Key result
Oral telmisartan fails to reliably distinguish primary hyperaldosteronism from secondary causes in cats.
Why the study?
Previous findings showed telmisartan suppressed aldosterone in healthy cats but not in cats with primary hyperaldosteronism, prompting evaluation of its ability to distinguish primary hyperaldosteronism from secondary hyperaldosteronism or health.
Does an oral telmisartan suppression test accurately discriminate primary hyperaldosteronism from secondary hyperaldosteronism and healthy states in cats?
Cross-Sectional (n=38)
No
Does an oral telmisartan suppression test accurately discriminate primary hyperaldosteronism from secondary hyperaldosteronism and healthy states in cats?
A single-dose oral telmisartan suppression test does not appear to be a reliable diagnostic tool for identifying primary hyperaldosteronism in older cats with complex comorbidities.
Does not support telmisartan suppression testing for feline primary hyperaldosteronism; leaves open need for validated diagnostics in cats with comorbidities.
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.
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Kurtz et al. (2023) conducted a cross-sectional in Primary hyperaldosteronism (feline) (n=38). Telmisartan vs. Other diagnostic groups (CKD, HTH, ISH) and healthy controls was evaluated on Minimum aldosterone variation rate (AVR) at 1 and 1.5 hours after telmisartan administration (p=.05). A single 2 mg/kg oral dose of telmisartan did not significantly discriminate cats with primary hyperaldosteronism from healthy middle-aged cats or those with diseases causing secondary hyperaldosteronism (P=.05 for AVR).
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