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The liver and the kidney: two critical organs influencing the atherothrombotic risk in metabolic syndrome

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
Topic:

Theme Issue
Platelets: basic mechanisms and translational implications

DOI: https://doi.org/10.1160/TH13-06-0499
Issue: 2013: 110/5 (Nov) pp. 857-1085
Pages: 940-958

The liver and the kidney: two critical organs influencing the atherothrombotic risk in metabolic syndrome

F. Carbone (1, 2), F. Montecucco (1, 2), F. Mach (2), R. Pontremoli (3), F. Viazzi (3)

(1) Department of Internal Medicine, University of Genoa School of Medicine. IRCCS Azienda Ospedaliera Universitaria San Martino–IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy; (2) Cardiology Division, Foundation for Medical Researches, Department of Internal Medicine, University of Geneva, Geneva, Switzerland; (3) Departments of Cardio- Nephrology and Internal Medicine University of Genoa, School of Medicine, IRCCS Azienda Ospedaliera Universitaria San Martino–IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy

Keywords

metabolic syndrome, atherothrombosis, liver, kidney

Summary

The increased atherothrombotic risk in patients with metabolic syndrome (MetS) has been classically explained by the multiplicative effect of systemic concomitant pro-atherosclerotic factors. In particular, centripetal obesity, dyslipidaemia, glucose intolerance, hypertension (differently combined in the diagnosis of the disease) would be expected to act as classical cardiovascular risk conditions underlying accelerated atherogenesis. In order to better understand specific atherosclerotic pathophysiology in MetS, emerging evidence focused on the alterations in different organs that could serve as both pathophysiological targets and active players in the disease. Abnormalities in adipose tissue, heart and arteries have been widely investigated in a variety of basic research and clinical studies in MetS. In this narrative review, we focus on pathophysiological activities of the liver and kidney. Considering its key role in metabolism and production of soluble inflammatory mediators (such as C-reactive protein [CRP]), the liver in MetS has been shown to be altered both in its structure and function. In particular, a relevant amount of the fat accumulated within this organ has been shown to be associated with different degrees of inflammation and potential insulin resistance. In humans, non-alcoholic fatty liver disease (NAFLD) has been described as the hepatic manifestation of MetS. In an analogous manner, epidemiological evidence strongly suggested a “guilty” association between MetS and chronic kidney disease (CKD). Some biomarkers of hepatic (such as C-reactive protein, TNF-alpha or other cytokines) and renal diseases (such as uric acid) associated with MetS might be particularly useful to better manage and prevent the atherothrombotic risk.

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