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Serum amyloid A in cats with renal azotemia

BACKGROUND AND AIM: The concentration of the feline acute-phase protein serum amyloid A (SAA) increases in cats with acute inflammatory diseases. However, it is unclear whether SAA concentration increases in cats with azotemic kidney disease or whether it can aid in differentiating acute kidney inju...

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Detalles Bibliográficos
Autores principales: Degenhardt, Laura, Dorsch, Roswitha, Hartmann, Katrin, Dörfelt, René
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Veterinary World 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10521177/
https://www.ncbi.nlm.nih.gov/pubmed/37766698
http://dx.doi.org/10.14202/vetworld.2023.1673-1681
Descripción
Sumario:BACKGROUND AND AIM: The concentration of the feline acute-phase protein serum amyloid A (SAA) increases in cats with acute inflammatory diseases. However, it is unclear whether SAA concentration increases in cats with azotemic kidney disease or whether it can aid in differentiating acute kidney injury (AKI) from chronic kidney disease (CKD). Similarly, whether SAA concentration can be used as a prognostic marker is also unclear. Therefore, this study aimed to evaluate the SAA concentrations in cats with azotemic kidney disease and determine whether SAA concentrations can be used to differentiate between AKI, CKD, and “acute on CKD” (AoC). In addition, we evaluated whether SAA concentration could serve as a prognostic parameter. Moreover, we determined the correlations between SAA concentration and temperature; creatinine, urea, and albumin concentrations; leukocyte count; and urine protein/creatinine (UP/C). MATERIALS AND METHODS: Forty-eight client-owned azotemic cats (creatinine >250 μmol/L) were included in this prospective study. Cats with pre- and post-renal azotemia were excluded from the study. The causes of azotemia were differentiated into AKI, CKD, and AoC. The SAA concentrations were analyzed through turbidimetric immunoassay at the time of admission. Data were analyzed using the Mann–Whitney U, Kruskal–Wallis, Chi-Square, Fisher’s exact, and Spearman correlation tests. p ≤ 0.05 was considered statistically significant. RESULTS: Serum amyloid A concentration increased in 5/12 cats with AKI, 7/22 cats with CKD, and 9/14 cats with AoC (p = 0.234). The median SAA concentration in cats with AKI, CKD, and AoC whose SAA concentration was ≥5 mg/L was 174 mg/L (10–281 mg/L), 125 mg/L (6–269 mg/L), and 143 mg/L (7–316 mg/L), respectively (p = 0.697), with no significant differences observed between the groups. The median SAA concentration did not differ significantly between survivors (125 mg/L, 10–316 mg/L) and non-survivors (149 mg/L, 6–281 mg/L; p = 0.915) with SAA concentration ≥5 mg/L. CONCLUSION: Serum amyloid A concentration increased in 44% of the cats with azotemia. However, it cannot be used to differentiate AKI from CKD or as a prognostic marker. Serum amyloid A concentration was correlated with neutrophil count, albumin concentration, and UP/C, and the presence of comorbidities may influence SAA concentration.