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Secondary hyperaldosteronism and liver fibrosis in patients with compensated chronic liver disease or portal hypertension

  • Giovanni Vitale
    Affiliations
    Internal Medicine Unit for the Treatment of Severe Organ Failure, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Policlinico di Sant'Orsola, Bologna, Italy
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  • Kimberly Coscia
    Affiliations
    Unit of Endocrinology and Prevention and Care of Diabetes, Department of Medical and Surgical Sciences (DIMEC), IRCCS Azienda Ospedaliero-Universitaria di Bologna, Policlinico di Sant'Orsola, Bologna, Italy
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  • Guido Zavatta
    Affiliations
    Unit of Endocrinology and Prevention and Care of Diabetes, Department of Medical and Surgical Sciences (DIMEC), IRCCS Azienda Ospedaliero-Universitaria di Bologna, Policlinico di Sant'Orsola, Bologna, Italy
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  • Maria Cristina Morelli
    Affiliations
    Internal Medicine Unit for the Treatment of Severe Organ Failure, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Policlinico di Sant'Orsola, Bologna, Italy
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  • Valentina Vicennati
    Correspondence
    Corresponding author at: Dipartimento di Scienze Mediche e Chirurgiche, University of Bologna, Via Massarenti, 9, 40138 Bologna, Italy.
    Affiliations
    Unit of Endocrinology and Prevention and Care of Diabetes, Department of Medical and Surgical Sciences (DIMEC), IRCCS Azienda Ospedaliero-Universitaria di Bologna, Policlinico di Sant'Orsola, Bologna, Italy
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Published:January 15, 2022DOI:https://doi.org/10.1016/j.ejim.2022.01.020
      Among edematous disorders, liver cirrhosis (LC) is considered one of the main models of secondary hyperaldosteronism (SH), as pointed out by several studies in the past [
      • Bernardi M.
      • Domenicali M.
      The renin–angiotensin–aldosterone system in cirrhosis.
      ]. Aldosterone is expected to be increased in patients with liver disease when pH occurs. The RAAS may also be implicated in the onset and progression of liver fibrosis. Since the etiology of cirrhosis and its treatments have profoundly changed over the years we aimed to evaluate the presence and severity of secondary hyperaldosteronism in patients with ACLD or mild pH. A secondary objective was to correlate RAAS components with noninvasive indices of liver fibrosis. The Ethical Committee of the S. Orsola-Malpighi Hospital approved the study. Written informed consent was obtained from all patients.

      Keywords

      Abbreviations:

      AT1 (Angiotensin Type1), ACE (Angiotensin-Converting Enzyme), ACLD (Advanced Chronic Liver Disease), ARR (Aldosterone-to-Renin Ratio), APRI (AST to Platelet Ratio Index), AxR (Aldosterone x Renin), CLIA (Chemiluminescent Immunoassay), DAAs (Direct Antiviral Agents), FIB-4 (Fibrosis Index-4), HCC (Hepatocellular Carcinoma), LC (Liver Cirrhosis), pH (Portal Hypertension), PRA (Plasma Renin Activity), RAAS (Renin-Angiotensin-Aldosterone System), SH (Secondary Hyperaldosteronism)
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