SAA as a Feline Respiratory Diagnostic Split: Two 2026 Studies Disagree

A cutoff of 8.6 μg/mL for serum amyloid A separated inflammatory from cardiac or neoplastic respiratory disease in a 22-cat French study — while a 122-cat German study concluded the same marker cannot clearly distinguish feline respiratory conditions at all.

Both studies were published in 2026 and both asked the same question: can SAA, the major acute-phase protein in cats, help clinicians sort out what lies behind respiratory signs? The two teams reached opposite answers, and the gap between them maps onto real decisions at the exam table.

What did the French study find?

Eva Berro, DVM, an internal medicine resident at Centre Hospitalier Vétérinaire AniCura Nordvet in La Madeleine, worked with specialists Aline Fastrès, DVM, PhD, DipECVIM-CA, and Anaïs Lamoureux, DVM, DipECVIM-CA. They retrospectively reviewed cats presented to the emergency unit for respiratory distress between October 2021 and December 2024. The final sample was 22 cats with SAA measured within 48 hours of admission, reported in the Journal of Small Animal Practice on October 12, 2026.

Two board-certified internists classified the cats blind to SAA results. The inflammatory group held 15 cats: 7 with aspiration pneumonia, 7 with feline lower airway disease and 1 with pulmonary toxoplasmosis. The cardiac/neoplastic group held 7: 3 with left-sided congestive heart failure and 4 with neoplastic disease.

Median SAA was 57.5 μg/mL in the inflammatory group versus 5 μg/mL in the cardiac/neoplastic group — a more than elevenfold difference. The assay could not read below 5 μg/mL, so lower results were recorded at that floor. A cutoff of 8.6 μg/mL delivered 80% sensitivity and 100% specificity.

Berro and colleagues called SAA a potential supportive tool for rapid triage, but urged restraint: the results "should be interpreted with caution given the small sample size," and the proposed cutoff cannot yet serve as a definitive rule-out threshold.

What did the German study find?

In Frontiers in Veterinary Science, Hannah Gareis, DVM, Dr med vet, and Bianka Schulz, Dr med vet, DipECVIM-CA, of Ludwig-Maximilians-University of Munich tested serum from 102 cats with respiratory signs and 20 healthy controls. The diseased cats split into five groups:

• Feline lower airway disease (n = 26)
• Infectious lower airway or pleural space disease (n = 12)
• Neoplastic lower airway or pleural space disease (n = 17)
• Congestive heart failure (n = 29)
• Upper airway disease (n = 18)

Only one comparison reached significance: median SAA of 2.61 μg/mL in the infectious group versus 0.14 μg/mL in cats with feline lower airway disease. Every group median sat within the laboratory reference range of less than 6.7 μg/mL, and SAA did not differ between diseased and healthy cats.

The infectious signal was also narrow. Elevated values came mainly from cats with pyothorax; most other infections stayed within reference range. The 3 neoplastic-group cats above 15 μg/mL all had pleural effusion secondary to intrathoracic neoplasia. Gareis and Schulz wrote that a normal SAA does not rule out infection and that SAA "should be used as supporting diagnostic information only."

Why do the results diverge?

Methodological differences explain much of the split:

• The assay. The French team ran an in-house feline-specific immunofluorescence assay on fresh serum — an assay the authors note lacks peer-reviewed validation data. The German team used an external immunoturbidimetric laboratory assay.
• Grouping. The French inflammatory group mixed infectious and noninfectious disease, which the retrospective design could not separate. The German study separated them — and that separation produced its only significant finding.
• Patients. All 22 French cats were in respiratory distress. In Germany, 71 of 102 were, and distressed cats had significantly higher SAA than non-distressed cats, though both medians stayed within reference range.
• Timing. Germany sampled all cats before treatment; the French team tested 17 of 22 at admission and 5 within 48 hours after drug administration. The German authors noted many cats were likely sampled before peak acute-phase response.
• Survival. France found no SAA difference between survivors and non-survivors. Germany found cats that died or were euthanized had significantly higher admission SAA — yet cautioned against using acute-phase proteins for prognosis.

The studies also brush against cardiology. The French authors attributed normal SAA in cardiac cats to SAA marking acute rather than chronic inflammation, plus low cardiac case numbers. German CHF cats had a median of 0.70 μg/mL, within range. A 2020 Journal of Veterinary Internal Medicine study complicates the picture further, reporting significantly higher SAA in cats with CHF from primary cardiomyopathy than in preclinical or healthy cats.

On one point both teams converge: larger prospective studies are needed before SAA earns a fixed place in the feline respiratory workup.