ArticleFrontiers in medicine2023
Hepatorenal dysfunction in patients with chronic thromboembolic pulmonary hypertension.
Article in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Pulmonary arterial hypertension induces a metabolic and inflammatory hepatopathy.The Journal of clinical investigation · 2026Article
- Pulmonary Arterial Hypertension Induces a Metabolic and Inflammatory Hepatopathy.bioRxiv : the preprint server for biology · 2026Article
- Acidosis and in-hospital mortality in patients with pulmonary hypertension: a retrospective cohort study based on the MIMIC-IV database.Frontiers in medicine · 2025Article
- Beyond the Lung: Viewing Treatment Response through the Liver in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2024Article
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11 authors.
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Abstract
Background: Cardiac interactions with organs such as the liver or kidneys have been described in different cardiovascular diseases. However, the clinical relevance of hepatorenal dysfunction in chronic thromboembolic pulmonary hypertension (CTEPH) remains unclear. We determined the association of hepatorenal dysfunction (measured using the Model for End-stage Liver Disease Sodium [MELDNa] score) with right heart function and survival in patients with CTEPH. Methods: We analyzed all patients with CTEPH in the Giessen Pulmonary Hypertension Registry who had available MELDNa scores and were not taking vitamin K antagonists. The MELDNa score was calculated as MELD score - serum Na - (0.025 * MELD score * (140 - serum Na)) + 140; the MELD score was calculated as 10*(0.957*ln(creatinine)+0.378*ln(bilirubin)+1.12*ln(International Normalized Ratio))+6.43. Results: Seventy-two patients were included (74% female; median [Q1, Q3] MELDNa: 9 [6, 11]). MELDNa correlated well with right atrial and ventricular function and pulmonary hemodynamics. Forward regression analysis revealed that hepatorenal dysfunction mainly depends on right atrial strain and tricuspid regurgitation, but not right ventricular systolic dysfunction. Hepatorenal dysfunction predicted mortality at baseline and follow-up (adjusted hazard ratios [95% confidence intervals] per unit increase of MELDNa: 1.6 [1.1, 2.4] and 1.8 [1.1, 2.9], respectively). Changes in hepatorenal function also predicted mortality. Conclusion: Hepatorenal dysfunction in CTEPH is primarily associated with venous congestion rather than cardiac forward failure. As a surrogate parameter for hepatorenal dysfunction, MELDNa is a simple method to identify at-risk patients at baseline and follow-up.
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