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. 2025 Nov;168(5):1200-1214.
doi: 10.1016/j.chest.2025.05.024. Epub 2025 May 29.

Longitudinal Pulmonary Arterial Pressure Trajectories and Clinical Outcome in Kidney Transplantation Patients

Katarina Zeder  1 , Suman Kundu  2 , Edward D Siew  3 , Jeffrey S Annis  2 , Laurel Y Lee  4 , Jonah Garry  2 , Kelly A Birdwell  3 , Matthew S Freiberg  2 , Gabor Kovacs  5 , Evan L Brittain  2 , Bradley A Maron  6
Affiliations

Longitudinal Pulmonary Arterial Pressure Trajectories and Clinical Outcome in Kidney Transplantation Patients

Katarina Zeder et al. Chest. 2025 Nov.

Abstract

Background: Pulmonary hypertension (PH) is a high-risk finding in end-stage kidney disease (ESKD) and is independently associated with increased mortality.

Research question: What is the relationship between pulmonary artery pressure (PAP) trajectories from before kidney transplantation (KT) to after KT, as well as the role of PH after KT?

Study design and methods: We retrospectively analyzed patients in the Veterans Affairs Healthcare System with PAP values both before KT and after KT using echocardiography. The primary exposure was all-cause mortality, stratified according to PH status (systolic PAP > 35 mm Hg) into four groups: No-PH (no PH pre-KT or post-KT), New-PH (no PH pre-KT but PH post-KT), Resolved-PH (PH pre-KT but no PH post-KT), and Persistent-PH (PH pre-KT and post-KT). Findings were validated in the sex-balanced Vanderbilt University Medical System using echocardiography and right heart catheterization.

Results: From 631 patients (aged 60 ± 6 years; 96% male) in the primary cohort, there were 231 (36.6%), 184 (29.2%), 133 (21.1%), and 83 (13.1%) patients in the Persistent-PH, Never-PH, Resolved-PH, and New-PH groups, respectively. New-PH and Persistent-PH were associated with a 51% (hazard ratio [HR], 1.51; 95% CI, 1.06-2.15; P = .023) and 37% (HR, 1.37; 95% CI, 1.03-1.82; P = .029) increase in age- and sex-adjusted mortality risk compared with No-PH. Of all groups, Resolved PH was associated with the most favorable survival rate (adjusted HR, 0.73; 95% CI, 0.51-1.05; P = .087, compared with No-PH). Longitudinal mortality risk increased continuously with ≥ 1 mm Hg PAP increase from pre-KT to post-KT. Overall, a 21% increase in mortality risk per 10 mm Hg increment increase in echocardiographic systolic PAP (sPAP) was observed from pre-KT to post-KT, adjusted for age, sex, and baseline sPAP (HR, 1.21; 95% CI, 1.11-1.31; P < .001); a 10 mm Hg sPAP decrease was associated with a 17% decrease in adjusted mortality risk (HR, 0.83; 95% CI, 0.76-0.90; P < .001). Results were reproducible in the validation cohort.

Interpretation: Our results indicate that in patients with ESKD referred for KT as well as hemodynamic assessment, outcome is strongly associated with PAP trajectory. These data suggest that PAP may be a novel biomarker for risk stratifying KT candidacy, supporting prospective ESKD studies investigating the role of PH in clinical decision-making.

Keywords: kidney failure; kidney transplantation; outcome; pulmonary artery pressure; pulmonary hypertension.

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Conflict of interest statement

Financial/Nonfinancial Disclosures The authors have reported to CHEST the following: B. A. M. has a patent PCT/US2019/059890 pending to None, a patent #9,605,047 issued to None, a patent PCT/US2020/066886, pending to None, and a patent BWH 2023-152-29618-0438P02 pending to None. B. A. M. reports grants from the National Institutes of Health (NIH): 5R01HL139613-03, R01HL163960, R01HL153502, R01HL155096-01; and is an investigator at the University of Maryland-Institute for Health Computing, which is supported by funding from Montgomery County, Maryland, and The University of Maryland Strategic Partnership: MPowering the State, a formal collaboration between the University of Maryland, College Park, and the University of Maryland, Baltimore. E. L. B. reports grants from 01 HL 155278, R34 HL173389, R61/R33 HL 158941, R01 FD 007627, R01 HL 163960, R01 HL146588, and investigator-initiated grant funding from United Therapeutics. L. Y. L. is funded by NIH K08 HL165047. K. Z. reports support from Max Kade Fellowship of the Max Kade Foundation; funding from the Cardiovascular Medical Research and Education Fund (CMREF); consulting fees from Fa. Ferrer and AstraZeneca; support for attending scientific meetings from Fa. Janssen and Grupo Ferrer Internacional (all outside the scope of this work). G. K. reports grants or contracts from Boehringer Ingelheim Janssen, and MSD; consulting fees and payment honoraria from Boehringer Ingelheim, Janssen, MSD, AstraZeneca, Chiesi, AOP, and Ferrer; support for attending scientific meetings from AOP, VitalAire, MSD, and Boehringer Ingelheim; and a leadership role as a Member of the European Respiratory Society Guideline Group. None declared: (S. K., K. A. B., J. G., E. D. S., J. S. A., M. S. F.).

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