Update (June 13, 2026): No Circulating RAAS Activation Found in Cats with Non-Hypertensive CKD or Untreated Hypertension — Angiotensin Peptide Data

TL;DR

Lourenco 2026 (prospective observational study, cats with non-hypertensive CKD and untreated systemic hypertension) found mean serum angiotensin I, II, and III were lower in hypertensive cats versus healthy controls, and serum aldosterone did not differ between groups — providing no evidence of circulating RAAS activation in these populations. Amlodipine treatment significantly increased all angiotensin peptides (except angiotensin IV).

What just dropped

• Lourenco and colleagues (2026) conducted a prospective single-centre observational study comparing serum angiotensin peptides and aldosterone in cats with CKD without systemic arterial hypertension (SAH), cats with untreated SAH (with or without CKD), and healthy controls. Mean serum angiotensin I, II, and III were lower in untreated SAH cats versus healthy controls. Serum aldosterone did not differ between groups. (https://pubmed.ncbi.nlm.nih.gov/42117720/)
• A companion review by Coleman and Lourenco (2026) contextualises these findings within the broader cardiorenal-metabolic comorbidity landscape in cats, noting the complexity of RAAS assessment in feline hypertension and CKD. (https://pubmed.ncbi.nlm.nih.gov/41863293/)
• Amlodipine treatment was associated with significant increases in all angiotensin peptides except angiotensin IV in the study population. (https://pubmed.ncbi.nlm.nih.gov/42117720/)

Context

Telmisartan (Semintra) is an angiotensin receptor blocker approved for reducing proteinuria in cats with CKD. Its clinical rationale rests on RAAS blockade — specifically AT1 receptor antagonism to reduce the downstream effects of angiotensin II on glomerular filtration and renal perfusion pressure. The assumption underlying this indication is that the RAAS contributes to the pathophysiology of feline CKD-related hypertension and proteinuria.

The Lourenco 2026 findings challenge part of this assumption: circulating angiotensin peptides and aldosterone were not elevated in cats with CKD without hypertension or in cats with untreated hypertension relative to controls. This does not necessarily invalidate telmisartan's antiproteinuric efficacy — the drug's benefits may operate through intrarenal RAAS rather than circulating peptide levels, or through direct anti-fibrotic effects — but it adds nuance to the physiological model.

The amlodipine finding (increased angiotensin peptides with treatment) is consistent with compensatory RAAS activation during blood pressure lowering — a known pharmacodynamic phenomenon in other species that may have implications for monitoring in cats on long-term antihypertensive therapy.

What this changes in Telmisartan (Semintra) for Proteinuria and Hypertension in Cats with CKD (https://www.thevoyage.ai/forvets/knowledge/telmisartan-feline-ckd-proteinuria)

The Lourenco 2026 circulating RAAS data add a mechanistic-context dimension to this page. The existing evergreen documents telmisartan's efficacy against placebo; this update adds the physiological nuance that circulating RAAS activation may not be the dominant driver of feline CKD-associated hypertension, which informs how clinicians explain the drug's mechanism and expected benefit to colleagues and owners.

References

1. Lourenco BN et al. 2026. Serum angiotensin peptides and aldosterone in cats with CKD and untreated hypertension: prospective observational study. PMID 42117720. https://pubmed.ncbi.nlm.nih.gov/42117720/
2. Coleman AE, Lourenco BN. 2026. Cardiorenal-metabolic comorbidities in cats: review. PMID 41863293. https://pubmed.ncbi.nlm.nih.gov/41863293/

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• Telmisartan (Semintra) for Proteinuria and Hypertension in Cats with CKD
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