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The pathophysiology of the chronic cardiorenal syndrome: a magnetic resonance imaging study

Breidthardt, Tobias ; Cox, Eleanor ; Squire, Iain ; Odudu, Aghogho ; Omar, Nur ; Eldehni, Mohamed ; Francis, Susan ; McIntyre, Christopher

In: European Radiology, 2015, vol. 25, no. 6, p. 1684-1691

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    Titre
    • The pathophysiology of the chronic cardiorenal syndrome: a magnetic resonance imaging study
    Auteur
    • Breidthardt, Tobias. Clinic of Internal Medicine and Clinic for Transplant-Immunology and Nephrology, University Hospital Basel, Basel, Switzerland
    • Cox, Eleanor. Sir Peter Mansfield Magnetic Resonance Centre, University of Nottingham, Nottingham, UK
    • Squire, Iain. Department of Cardiovascular Sciences, University of Leicester and NIHR Cardiovascular Biomedical Research Unit, Glenfield Hospital, Leicester, UK
    • Odudu, Aghogho. Department of Renal Medicine, Royal Derby Hospital, Derby, UK
    • Omar, Nur. Sir Peter Mansfield Magnetic Resonance Centre, University of Nottingham, Nottingham, UK
    • Eldehni, Mohamed. Department of Renal Medicine, Royal Derby Hospital, Derby, UK
    • Francis, Susan. Sir Peter Mansfield Magnetic Resonance Centre, University of Nottingham, Nottingham, UK
    • McIntyre, Christopher. Department of Renal Medicine, Royal Derby Hospital, Derby, UK
    Type de document
    • Postprint
    Langue
    • Inglese
    Publié dans
    • European Radiology, 2015, vol. 25, no. 6, p. 1684-1691. Springer Berlin Heidelberg
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:331260
    Summary
    Objective: To study the association of renal function with renal perfusion and renal parenchymal structure (T1 relaxation) in patients with chronic heart failure (HF). Methods: After IRB approval, 40 participants were enrolled according to HF and renal function status [10 healthy volunteers < 40years; 10 healthy age-matched volunteers; 10 HF patients eGFR > 60ml/min/1.73m2; 10 HF patients eGFR < 60ml/min/1.73m2] and assessed by MRI. To be eligible for enrolment all HF patients with renal dysfunction (RD) needed to be diagnosed as having chronic cardiorenal syndrome based on current guidelines. Patients with primary kidney disease were excluded. Results: Renal cortical perfusion correlated with eGFR values (r = 0.52;p < 0.01) and was similar between HF patients with and without RD (p = 0.27). T1 relaxation correlated negatively with eGFR values (r = -0.41;p > 0.01) and was higher in HF patients compared to volunteers (1121 ± 102ms vs. 1054 ± 65ms;p = 0.03). T1 relaxation was selectively prolonged in HF patients with RD (1169ms ± 100 vs. HF without RD 1067ms ± 79;p = 0.047). In linear regression analyses coronary artery disease (p = 0.01), hypertension (p = 0.04), and diabetes mellitus (p < 0.01) were associated with T1 relaxation. Conclusion: RD in HF is not primarily mediated by decreased renal perfusion. Instead, chronic reno-parenchymal damage, as indicated by prolonged T1 relaxation, appears to underly chronic cardiorenal syndrome. Key points : • The pathophysiology underlying chronic cardiorenal syndrome is not completely understood. • Chronic cardiorenal syndrome is independent of cardiac output or renal perfusion. • Renal T 1 relaxation appears to be prolonged in HF with renal impairment. • Renal T 1 relaxation is associated with classic cardiovascular risk factors. • Association of renal T 1 relaxation with parenchymal damage should be validated further.