Chronic Renin-angiotensin-aldosterone System Research Articles

Evaluation of Renin-Angiotensin-Aldosterone System Components and Enzymes in Systemically Hypertensive Cats Receiving Amlodipine.

Chronic renin-angiotensin-aldosterone system (RAAS) activation is harmful. Amlodipine activates RAAS in humans and dogs, but contradictory data exist for systemically hypertensive (SHT) cats. Cats with SHT and chronic kidney disease treated with amlodipine (SHT/CKD-A) are RAAS activated. Client-owned cats: unmedicated normotensive (NT) cats (n = 9); SHT/CKD-A cats (n = 5) with median systolic blood pressure of 170 mmHg (vs. 195 mmHg, pre-treatment), chronic kidney disease, and receiving no RAAS-suppressive therapy. Serum was frozen (-80 °C) until RAAS analysis via equilibrium analysis. The RAAS variables (reported as median (minimum-maximum)) were compared between groups, using Mann-Whitney U test. Angiotensin 1, angiotensin 1,7, angiotensin III, and angiotensin 1,5, and angiotensin-converting enzyme (ACE)-2 activity were higher in SHT/CKD-A cats compared to NT cats, while ACE activity was lower in SHT/CKD-A cats compared to NT cats (p < 0.05 all). A marker for alternative RAAS influence (ALT-S) was significantly higher (69; 58-73 pmol/pmol) in SHT/CKD-A cats compared to NT cats (35; 14-63 pmol/pmol; p = 0.001). Aldosterone concentrations were significantly higher (393; 137-564 pmol/L) in SHT/CKD-A cats compared to NT cats (129; 28-206 pmol/L; p = 0.007). Circulating RAAS is activated in systemically hypertensive cats receiving amlodipine. Although this study did not parse out the individual contributions of SHT, chronic kidney disease, and amlodipine, the findings suggest that the use of concurrent RAAS-suppressant therapy, specifically aldosterone antagonism, in amlodipine-treated SHT cats with chronic kidney disease might be indicated.

MO421THE EFFECT OF RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM BLOCKADE MEDICATIONS ON CONTRAST-INDUCED NEPHROPATHY IN PATIENTS UNDERGOING CORONARY ANGIOGRAPHY

Abstract Background and Aims Contrast-induced nephropathy (CIN) is the main complication of contrast media administration in patients undergoing coronary angiography (CAG). This complication may be accelerated by concurrent renin-angiotensin-aldosterone system (RAAS) blockers . Current literature is inconclusive. We investigated the impact of RAAS blockade on the occurrence of CIN in patients undergoing CAG. Method We prospectively enrolled 158 patients who underwent CAG with or without percutaneous coronary intervention from December 2017 to February 2018 at a cardiology department . CIN was defined as an increase in serum creatinine level &amp;gt;25% or 0.5 mg/dL after 48 hours postcardiac catheterization. Results Of 158 patients (females=36.1%, mean age 60.0 ± 11 years) who underwent CAG , 15 (9,5%) developed CIN . Eighty one patients (51,2%) were chronic RAAS blockade users. There was no significant difference between the two groups, RAAS blockade 'used' versus 'not-used', in the incidence of postprocedural CIN (7,5% vs 11,5%, p=0,38). However , the pre-contrast use of RASS blockers decrease the risk of CIN in patients with chronic renal failure (12,5% vs 66,6% , p=0,042) . Conclusion RAAS blockade isn’t associated with a significantly higher incidence of CIN, whereas it has the potential to mitigate the incidence of CIN in patients with chronic renal failure. This low cost intervention could be considered when referring a patient for cardiac catheterization.

Underestimated role of MMP2 and 9 in albuminuria developed under chronic renin angiotensin aldosterone system suppression

Underestimated role of MMP2 and 9 in albuminuria developed under chronic renin angiotensin aldosterone system suppression

The evolving landscape of RAAS inhibition: from ACE inhibitors to ARBs, to DRIs and beyond

Chronic renin–angiotensin–aldosterone system (RAAS) activation has far-reaching effects on cardiometabolic risk and is a substantial contributor to cardiovascular (CV) disease and renal dysfunction. The vascular effects of sustained RAAS activation are associated with hemodynamic imbalances, as well as inflammatory stimulation and prothrombotic processes that lead to fibrosis, endothelial dysfunction and cellular remodeling. RAAS inhibition therapies, which include the use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and more recently, direct renin inhibitors, have been used in clinical practice for more than 30 years. Our understanding of how these drugs work, alone and in combination, has contributed to an expanding landscape of treatment options and established RAAS inhibition as essential for reducing the risk of CV and renal disease. This perspective provides a historical overview of how RAAS inhibitors have evolved to their present-day status and will discuss recently discovered functions for components of this complicated and powerful regulatory system.

Direct Renin Inhibition: Promising Treatment in Renoprotection?

Interruption of the Renin-Angiotensin-Aldosterone System (RAAS) with Angiotensin-Converting Enzyme (ACE) inhibitors and Angiotensin-Receptor Blockers (ARBs), alone or in combination, has become a leading therapeutic strategy to slow down the progression of chronic kidney disease. Nevertheless, a considerable proportion of patients progress despite this therapy. New alternative arms are available today to treat hypertension in uncontrolled patients that might have a role in renoprotection. The role of aliskiren, the recently available renin inhibitor may be assumed, based on the pathophysiology of RAAS related renal damage and from data derived on experimental and clinical studies in-patient with type 2 diabetes related nephropathy. The review focuses on the potential consequences of (pro)renin blockade in glomerular hypertension and renal scarring along with some patented treatment methods. The benefit of this additional therapy is still only hypothetical. Ad hoc clinical trials have been conducted to confirm the expected results. Finding that prolonged inhibition of renin vasoconstrictor effect, suppression of plasma renin activity and a more effective RAAS blockade, in patients with chronic RAAS inhibition may help to achieve a sustained reduction of proteinuria, would suggest that renin inhibitors may represent a new weapon to fight progressive nephropathies.