The Role of Renin-Angiotensin-Aldosterone System (RAAS) in the Development of Systemic Hypertension in Cats Treated for Hyperthyroidism.
R.E. Jepson; J. Elliott; H.M. Syme.
Proceeding of the 23rd Annual Forum of the American College of Veterinary Internal Medicine, 2005

A proportion of hyperthyroid cats that have normal blood pressure at diagnosis become hypertensive following treatment. The aim of this study was to evaluate the role of RAAS in the pathogenesis of systemic hypertension following treatment for hyperthyroidism by measurement of plasma renin activity (PRA) and aldosterone (ALDO) concentration.

Cats were selected retrospectively for inclusion in the study if they were diagnosed as hyperthyroid (T4 >55nmol/L) and developed systemic hypertension within six months of documented stable euthyroidism (HT group, n=11). A control group of cats that remained normotensive during treatment for hyperthyroidism were selected at random (NT group, n=10). All cats were normotensive and non-azotemic (plasma creatinine <1.9mg/dl) prior to treatment. Systolic blood pressure (SBP) was measured using the Doppler technique and hypertension was defined as SBP>175mmHg on multiple occasions or in association with clinical manifestations of hypertension. Treatment was with carbimazole therapy alone or in combination with surgical thyroidectomy. PRA and ALDO concentrations were measured using commercially available radioimmunoassays (Diasorin GammaCoat, DPC Coat-A-Count Aldosterone) before treatment and after euthyroidism was established in both NT and HT cats. Wilcoxon signed rank tests were used to compare data before and after treatment. Mann-Whitney U tests were used to make comparisons between NT and HT groups. Data are reported as the median [25th, 75th percentiles].

PRA did not decrease significantly with treatment of hyperthyroidism in either group (pre 1.52 [1.09, 2.14], post 0.65 [0.19, 1.97] ng/ml/hr, P=0.18; NT and HT combined). ALDO declined significantly in both groups (pre 202 [125, 268], post 159 [92, 206] pg/ml, P=0.012; NT and HT combined), and plasma creatinine increased significantly (pre 1.3 [0.9, 1.5], post 1.9 [1.6, 2.9] mg/dl, P<0.001) with treatment. There was no difference in PRA, ALDO or creatinine concentrations between NT and HT groups either before or after treatment.

The cause for the development of hypertension in cats that are being treated for hyperthyroidism remains enigmatic. Activation of the RAAS tends to decrease with treatment both in cats that remain normotensive and those that develop hypertension. Although renal function declined significantly with treatment, cats in both NT (3/10) and HT (6/11) groups developed azotemia, and creatinine concentrations were not significantly different between the groups. The role of declining renal function in development of hypertension is worthy of further study.