The Impact of Donor Renal Function on Cardiac Allograft Survival: Insights into Reno-Cardiac Interactions
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文摘

Purpose

Myocardial necrosis and apoptosis have been observed following experimentally induced renal dysfunction (RD). Given that adverse cardiac outcomes remain strongly associated with acute kidney injury even after RD completely normalizes, many have theorized that the adverse outcomes directly result from RD-induced myocardial injury. However, it remains unclear whether this risk is the result of the RD itself, or if RD is identifying a ¡°sicker¡± population. As such, we hypothesized that if the adverse cardiovascular outcomes associated with RD result primarily from irreversible RD-induced myocardial injury, transplantation of a heart from a donor with RD should lead to inferior graft survival.

Methods and Materials

Adult patients in the UNOS registry who underwent cardiac transplantation from 1994 through June 30, 2011 with donor creatinine and urine protein available were evaluated (n=20,438).

Results

Mean donor GFR was 90.5 ¡À 48.4 ml/min and 22.3 % of donors had RD (GFR<60 ml/min). Ejection fraction was similar between donors with (61.8 % ¡À 7.8 % ) and without RD (61.5 % ¡À 7.8 % , p=0.05). Both donor GFR (HR=1.000, p=0.19) and donor proteinuria (HR=0.999, p=0.96) were unrelated to graft survival. Paradoxically, after adjustment for donor and recipient characteristics, better donor GFR was actually associated with significantly worsened graft survival (HR=1.01 per 10 ml/min higher GFR, p=0.03). However, other donor/pre-transplant factors linked to subclinical myocardial injury such as age > 40 (HR=1.4, p<0.001), diabetes (HR=1.09, p=0.04), hypertension (HR=1.09, p<0.001), smoking (HR=1.21, p<0.001), and ischemic time > 4 hrs (HR=1.2, p<0.001) were associated with reduced graft survival.

Conclusions

RD in cardiac allograft donors is not associated with reduced post-transplant graft survival. These data support the hypothesis that irreversible myocardial injury induced by RD is not primarily responsible for the strong epidemiologic association between RD and adverse cardiovascular outcomes.

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