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Circulating renin-angiotensin-aldosterone system markers in cats with non-hypertensive chronic kidney disease or
Bianca N Lourenço1, Jane H C Huang1, Lisa Reno1
1Department of Small Animal Medicine & Surgery, University of Georgia College of Veterinary Medicine, Athens, GA, United States.
Insights
This study found no evidence of renin-angiotensin-aldosterone system (RAAS) activation in cats with non-hypertensive chronic kidney disease (NHT-CKD) or systemic arterial hypertension (SAH). Angiotensin peptides increased in hypertensive cats treated with amlodipine.
Area of Science:
- Veterinary Medicine
- Cardiovascular Physiology
- Nephrology
Background:
- Limited information exists on the renin-angiotensin-aldosterone system (RAAS) in cats with non-hypertensive chronic kidney disease (NHT-CKD) or systemic arterial hypertension (SAH).
- Age and diet are known factors influencing RAAS activity.
Purpose of the Study:
- To compare serum concentrations of angiotensin peptides and aldosterone in healthy cats, cats with NHT-CKD, and cats with untreated SAH.
- To assess changes in these concentrations following amlodipine treatment in hypertensive cats.
Main Methods:
- A prospective, observational study involving client-owned cats with NHT-CKD, SAH, or normal kidney function and blood pressure.
- Serum samples were analyzed for angiotensin I, II, III, IV, 1-5, and 1-7, and aldosterone.
- Hypertensive cats were re-evaluated after 2-4 weeks of amlodipine therapy.
Main Results:
- Serum angiotensin I, II, and III concentrations were lower in cats with untreated SAH compared to healthy controls, even after adjusting for diet and age.
- Angiotensin II and III were also lower in cats with NHT-CKD compared to controls when diet was considered.
- All angiotensin peptides, except angiotensin IV, increased significantly in hypertensive cats during amlodipine treatment. Aldosterone levels did not differ significantly between groups or with treatment.
Conclusions:
- The study did not find evidence of circulating RAAS activation in cats with NHT-CKD or untreated SAH.
- These findings suggest that RAAS may not be a primary driver in these feline conditions.
- Further research is needed to fully elucidate the role of RAAS in feline kidney disease and hypertension.
Background:
Information on the classical and alternative circulating renin-angiotensin-aldosterone systems (RAAS) in cats with non-hypertensive chronic kidney disease (NHT-CKD) or systemic arterial hypertension (SAH) is limited. Age and diet affect the RAAS.
Hypothesis/Objectives:
To compare serum equilibrium concentrations of angiotensin peptides and aldosterone in healthy cats and cats with NHT-CKD or untreated SAH, and to evaluate changes in these concentrations in hypertensive cats administered amlodipine.
Animals:
Client-owned cats with NHT-CKD (serum creatinine ≥ 1.6 mg/dL, systolic blood pressure [SBP] < 160 mmHg; n = 17), SAH (SBP ≥ 160 mmHg or ≥ 150 mmHg with hypertensive ocular lesions; n = 6), or normal SBP (<140 mmHg) and kidney function (n = 17).
Methods:
Prospective, single-center, observational study. Cats underwent indirect SBP measurement and clinicopathologic analyses. Serum was obtained contemporaneously in all cats, and after 2-4 weeks of amlodipine therapy in hypertensive cats, for evaluation of angiotensin I, II, III, IV, 1-5, and 1-7, and aldosterone.
Results:
Adjusting for diet, age, or both modified the conclusions of statistical comparisons for several variables. Mean serum angiotensin I, II, and III concentrations were lower in cats with untreated SAH vs healthy controls across unadjusted and diet-, age-, or both diet- and age-adjusted linear mixed models (geometric mean [95% CI] angiotensin I, 9.02 [3.05-26.62] vs 29.78 [21.15-41.94] pmol/L; angiotensin II, 33.63 [12.25-92.26] vs 124.24 [90.52-170.51] pmol/L; angiotensin III, 1.56 [0.88-2.79] vs 7.96 [5.35-11.86] pmol/L; all P ≤ .038). Controlling for diet but not age, angiotensin II (P = .043) and III (P = .019) were also lower in cats with NHT-CKD vs controls. All angiotensin peptides, except for angiotensin IV, significantly increased in hypertensive cats during amlodipine therapy. Serum aldosterone did not differ between groups, or before and after amlodipine in hypertensive cats.
Conclusions And Clinical Importance:
Evidence of circulating RAAS activation in cats with NHT-CKD or untreated SAH was not found.
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