13 research outputs found
Effects of direct renin inhibition versus angiotensin II receptor blockade on angiotensin profiles in non-diabetic chronic kidney disease
<p><b>Background:</b> Direct renin inhibition (DRI) is clinically inferior to other blockers of the renin–angiotensin system (RAS). Thus far, the underlying molecular causes of this finding remain unknown.</p> <p><b>Methods:</b> Twenty four patients with non-diabetic chronic kidney disease (CKD) stages III–IV and albuminuria were randomized to DRI or angiotensin receptor blocker (ARB). Employing a novel mass-spectrometry method, the concentrations of renin, aldosterone and plasma angiotensin peptides [Ang I, Ang II, Ang-(1-7), Ang-(1-5), Ang-(2-8), Ang-(3-8)] were quantified before and after an 8-week treatment.</p> <p><b>Results:</b> While blood pressure, renal function and albuminuria decreased comparably in both groups, profound RAS component differences were observed: DRI led to a massive renin increase, while suppressing both vasoconstrictive (Ang I and Ang II) and vasodilatory RAS metabolites (Ang-(1-7) and Ang-(1-5)). In contrast, ARB led to a four-fold increase of Ang I and Ang II, while Ang-(1-7) and Ang-(1-5) increased moderately but significantly. With ARB treatment, a decreased aldosterone-to-Ang II ratio suggested efficacy in blocking AT1 receptor.</p> <p><b>Conclusions:</b> DRI therapy abolishes all RAS effector peptides. ARB increases both vasoconstrictive and vasodilative angiotensins, while this is accompanied by efficient blockade of vasoconstrictive effects. These differential molecular regulations should be considered when selecting optimal antihypertensive and disease-modifying therapy in CKD patients.Key messages</p><p>Direct renin inhibition leads to a complete and lasting abolition of both classical and alternative RAS components.</p><p>Angiotensin receptor blockade leads to effective receptor blockade and up-regulation of alternative RAS components.</p><p>Differential molecular regulations of the RAS should be considered when selecting optimal antihypertensive and disease-modifying therapy in CKD patients.</p><p></p> <p>Direct renin inhibition leads to a complete and lasting abolition of both classical and alternative RAS components.</p> <p>Angiotensin receptor blockade leads to effective receptor blockade and up-regulation of alternative RAS components.</p> <p>Differential molecular regulations of the RAS should be considered when selecting optimal antihypertensive and disease-modifying therapy in CKD patients.</p
Factors associated with prevalence of atrial fibrillation Model 1 (N = 626).
<p>Factors associated with prevalence of atrial fibrillation Model 1 (N = 626).</p
Prevalence of atrial fibrillation in patients with increasing age and time on hemodialysis.
<p>Prevalence of atrial fibrillation in patients with increasing age and time on hemodialysis.</p
Practice patterns of antithrombotics in patients on HD.
<p>Practice patterns of antithrombotics in patients on HD.</p
Distribution of patients with AF across CHA2DS2-VASc Scores and frequency of corresponding anticoagulation treatment.
<p>Distribution of patients with AF across CHA2DS2-VASc Scores and frequency of corresponding anticoagulation treatment.</p
Enrollment and randomization of the SAPT-NODAT and ITP-NODAT trial participants at the Medical University of Vienna.
<p>Enrollment and randomization of the SAPT-NODAT and ITP-NODAT trial participants at the Medical University of Vienna.</p
Distribution of patients with AF across HAS-BLED Scores and frequency of corresponding anticoagulation treatment.
<p>Distribution of patients with AF across HAS-BLED Scores and frequency of corresponding anticoagulation treatment.</p
Adverse events, insulin therapy-related only.
<p>Adverse events, insulin therapy-related only.</p