NU11 - Circulating Renin-angiotensin-aldosterone System Markers in Cats with Non-hypertensive Chronic Kidney Disease or Systemic Arterial Hypertension

Abstract: Background – Information on the classical and alternative pathways of the circulating renin-angiotensin-aldosterone system (cRAAS) in cats is limited. Objectives – To describe and compare serum equilibrium concentrations of angiotensin peptides and aldosterone in apparently healthy cats and cats with azotemic, non-hypertensive CKD (Azo-NHT-CKD) or untreated systemic arterial hypertension (SAH); and to characterize changes in these concentrations in hypertensive cats treated with amlodipine. Animals – Client-owned cats with Azo-NHT-CKD (serum creatinine≥1.6mg/dL, systemic arterial blood pressure [SBP]< 160mmHg; n=17), SAH (SBP≥160mmHg or ≥150mmHg with hypertensive ocular lesions; n=6), or normal SBP (< 140mmHg) and kidney function (n=17). Methods – Prospective, single-center, observational study. Cats underwent indirect SBP measurement and hematologic, serum, and urinary analyses to determine group assignment. Serum was obtained contemporaneously in all cats, and after 2-4 weeks of amlodipine therapy in cats with SAH, for evaluation of equilibrium concentrations of angiotensin I, II, III, IV, 1-5, and 1-7, and aldosterone using liquid chromatography-tandem mass spectrometry. Results – No differences in mean serum equilibrium concentration were detected between the Azo-NHT-CKD and control groups for any angiotensin peptide. Cats with untreated SAH had significantly lower mean concentrations of angiotensin I, II, III, IV, and 1-5 versus controls, and of angiotensin I and III versus the Azo-NHT-CKD group. Hypertensive cats treated with amlodipine experienced a significant increase in all angiotensin peptides. Serum aldosterone did not differ between groups, or before and after amlodipine in hypertensives. Conclusions and clinical importance – Evidence of cRAAS activation in cats with Azo-NHT-CKD or untreated SAH was not found.