Background: The renin-angiotensin-aldosterone system (RAAS) plays a key role in chronic kidney disease (CKD) in multiple species; however, little is known about this system in cats with CKD.
Objectives: To describe the classic and alternative circulating RAAS pathway components in cats with CKD, and to evaluate their correlation with CKD progression and amlodipine administration. Animals: 15 cats with surgically induced CKD and 15 healthy cats with comparable age and sex ratios.
Methods: Observational case-control study. Serum equilibrium concentrations of angiotensin I, II, III, IV, 1-5, and 1-7, and aldosterone were evaluated using liquid chromatography-mass spectrometry twice (6 months apart) for CKD cats and once for healthy cats. Data were analyzed using linear mixed models or Mann-Whitney U test, when appropriate. CKD progression was defined as >25% increase in serum concentrations of creatinine, symmetric dimethylarginine, or both within a 10-month follow-up period.
Results: Relative to healthy cats, CKD cats had significantly higher serum aldosterone concentrations (median, 205.3 vs. 399.1 pmol/L; p-value <0.01). No differences in angiotensin peptide concentrations were found. Among CKD cats, amlodipine-treated cats had higher concentrations of all angiotensins and aldosterone. In CKD cats with follow-up data available, those who experienced progression (n=3) had lower baseline aldosterone concentrations compared to those who did not (n=9) (median 162.2 vs. 430.4 pmol/L; p-value=0.021). Conclusions and clinical importance: Amlodipine administration was associated with activation of the circulating classic and alternative RAAS pathways. Further study is warranted to clarify the correlation between circulating aldosterone and CKD progression in cats.
