Ventilatory compensation for metabolic acidosis is independent of hypertension in dogs with chronic kidney disease

Abstract 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 (PCO 2 ) 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 PCO 2 . Results Metabolic acidosis severity (BE) was associated with ventilatory response (PCO 2 ) ( p < 0.001), whereas SBP showed no association. Mean PCO 2 did not differ between normotensive and hypertensive dogs ( p = 0.373). Serum creatinine independently predicted PCO 2 ( p < 0.001), with higher concentrations associated with higher PCO 2 . 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 PCO 2 , 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.