Purpose: Pulmonary hypertension (PH) is common in patients undergoing lung transplantation. The association of pretransplant mean pulmonary artery pressure (mPAP) and the risk of perioperative acute kidney injury (AKI) remains unknown. Methods: We identified 354 lung allograft recipients transplanted between 1997 and 2009 with available preoperative pulmonary artery pressure measurements. We categorized patients as having no PH (mPAP < 25mmHg, n=162), mild PH (mPAP 25-34mmHg, n=133), moderate PH (mPAP 35-45mmHg, n=39), and severe PH (mPAP > 45mmHg, n=20) prior to transplant. AKI was defined by an absolute rise in creatinine within 48 hours of transplant by > 0.3mg/dl according to the Acute Kidney Injury Network classification schema. Results: We identified a graded incidence of perioperative AKI based on baseline PH status [no PH n=60(37%), mild PH n=68(51%), moderate PH n=26(67%), severe PH n=17(85%), p<0.001]. For every 10mmHg increase in baseline mPAP there was an associated 1.7 (95%CI 1.4, 2.2) increased odds of AKI. Controlling for age, gender, race, single vs. double lung transplant, pretransplant diabetes, baseline creatinine, COPD as etiology of lung disease, intraoperative administration of pressors and/or inotropes, baseline mPAP, and initial postoperative PaO2/FiO2 those independent covariates that remained significantly associated with AKI post-transplant included vasopressor/inotrope use [OR 2.3, (95%CI 1.3,4.2)], age [OR 0.72, (95%CI 0.55,0.95) per decade increase], baseline creatinine [OR 7.6, (95%CI 1.1,18.6) per 1mg/dl increase], initial PaO2/FiO2 [0.83, (95%CI 0.74,0.92) per 50 unit increase], and mPAP [OR 1.6, (95%CI 1.2,2.0) per 10mmHg increase].Conclusions: Higher baseline pulmonary artery pressures independently predict in a dose dependent fashion an increased risk of AKI immediately after lung tranplant.

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