Browsing by Subject "Renal disease"

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    Epicardial Adipose Tissue and Renal Disease
    (MDPI, 2019-03-02) Aeddula, Narothama Reddy; Cheungpasitporn, Wisit; Thongprayoon, Charat; Pathireddy, Samata; Medicine, School of Medicine
    Epicardial adipose tissue (EAT) is derived from splanchnic mesoderm, localized anatomically between the myocardium and pericardial visceral layer, and surrounds the coronary arteries. Being a metabolically active organ, EAT secretes numerous cytokines, which moderate cardiovascular morphology and function. Through its paracrine and vasocrine secretions, EAT may play a prominent role in modulating cardiac function. EAT protects the heart in normal physiological conditions by secreting a variety of adipokines with anti-atherosclerotic properties, and in contrast, secretes inflammatory molecules in pathologic conditions that may play a dynamic role in the pathogenesis of cardiovascular diseases by promoting atherosclerosis. Considerable research has been focused on comparing the anatomical and biochemical features of EAT in healthy people, and a variety of disease conditions such as cardiovascular diseases and renal diseases. The global cardiovascular morbidity and mortality in renal disease are high, and there is a paucity of concrete evidence and societal guidelines to detect early cardiovascular disease (CVD) in this group of patients. Here we performed a clinical review on the existing evidence and knowledge on EAT in patients with renal disease, to evaluate its application as a reliable, early, noninvasive biomarker and indicator for CVD, and to assess its significance in cardiovascular risk stratification.
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    Vascular complications of sickle cell disease
    (IOS Press, 2020-05-01) Usmani, Ashar; Machado, Roberto F.; Medicine, School of Medicine
    Sickle cell disease (SCD) is a monogenetic disorder caused by a mutation in the [H9252]-globin gene HBB leading to polymerization of red blood cells causing damage to cell membranes, increasing its rigidity and intravascular hemolysis. Multiple lines of evidence suggest that SCD can be viewed as pan-vasculopathy associated with multiple mechanisms but driven by hemoglobin S polymerization. Here we review the pathophysiology, clinical manifestations and management strategies for cerebrovascular disease, pulmonary hypertension and renal disease associated with SCD. These “vascular phenotypes” reflect the systemic nature of the complications of SCD and are a major threat to the well-being of patients with the disorder.