Zeder Katarina, Kundu Suman, Siew Edward D, Annis Jeffrey S, Lee Laurel Y, Garry Jonah, Birdwell Kelly A, Freiberg Matthew S, Kovacs Gabor, Brittain Evan L, Maron Bradley A
Division of Cardiovascular Medicine, University of Maryland School of Medicine, Baltimore; University of Maryland-Institute for Health Computing, Bethesda, MD; Division of Cardiovascular Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Division of Pulmonology, Medical University of Graz, Graz, Austria.
Department of Medicine, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN; Vanderbilt Pulmonary Circulation Center and Vanderbilt Institute for Clinical and Translational Medicine, Vanderbilt University Medical Center, Nashville, TN.
Chest. 2025 May 29. doi: 10.1016/j.chest.2025.05.024.
Pulmonary hypertension (PH) is a high-risk finding in end-stage kidney disease (ESKD) and is independently associated with increased mortality.
What is the relationship between pulmonary artery pressure (PAP) trajectories from pre-kidney transplantation (KT) to post-KT, as well as the role of PH post-KT?
We retrospectively analyzed patients in the Veterans Affairs Healthcare System with PAP values both pre-KT and post-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.
From 631 patients (60 ± 6 years; 96% male) in the primary cohort, 364 (58%) 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.
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.