocardial ischemia has, for many decades, been viewed as an all-or-none process that causes myocardial necrosis when prolonged and severe, but whose effects are transient when it is brief or mild. In view of the evidence that the ischemic process may "hit, run and stun," perhaps our thinking about the consequences of myocardial ischemia should be expanded. According to this formulation, an ischemic insult not of sufficient severity of duration to produce myocardial necrosis may acutely affect myocardial repolarization and cause angina (hit); but these changes wane rapidly (run), when the balance between myocardial oxygen supply and demand has been reestablished. However, the ischemia may interfere with normal myocardial function, biochemical processes and ultrastructure for prolonged periods (stun). The severity and duration of these postischemic changes depend on the length and intensity of the ischemia, as well as on the condition of the myocardium at the onset of the ischemic episode. Furthermore, it is likely that when the myocardium is repeatedly stunned, it may exhibit chronic postischemic left ventricular dysfunction, an ill-defined condition. If prolonged, chronic postischemic left ventricular dysfunction can progress to myocardial scarring and ischemic cardiomyopathy, it may be important to determine how often it can be ameliorated by permanent improvement of myocardial perfusion by surgical treatment.
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              Comparison of survival probabilities for dialysis patients vs cadaveric renal transplant recipients.

              Robert Port, K Jiang, E A Mauger … (1993)
              To compare mortality risk among cadaveric renal transplant recipients vs transplant candidates on dialysis in the cyclosporine era. Patient mortality risk was analyzed by treatment modality for a completed statewide patient population. All Michigan residents younger than age 65 years who started endstage renal disease (ESRD) therapy between January 1, 1984, and December 31, 1989, were included. Patients were followed up from ESRD onset (n = 5020), to wait-listing for renal transplant (n = 1569), to receiving a cadaveric first transplant (n = 799), and to December 31, 1989. Mortality rates. Using a time-dependent variable based on the waiting time from date of wait-listing to transplantation and adjusting for age, sex, race, and primary cause of ESRD, the relative risk (RR) of dying was increased early after transplantation and then decreased to a beneficial long-term effect, given survival to 365 days after transplantation (RR, 0.36; P .05). Overall, the estimated times from transplantation to equal mortality risk was 117 +/- 28 days and to equal cumulative mortality was 325 +/- 91 days. The overall mortality risk following renal transplantation was initially increased, but there was a long-term survival benefit compared with similar patients on dialysis. These analyses allow improved description of comparative mortality risks for dialysis and transplant patients and allow advising patients regarding comparative survival outcomes.
              Article 0 comments Cited 112 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ž. Večerić-Haler:
                ORCID: http://orcid.org/0000-0003-3318-9850
                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date Collection: 2018
                Publication date (Electronic): 25 July 2018
                Volume: 2018
                Electronic Location Identifier: 4074209
                Affiliations
                1Institute of Pathology, Faculty of Medicine, University of Ljubljana, 1000 Ljubljana, Slovenia
                2Institute of Pathology, Medical Experimental Centre, Faculty of Medicine, University of Ljubljana, 1000 Ljubljana, Slovenia
                3Department of Nephrology, University Medical Centre Ljubljana, 1000 Ljubljana, Slovenia
                Author notes

                Academic Editor: Karine Hadaya

                Author information
                http://orcid.org/0000-0003-1893-4349
                http://orcid.org/0000-0001-9397-9366
                http://orcid.org/0000-0003-3318-9850
                Article
                DOI: 10.1155/2018/4074209
                PMC ID: 6083599
                SO-VID: d23c3087-5bcc-49eb-8991-a89fea0f9ac5
                Copyright © Copyright © 2018 N. Kojc et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 22 June 2018
                Date accepted : 18 July 2018
                Funding
                Funded by: ARRS
                Award ID: P3-054
                Award ID: P3-0323
                Categories
                Subject: Research Article

                Data availability:

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