Background: Hypochloremia is associated with poor outcomes in people with congestive heart failure (CHF) and advanced heart disease in dogs, but etiology is uncertain. Hypothesis/
Objectives: We hypothesized that dogs with serum chloride concentrations ([Cl-])< 100 mEq/L would show greater renin-angiotensin-aldosterone system (RAAS) activation than dogs with [Cl-]≥100 mEq/L. Animals: Eighty-nine dogs with CHF.
Methods: Prospective study. RAAS metabolites and enzymes were quantified by liquid chromatography-mass spectrometry/mass-spectroscopy using previously validated methods and compared between dogs with [Cl-]≥ or <100 mEq/L using Mann-Whitney test. Comparison of the proportion of dogs with active (pulmonary edema or effusions requiring intravenous furosemide) and stable (no edema or effusions and receiving oral furosemide or torsemide) CHF in each group was tested with Fisher’s exact test. Significance was set at P< 0.05.
Results: Sixteen dogs had [Cl-] <100 (all degenerative valve disease) and 73 CHF dogs had [Cl-] ≥100 (55 degenerative valve disease, 15 DCM, 3 congenital). Angiotensin II (P=0.002), angiotensin III (P=0.002), angiotensin 1-5 (P=0.0005), and angiotensin IV (P=0.002) were higher in dogs with [Cl-] <100 compared to dogs with [Cl-] ≥100. No group differences were found for angiotensin I, angiotensin 1-7, aldosterone, angiotensin-converting enzyme (ACE) activity, or ACE2 activity. Approximately half of the dogs with [Cl-] <100 had active CHF (44%) and half had stable CHF (56%), although the proportion of dogs with active CHF was greater in the group with [Cl-] <100 (P=0.01). Conclusions and Clinical Importance: Dogs with moderate to severe hypochloremia have greater RAAS activation compared to dogs with [Cl-] ≥100 mEq/L, which might contribute to poor outcomes.
