Journal of Cholesterol and Heart Disease

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Short Communication - Journal of Cholesterol and Heart Disease (2023) Volume 7, Issue 4

Cardiorenal-hepatic syndrome: Interactions between cardiac, renal, and hepatic dysfunction in cardiac cirrhosis and congestive hepatopathy.

Gracia Fabiane *

Department of Medicine, Sao Paulo State University, Botucatu, Brazil

*Corresponding Author:
Gracia Fabiane
Department of Medicine
Sao Paulo State University
Botucatu, Brazil
E-mail: gracia@fab.br

Received: 29-Jul-2023, Manuscript No. AACHD-23-112264; Editor assigned: 01-Aug-2023, PreQC No. AACHD-23-112264 (PQ); Reviewed: 15-Aug-2023, QC No. AACHD -23-112264; Revised: 18-Aug-2023, Manuscript No. AACHD-23-112264 (R); Published: 25-Aug-2023, DOI: 10.35841/aachd-7.4.157

Citation: Fabiane G. Cardiorenal-hepatic syndrome: Interactions between cardiac, renal, and hepatic dysfunction in cardiac cirrhosis and congestive hepatopathy. J Cholest Heart Dis 2023;7(4):157

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Introduction

Cardiorenal-hepatic syndrome (CRHS) is a complex condition characterized by the simultaneous dysfunction of the heart, kidneys, and liver. It is commonly observed in patients with cardiac cirrhosis and congestive hepatopathy, conditions that arise due to chronic heart failure. The intricate interplay between the cardiovascular, renal, and hepatic systems in CRHS poses significant challenges for diagnosis, management, and treatment. This article aims to explore the interactions between cardiac, renal, and hepatic dysfunction in CRHS, emphasizing the underlying pathophysiology, diagnostic criteria, and therapeutic approaches [1].

CRHS occurs due to the hemodynamic disturbances associated with chronic heart failure. The reduced cardiac output in heart failure leads to renal hypoperfusion, activation of the renin-angiotensin-aldosterone system, and subsequent sodium and water retention. These mechanisms contribute to the development of renal dysfunction, commonly manifested as acute kidney injury or chronic kidney disease. Concurrently, the impaired cardiac function causes portal hypertension, resulting in hepatic congestion and ultimately leading to hepatic dysfunction, often referred to as congestive hepatopathy or cardiac cirrhosis. Additionally, systemic inflammation and oxidative stress further exacerbate the pathophysiological processes in CRHS [2].

The diagnosis of CRHS requires the identification of cardiac, renal, and hepatic dysfunction in a patient with chronic heart failure. Various diagnostic criteria have been proposed, including the consensus definitions put forth by the International Club of Ascites and the Acute Dialysis Quality Initiative. These criteria consider the presence of heart failure, impaired renal function (e.g., reduced glomerular filtration rate or increased serum creatinine), and evidence of hepatic dysfunction (e.g., elevated liver enzymes, hypoalbuminemia, or coagulation abnormalities). Imaging modalities such as echocardiography, abdominal ultrasound, and liver biopsy may provide additional insights into the structural and functional changes within the cardiovascular, renal, and hepatic systems [3].

CRHS poses significant challenges in terms of management and treatment. The therapeutic approach primarily focuses on addressing the underlying cardiac dysfunction and improving hemodynamics. This involves optimizing heart failure treatment with diuretics, angiotensin-converting enzyme inhibitors, beta-blockers, and mineralocorticoid receptor antagonists. Renal support, such as diuretics, may be necessary to manage fluid overload and prevent further renal impairment. In severe cases, renal replacement therapy, including hemodialysis or continuous renal replacement therapy, may be required. The management of hepatic dysfunction in CRHS often involves maintaining adequate nutritional support, managing complications such as ascites and hepatic encephalopathy, and considering liver transplantation in selected cases [4].

Cardiorenal-hepatic syndrome represents a complex clinical entity characterized by the simultaneous dysfunction of the heart, kidneys, and liver. Understanding the underlying pathophysiology and recognizing the diagnostic criteria for CRHS is crucial for early detection and appropriate management. Multidisciplinary collaboration among cardiologists, nephrologists, hepatologists, and other healthcare professionals is essential for optimizing patient outcomes and improving the quality of life for individuals affected by this syndrome. Future research endeavors should focus on identifying novel therapeutic strategies that target the complex interactions between the cardiovascular, renal, and hepatic systems in CRHS [5].

References

  1. Wells ML, Fenstad ER, Poterucha JT, et al Imaging findings of congestive hepatopathy. Radiograph. 2016;36(4):1024-37.
  2. Indexed at, Google Scholar, Cross Ref

  3. Hussein MS, Almujil SJ, Banheem AS, et al. Overview on cardiac cirrhosis and congestive hepatopathy-A review. J Pharmaceut Res Int. 2021;33(47A):212-20.
  4. Indexed at, Google Scholar, Cross Ref

  5. Lemmer A, VanWagner L, Ganger D. Congestive hepatopathy: Differentiating congestion from fibrosis.. Clin Liv Dis. 2017;10(6):139.
  6. Indexed at, Google Scholar, Cross Ref

  7. Khalife M, Faraj W, Salah F, et al. Congestive hepatopathy secondary to large renal arteriovenous malformation. Case Rep. 2013;2013:bcr2012007818.
  8. Indexed at, Google Scholar, Cross Ref

  9. Gewehr DM, Giovanini AF, Mattar BA, et al. Congestive hepatopathy secondary to right ventricular hypertrophy related to monocrotaline-induced pulmonary arterial hypertension. Int J Mol Sci. 2021;22(21):11891.
  10. Indexed at, Google Scholar, Cross Ref

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