Early Lung Allograft Function in Twin Recipients From the Same Donor: Risk Factor Analysis

Sommers, K. Eric; Griffith, Bartley P.; Hardesty, Robert L.; Keenan, Robert J.

doi:10.1016/s0003-4975(96)00371-2

Cited by 55 publications

(48 citation statements)

References 6 publications

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“…The primary definition of grade 3 PGD at 48 or 72 hours after transplant was associated with a relative risk (RR) of 4.8 (95% CI, 3.3-7.0; P , 0.001) for death within 90 days of transplant compared with those without grade 3 PGD and an ARI of 18% (95% CI, 12-24). Grade 3 PGD was associated with a significantly increased 1-year mortality (RR, 3.0; 95% CI, 2.3-3.9; P , 0.001) compared with those without grade 3 PGD, and an ARI of 23% (95% CI, [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]. Although the magnitude of the association between grade 3 PGD and mortality was attenuated when the alternate definition of any grade 3 PGD within 72 hours was used in the sensitivity analyses, the association remained significant at 90 days (RR, 3.5; 95% CI, 2.3-5.1; P , 0.001) and 1 year (RR, 2.5; 95% CI, 1.9-3.3; P , 0.001) (see Table E6).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Clinical Risk Factors for Primary Graft Dysfunction after Lung Transplantation

Diamond¹,

Lee²,

Kawut³

et al. 2013

The Journal of Heart and Lung Transplantation

154

294

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Rationale: Primary graft dysfunction (PGD) is the main cause of early morbidity and mortality after lung transplantation. Previous studies have yielded conflicting results for PGD risk factors. Objectives: We sought to identify donor, recipient, and perioperative risk factors for PGD. Methods: We performed a 10-center prospective cohort study enrolled between March 2002 and December 2010 (the Lung Transplant Outcomes Group). The primary outcome was International Society for Heart and Lung Transplantation grade 3 PGD at 48 or 72 hours posttransplant. The association of potential risk factors with PGD was analyzed using multivariable conditional logistic regression. Measurements and Main Results: A total of 1,255 patients from 10 centers were enrolled; 211 subjects (16.8%) developed grade 3 PGD. In multivariable models, independent risk factors for PGD were any history of donor smoking (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.2-2.6; P ¼ 0.002); FI O 2 during allograft reperfusion (OR, 1.1 per 10% increase in FI O 2 ; 95% CI, 1.0-1.2; P ¼ 0.01); single lung transplant (OR, 2; 95% CI, 1.2-3.3; P ¼ 0.008); use of cardiopulmonary bypass (OR, 3.4; 95% CI, 2.2-5.3; P , 0.001); overweight (OR, 1.8; 95% CI, 1.2-2.7; P ¼ 0.01) and obese (OR, 2.3; 95% CI, 1.3-3.9; P ¼ 0.004) recipient body mass index; preoperative sarcoidosis (OR, 2.5; 95% CI, 1.1-5.6; P ¼ 0.03) or pulmonary arterial hypertension (OR, 3.5; 95% CI, 1.6-7.7; P ¼ 0.002); and mean pulmonary artery pressure (OR, 1.3 per 10 mm Hg increase; 95% CI, 1.1-1.5; P , 0.001). PGD was significantly associated with 90-day (relative risk, 4.8; absolute risk increase, 18%; P , 0.001) and 1-year (relative risk, 3; absolute risk increase, 23%; P , 0.001) mortality. Conclusions: We identified grade 3 PGD risk factors, several of which are potentially modifiable and should be prioritized for future research aimed at preventative strategies. Clinical trial registered with www.clinicaltrials.gov (NCT 00552357). What This Study Adds to the FieldWe performed a multicenter, prospective cohort study of 1,255 lung transplant recipients across 10 US transplant centers. We identified receipt of an organ from a donor with any smoking history, elevated FI O 2 during allograft reperfusion, preoperative sarcoidosis or pulmonary arterial hypertension, use of cardiopulmonary bypass, single lung transplant, large-volume blood product transfusion, elevated pulmonary arterial pressures, and overweight or obese recipient body habitus as risk factors for grade 3 PGD. Several of these risk factors are potentially modifiable, and thus may suggest preventative strategies, whereas other risk factors should be prioritized for future mechanistic research efforts.

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Section: Resultsmentioning

confidence: 99%

“…Potential risk factors for grade 3 PGD previously identified in the literature or with hypothetical clinical or biologic plausibility were selected for analysis a priori (5)(6)(7)(14)(15)(16)(17)(18)(19)(20). Details of covariate definitions are included in the online supplement.…”

Section: Candidate Risk Factor Selection and Definitionmentioning

confidence: 99%

Clinical Risk Factors for Primary Graft Dysfunction after Lung Transplantation

Diamond¹,

Lee²,

Kawut³

et al. 2013

The Journal of Heart and Lung Transplantation

154

294

View full text Add to dashboard Cite

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“…The early phase of reperfusion depends primarily on donor characteristics, but these lose importance during the ensuing 24 h, and recipients characteristics then become predominant (8). Donor/passenger macrophages have been shown to be activated during ischemia and to mediate the early phase of reperfusion injury, whereas neutrophils are primarily involved in the late phase of reperfusion injury (9,10).…”

Section: Recipient T Cells Mediate Reperfusion Injury After Lung Tranmentioning

confidence: 99%

“…Previous studies have suggested that IR injury can be differentiated into two phases: the early phase of reperfusion injury, which corresponds to the first few hours of reperfusion during which function of the transplanted lung is mainly dependent of donor characteristics; and the late phase of reperfusion, which occurs thereafter and is principally dependent of recipient factors (7,8).…”

Section: Late Reperfusion Injury Is Dependent Of Recipient T Cellsmentioning

confidence: 99%

Recipient T Cells Mediate Reperfusion Injury after Lung Transplantation in the Rat

Perrot¹,

Young

Imai³

et al. 2003

The Journal of Immunology

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Leukocytes have been implicated in ischemia-reperfusion (IR) injury of the lung, but the individual role of T cells has not been explored. Recent evidence in mice suggests that T cells may play a role in IR injury. Using a syngeneic (Lewis to Lewis) rat lung transplant model, we observed that recipient CD4+ T cells infiltrated lung grafts within 1 h of reperfusion and up-regulated the expression of CD25 over the ensuing 12 h. Nude rats (rnu/rnu) and heterozygous rats (rnu/+) were used to determine the role of T cells in IR injury. No significant difference in lung function was observed between nude and heterozygous recipient rats after 2 h of reperfusion. However, after 12 h of reperfusion, recipient nude rats had significantly higher oxygenation and lower peak airway pressure than recipient heterozygous rats. This was associated with significantly lower levels of IFN-γ in transplanted lung tissue of recipient nude rats. Reconstitution of recipient nude rats with T cells from heterozygous rats restored IR injury after 12 h of reperfusion. The effect of T cells was independent of neutrophil recruitment and activation in the transplanted lung. These results demonstrate that recipient T cells are activated and mediate IR injury during lung transplantation in rats.

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“…Primers used for the selected eight genes are shown in (24) and interplay of donor lungs and the recipient (7,25 (28,29). Furthermore, donor-related fac- …”

Section: Verification Of Gene Expression By Quantitative Rt-pcrmentioning

confidence: 99%

Impact of Human Donor Lung Gene Expression Profiles on Survival after Lung Transplantation: A Case-Control Study

Anraku

Cameron

Waddell

et al. 2008

American Journal of Transplantation

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Primary graft dysfunction (PGD) continues to be a major cause of early death after lung transplantation. Moreover, there remains a lack of accurate pretransplant molecular markers for predicting PGD. To identify distinctive donor lung gene expression signatures associated with PGD, we profiled human donor lungs using microarray technology prior to implantation. The genomic profiles of 10 donor lung samples from patients who subsequently developed clinically defined severe PGD were compared with 16 case-matched donor lung samples from those who had a favorable outcome without PGD (development set, n = 26). Selected PCR validated predictive genes were tested by quantitative reverse transcription-polymerase chain reaction in an independent test set (n = 81). Our microarray analyses of the development set identified four significantly upregulated genes (ATP11B, FGFR2, EGLN1 and MCPH1) in the PGD samples. These genes were also significantly upregulated in donor samples of the test set of patients with poor outcomes when compared to those of patients with good outcomes after lung transplantation. This type of biological donor lung assessment shows significant promise for development of a more accurate diagnostic strategy to assess donor lungs prior to implantation.

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Early Lung Allograft Function in Twin Recipients From the Same Donor: Risk Factor Analysis

Cited by 55 publications

References 6 publications

Clinical Risk Factors for Primary Graft Dysfunction after Lung Transplantation

Clinical Risk Factors for Primary Graft Dysfunction after Lung Transplantation

Recipient T Cells Mediate Reperfusion Injury after Lung Transplantation in the Rat

Impact of Human Donor Lung Gene Expression Profiles on Survival after Lung Transplantation: A Case-Control Study

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