Circulating renin–angiotensin–aldosterone system markers in cats with non-hypertensive chronic kidney disease or systemic arterial hypertension

Figures

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  Figure 1. Flow diagram illustrating the progress of cats through the present study, which evaluates the circulating renin–angiotensin–aldosterone system in cats with NHT-CKD in International Renal Interest Society stages 2 or higher, cats with SAH (all of which had CKD), and healthy controls. Abbreviations: NHT-CKD = non-hypertensive chronic kidney disease; SAH, systemic arterial hypertension.

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  Figure 2. Serum equilibrium concentrations of angiotensin peptides and aldosterone in cats with non-hypertensive-CKD (International Renal Interest Society stages 2 or higher), cats with systemic arterial hypertension naïve to antihypertensive therapy (all of which had CKD), and healthy controls that were age- and sex-matched to those in the non-hypertensive-CKD group. The size of each sphere is proportional to median concentrations of each analyte, with median concentrations (pmol/L) shown next to the spheres. Abbreviations: ACE, angiotensin-converting enzyme; ACE2, angiotensin-converting enzyme 2; Aldo, aldosterone; Ang, angiotensin; AP, aminopeptidase; AT1R, angiotensin type-1 receptor; CKD, chronic kidney disease; DAP, aspartyl aminopeptidase; NEP, neutral endopeptidase (neprilysin).

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  Figure 3. Dot plots of circulating renin-angiotensin-aldosterone system markers in cats with NHT-CKD of International Renal Interest Society stages 2 or higher (open squares; n = 17), cats with SAH naïve to antihypertensive therapy (open triangles; n = 6, all of which had CKD), and healthy controls that were age- and sex-matched to those in the NHT-CKD group (n = 17; open circles). Horizontal bars depict the median value for each group. Statistical comparisons between groups were conducted using linear mixed-effect models to account for paired matching between NHT-CKD and healthy control cats. No adjustment for the feeding of a therapeutic renal diet or age was included in this analysis. Significant P-values are noted above relevant brackets. Abbreviations: AA2, angiotensin-to-angiotensin II ratio, a surrogate measure of adrenal responsiveness to angiotensin II; ACE-S, surrogate measure of angiotensin-converting enzyme (ACE) activity; ACE2-S, surrogate measure of ACE2 activity; Ang, angiotensin; ns, not statistically significant; NHT-CKD, non-hypertensive chronic kidney disease; PRA-S, surrogate measure of plasma renin activity; SAH, systemic arterial hypertension.

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  Figure 4. Dot plots for systolic blood pressure (SBP), serum creatinine concentration, and urinary protein-to-creatinine ratio in systemically hypertensive cats (n = 6, all of which had CKD) before (open triangles) and 2-4 weeks after the start of treatment with amlodipine besylate (0.625 mg PO q24h; solid triangles). Data points from cats with hypertensive ocular damage are denoted in red. Lines connect data from the same cat.

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  Figure 5. Serum equilibrium concentrations of angiotensin peptides and aldosterone of cats with systemic arterial hypertension before (baseline) and 2-4 weeks after the start of treatment with amlodipine besylate (0.625 mg PO q24h). See Figure 2 legend for details and abbreviations.

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  Figure 6. Dot plots for serum equilibrium concentrations of circulating renin–angiotensin–aldosterone system markers in cats with systemic arterial hypertension (all of which had CKD) before (open triangles) and 2-4 weeks after the start of treatment with amlodipine besylate (0.625 mg PO q24h; solid triangles). Statistical comparisons between time points were conducted with the Wilcoxon signed-rank test. Significant P-values are noted above relevant brackets. Lines connect data from the same cat. See Figure 3 legend for abbreviations.