Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • Most of our DSAs were de novo and their development

    2018-10-23

    Most of our DSAs were “de-novo”, and their development was predicted by donor and recipient ages. Other studies reported younger age at LT and medication non-compliance to be predisposing factors, which was not confirmed in our cohort (Del et al., 2014). Only three children developed both Class II DSA and non-HLA antibodies, hinting at different etiopathogeneses. In line with previous results (Venturi et al., 2014), we found non-HLA antibodies to be associated with portal and lobular inflammation. Non-HLA antibodies were detected in 40–75% of post-LT cases (Chen et al., 2013), associated with acute rejections, chronic rejections, and DNAIH. Since transient positivity can occur with rejection episodes, we considered non-HLA antibodies as positive when detected at the last two PBs. HLA-DRB1*03/04 allele in LT recipients was an independent risk factor for portal fibrosis, with no significant association with inflammation. This corresponds to the AIH scenario Montano-Loza et al., 2006; Liberal et al., 2015. These 1-Deoxynojirimycin are believed to result in faulty antigen processing, with antigenic mimicry resulting in hepatic injury. Given that, within 4weeks, the recipient\'s Kuffer cells were shown to completely repopulate the allograft (Manns & Mix, 2013 Nov), any host antigen-presenting cell defects would be evident in the new graft, explaining our findings. Topographic fibrosis distribution was a unique aspect of this study. This enabled us to identify a stronger persistence versus a discontinuous evolution in central and sinusoidal area, respectively. We found deceased donor to be the only predisposing factor for central fibrosis. While vascular and biliary complications, chronic rejection have been reported in earlier studies (Venturi et al., 2014), these were exclusion criteria in the current study as they are known fibrogenic complications. Inflammation in non-portal, unlike portal, areas was neither predictive of fibrosis nor associated with Class II DSA, but rather associated with non-HLA antibodies. We speculate that inflammation-driven fibrosis, when mediated by DSA, is limited to portal areas.
    Conclusion The following are the supplementary data related to this article.
    Author Contributions
    Financial support
    Introduction Contrast induced nephropathy (CIN) has become one of the leading causes of hospital-acquired acute kidney injury (AKI) (Nash et al., 2002) as contrast agents are widely utilized in clinical diagnostic and interventional procedures (Asif and Epstein, 2004; Wang et al., 2013). CIN following cardiac angiogram or intervention is associated with significant morbidity and mortality, with an in-hospital mortality rate of 20% in unselected patients and a 1-year mortality rate of up to 66% (Rihal et al., 2002; Shlipak et al., 2002; Best et al., 2002). However, there is still no effective prophylactic regimen available to prevent occurrence of CIN (Gassanov et al., 2014). Therefore, it is urgent to develop novel strategies to decrease CIN incidence and to improve clinical outcomes. Accumulated evidence indicates that CIN is the result of combined direct toxic effects of contrast media and hypoxic renal injury (Sendeski, 2011). Renal ischemia-reperfusion (I/R) injury due to contrast induced hemodynamic alteration of renal blood flow plays a pivotal role in the pathogenesis of CIN (Evans et al., 2013; Persson et al., 2005). Besides, contrast media induced production of free oxygen radicals also contributes to renal tubular cell injury (Pisani et al., 2013). Thus, the strategies for protecting against hypoxic injury may also be effective for prevention and treatment of CIN. Remote ischemic preconditioning (IPC) is defined as temporal episodes of ischemia of remote organ before a subsequent prolonged I/R injury. It can facilitate other organs to tolerate a more severe injury and to reduce the extent of distant organ damage. The tissue protective effects of this approach have been reported in myocardial infarction and AKI (Przyklenk and Whittaker, 2011; Wever et al., 2011). Limb IPC, one of remote IPC represents a promising approach for clinical intervention, has been tested in the prevention of CIN in clinic trials and gained encouraging results, especially in patients with a high risk of CIN (Er et al., 2012, Menting et al., 2015). However, its reno-protective mechanism remains elusive.