The Veterinary record · 2026
Ventilatory compensation for metabolic acidosis is independent of hypertension in dogs with chronic kidney disease.
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da Silva Rueda Letícia, Pessina André Leal Raymundo, Senhorello Igor Luiz Salardani, Franco Rodrigo Prevedello, Dos Santos Paulo Sérgio Patto, Dias Maria Vitoria Magalhães, Gomes Lucas Ferreira, Ferreira Wagner Luis
Аннотация
INTRODUCTION: Metabolic acidosis is common in dogs with chronic kidney disease (CKD) and induces ventilatory compensation. Systemic arterial hypertension frequently accompanies CKD, but its influence on the ventilatory response remains unclear.
METHODS: This ambispective observational study included 42 dogs with CKD and metabolic acidosis. Venous partial pressure of carbon dioxide (PCO2) was compared between normotensive (systolic blood pressure [SBP] < 150 mmHg) and hypertensive (SBP ≥ 150 mmHg) dogs. Pearson's correlation and multiple linear regression were used to evaluate base excess (BE), SBP and serum creatinine as predictors of venous PCO2.
RESULTS: Metabolic acidosis severity (BE) was associated with ventilatory response (PCO2) (p < 0.001), whereas SBP showed no association. Mean PCO2 did not differ between normotensive and hypertensive dogs (p = 0.373). Serum creatinine independently predicted PCO2 (p < 0.001), with higher concentrations associated with higher PCO2.
LIMITATIONS: The observational design, limited sample size and incomplete International Renal Interest Society staging may limit the generalisability of the findings.
CONCLUSION: In dogs with CKD and metabolic acidosis, ventilatory compensation, assessed by venous PCO2, was primarily associated with the severity of the metabolic disturbance and showed no significant association with blood pressure status. Compensation may be attenuated as azotaemia worsens.
METHODS: This ambispective observational study included 42 dogs with CKD and metabolic acidosis. Venous partial pressure of carbon dioxide (PCO2) was compared between normotensive (systolic blood pressure [SBP] < 150 mmHg) and hypertensive (SBP ≥ 150 mmHg) dogs. Pearson's correlation and multiple linear regression were used to evaluate base excess (BE), SBP and serum creatinine as predictors of venous PCO2.
RESULTS: Metabolic acidosis severity (BE) was associated with ventilatory response (PCO2) (p < 0.001), whereas SBP showed no association. Mean PCO2 did not differ between normotensive and hypertensive dogs (p = 0.373). Serum creatinine independently predicted PCO2 (p < 0.001), with higher concentrations associated with higher PCO2.
LIMITATIONS: The observational design, limited sample size and incomplete International Renal Interest Society staging may limit the generalisability of the findings.
CONCLUSION: In dogs with CKD and metabolic acidosis, ventilatory compensation, assessed by venous PCO2, was primarily associated with the severity of the metabolic disturbance and showed no significant association with blood pressure status. Compensation may be attenuated as azotaemia worsens.