Comprehensive Characterization of Hematological, Renal, and Cardiovascular Profiles in Chronic Kidney Disease Patients With Pulmonary Hypertension

Objective: This study aimed to investigate the etiology, clinical consequences, and cardiovascular burden of pulmonary hypertension (PH) in patients with chronic kidney disease (CKD), particularly in severe CKD and end-stage renal disease. In addition, potential diagnostic markers were identified. Methods: In this single-center cross-sectional study, CKD patients (stage 3b–5) from the First Affiliated Hospital of Xi’an Jiaotong University were randomly matched 1:1 based on age, sex, and CKD stage between January 2020 and December 2022. Clinical and laboratory data—including blood cell counting, blood lipids, liver and kidney function, blood coagulation, N-terminal pro B-type natriuretic peptide, and troponin T—were collected from the Unified Digital Medical Record system. Additionally, transthoracic echocardiography and electrocardiogram results were collected upon patient admission. PH severity was classified as mild, moderate, or severe based on echocardiographic findings, and subgroup analyses were performed according to this classification. Results: A total of 440 CKD patients were enrolled with 220 patients diagnosed with PH (PH group) and 220 without PH (non-PH group). PH patients exhibited significantly lower red blood cell counts (2.76 (2.39, 3.2) × 10¹²/L vs. 3.14 (2.67, 3.73)×10¹²/L, P < 0.001), hemoglobin levels (82 (71, 93) g/L vs. 95 (79, 109) g/L, P < 0.001), and higher D-dimer (1.31(0.74, 2.75) mg/L vs. 0.83 (0.50, 1.47) mg/L, P < 0.001). Cardiac biomarkers, including N-terminal pro B-type natriuretic peptide (23,705 (6,809, 35,000) ng/L vs. 2,644 (665, 10,818) ng/L, P < 0.001) and troponin T (0.070 (0.032, 0.134) μg/L vs. 0.031 (0.013, 0.066) μg/L, P < 0.001), were markedly elevated in the PH group. Echocardiographic findings revealed significant right ventricular enlargement (29 (26, 32) mm vs. 27 (25,29) mm, P < 0.001) and a higher prevalence of pericardial effusion (62.7% vs. 25.0%, P < 0.001) in PH patients. Cardiac conduction abnormalities were more prevalent in PH patients, with significantly higher rates of atrial fibrillation, supraventricular premature beats, and right bundle branch block (all P < 0.05). There are 109 patients with mild PH, 83 with moderate PH, and 28 with severe PH. Left ventricular remodeling and functional impairment were observed in moderate and severe PH patients. Conclusion: Progressive PH in CKD patients is associated with significant cardiovascular abnormalities. Routine echocardiographic surveillance and biomarker monitoring are crucial for early risk stratification and management. Further research is needed to explore targeted therapies to improve outcomes in this high-risk population.