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. 2023 Jul-Aug;37(4):1348-1357.
doi: 10.1111/jvim.16741. Epub 2023 May 29.

Prospective evaluation of a telmisartan suppression test as a diagnostic tool for primary hyperaldosteronism in cats

Affiliations

Prospective evaluation of a telmisartan suppression test as a diagnostic tool for primary hyperaldosteronism in cats

Maxime Kurtz et al. J Vet Intern Med. 2023 Jul-Aug.

Abstract

Background: In a previous study, telmisartan suppressed aldosterone secretion in healthy cats but not in cats with primary hyperaldosteronism (PHA).

Hypotheses: Telmisartan suppresses aldosterone secretion in middle-aged healthy cat and cats with diseases that may result in secondary hyperaldosteronism, but not in those with PHA.

Animals: Thirty-eight cats: 5 with PHA; 16 with chronic kidney disease (CKD), subclassified as hypertensive (CKD-H) or non-hypertensive (CKD-NH); 9 with hyperthyroidism (HTH); 2 with idiopathic systemic arterial hypertension (ISH); and 6 healthy middle-aged cats.

Methods: Prospective, cross-sectional study. Serum aldosterone concentration, potassium concentration, and systolic blood pressure were measured before and 1 and 1.5 hours after PO administration of 2 mg/kg of telmisartan. The aldosterone variation rate (AVR) was calculated for each cat.

Results: No significant difference in the minimum AVR was observed among groups (median [quartile 1 (Q1); quartile 3 (Q3)]: 25 [0; 30]; 5 [-27; -75]; 10 [-6; -95]; 53 [19; 86]; 29 [5; 78]) for PHA, CKD, HTH, ISH, and healthy cats, respectively (P = .05). Basal serum aldosterone concentration (pmol/L) was significantly higher in PHA cats (median [Q1; Q3]: 2914 [2789; 4600]) than in CKD-H cats (median [Q1; Q3]: 239 [189; 577], corrected P value = .003) and CKD-NH cats (median [Q1; Q3]: 353 [136; 1371], corrected P value = .004).

Conclusions and clinical importance: The oral telmisartan suppression test using a single dose of 2 mg/kg telmisartan did not discriminate cats with PHA from healthy middle-aged cats or cats with diseases that may result in secondary hyperaldosteronism.

Keywords: adrenal; adrenal gland; aldosterone; cardiology; cardiovascular; endocrinology; hemodynamics; hypertension; hypertrophic cardiomyopathy; hypokalemia; retinopathy.

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Conflict of interest statement

Residency program of Maxime Kurtz has received financial support by Royal Canin. No other authors have a conflict of interest.

Figures

FIGURE 1
FIGURE 1
Baseline serum aldosterone concentration in each group. Asterisks (*, **) indicate significantly different values. Horizontal lines indicate the median values, and boxes delineate the 25th and 75th percentiles. Dots represent individual observations. CKD‐H and CKD‐NH, hypertensive and non‐hypertensive chronic kidney disease; HTH, hyperthyroidism; ISH, idiopathic systemic arterial hypertension; PHA, primary hyperaldosteronism.
FIGURE 2
FIGURE 2
Serum aldosterone concentration at T1.5 in each group. See Figure 1 for legends.
FIGURE 3
FIGURE 3
Aldosterone variation rate at T1.5 and minimal aldosterone variation rate between T1 and T1.5 in each group. See Figure 1 for legends.
FIGURE 4
FIGURE 4
Absolute variation in aldosterone concentration between T0 and T1.5, and minimal absolute variation in aldosterone concentration between T1 and T1.5 in each group. See Figure 1 for legends.
FIGURE 5
FIGURE 5
Aldosterone variation rate at T1.5 plotted against baseline plasma renin activity for the whole studied population.

References

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Supplementary concepts