American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons
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Donation after circulatory death (DCD) holds great promise for improving cardiac graft availability; however, concerns persist regarding injury following warm ischemia, after donor circulatory arrest, and subsequent reperfusion. Application of preischemic treatments is limited for ethical reasons; thus, cardioprotective strategies applied at graft procurement (reperfusion) are of particular importance in optimizing graft quality. ⋯ These reperfusion strategies, however, differentially affect mitochondria; mild hypothermia also increases phosphocreatine content, while mechanical postconditioning stimulates mitochondrial complex I activity and reduces cytochrome c release (marker of mitochondrial damage), whereas hypoxia upregulates the expression of peroxisome proliferator-activated receptor-gamma coactivator (regulator of mitochondrial biogenesis). Characterization of the role of mitochondria in cardioprotective reperfusion strategies should aid in the identification of new, mitochondrial-based therapeutic targets and the development of effective reperfusion strategies that could ultimately facilitate DCD heart transplantation.
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Letter Case Reports
Successful pregnancies after islet transplantation for type 1 diabetes.
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Chronic lung allograft dysfunction (CLAD) is a fatal condition that limits survival after lung transplantation (LTx). The pathological hallmark of CLAD is obliterative bronchiolitis (OB). A subset of patients present with a more aggressive CLAD phenotype, called restrictive allograft syndrome (RAS), characterized by lung parenchymal fibrosis (PF). ⋯ Most mice with OB also had PF with a pattern of pleuroparenchymal fibroelastosis, reminiscent of human RAS-related pathology. Grading of pathologic changes demonstrated variable severity of airway fibrosis, PF, acute rejection, vascular fibrosis, and epithelial changes, similar to those seen in human CLAD. These assessments can make the murine LTx model a more useful tool for further mechanistic studies of CLAD pathogenesis.
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Understanding risk factors for deceased-donor kidney nontransplantation is important since discard rates remain high. We analyzed DonorNet® data of consecutive deceased-donor nonmandatory share primary kidney-only offers to adult candidates at our center and beyond between July 1, 2015 and March 31, 2016 for donor- and system-level risk factors of discard, defined as nontransplantation at our or subsequent transplant centers. Exclusions were hepatitis C virus/hepatitis B virus core antibody status, blood type AB, and donor <1 year based on low candidate waitlist size. ⋯ On multivariate regression, factors significantly associated with discard were donor cerebrovascular accident (adjusted odds ratio [aOR]: 3.32), cancer transmission concern (aOR: 6.5), renal artery luminal compromise (aOR: 3.97), biopsy score ≥3 (aOR: 5.09), 2-hour pump resistive index >0.4 (aOR: 3.27), absence of pump (aOR: 2.58), nonspecific kidney abnormality (aOR: 2.76), increasing offer cold ischemia time category 11-15, 16-20, and >21 hours (aOR: 2.07, 2.33, 2.82), nighttime notification (aOR: 2.19), and neither kidney placed at time of offer (aOR: 2.74). Many traditional determinants of discard lack discriminatory value when granular factors are assessed. System-level factors also influence discard and warrant further study.
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En bloc kidney transplants (EBK) from very small pediatric donation after circulatory death (DCD) donors are infrequent because of the perception that DCD adversely impacts outcomes. We retrospectively studied 130 EBKs from donors ≤10 kg (65 consecutive DCD vs 65 donation after brain death [DBD] transplants; pair-matched for donor weight and terminal creatinine, and for preservation time). For DCD vs DBD, median donor weight was 5.0 vs 5.0 kg; median recipient age was 57 vs 48 years (P = .006). ⋯ Median estimated GFR (mL/min per 1.73 m2 ) was significantly lower for DCD recipients at 1 and 3 months; at 6 years it remained stable at 100 (DCD) and 99 (DBD). DCD impacted early posttransplant graft function, but did not appear to impart added risk for graft loss and long-term function. Very small (≤10 kg) DCD EBK donors should be considered as an option to augment the deceased kidney donor pool; larger studies with longer follow-up must confirm these findings.