Key result
Elevated ACE and RAS activation in hemodialysis link to progressive cardiovascular and renal disease.
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Understanding the balance between the classical renin-angiotensin system and the counter-regulatory ACE2 pathway could guide the development of targeted therapies for hemodialysis patients.
Understanding of the renin-angiotensin system (RAS) has changed remarkably over the past decade. Renin, angiotensin converting enzyme (ACE), angiotensin II (Ang II), and Ang II receptors are the main components of the RAS. Recent studies identified the ACE2/Ang 1-7/Mas receptor axis, which counter-regulates the classical RAS. Many studies have examined the effects of the RAS on the progression of cardiovascular disease and chronic kidney disease (CKD). In addition, many studies have documented increased levels of ACE in hemodialysis (HD) patients, raising concerns about the negative effects of RAS activation on the progression of renal disease. Elevated ACE increases the level of Ang II, leading to vasoconstriction and cell proliferation. Ang II stimulation of the sympathetic system leads to renal and cardiovascular complications that are secondary to uncontrolled hypertension. This review provides an overview of the RAS, evaluates new research on the role of ACE2 in dialysis, and reviews the evidence for potentially better treatments for patients undergoing HD. Further understanding of the role of ACE and ACE2 in HD patients may aid the development of targeted therapies that slow the progression of CKD and cardiovascular disease.
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Malik et al. (2015) conducted a review in Hemodialysis and chronic kidney disease. Renin-angiotensin system pathways and modulators was evaluated. Elevated ACE levels and renin-angiotensin system activation in hemodialysis patients may contribute to the progression of cardiovascular and renal diseases.
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