Plasma renin activity and aldosterone concentration in dogs with acquired portosystemic collaterals

Abstract

BackgroundThe renin‐angiotensin‐aldosterone system (RAAS) is activated in humans with portal hypertension (PH) associated with liver disease. However, involvement of RAAS in dogs with intrahepatic PH is not clear.ObjectiveTo measure plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in dogs with PH (chronic hepatitis [CH] and primary hypoplasia of the portal vein [PHPV]), dogs with extrahepatic congenital portosystemic shunt (EH‐CPSS), and healthy dogs and to determine whether the RAAS is activated in dogs with PH.AnimalsTwenty‐seven dogs with acquired portosystemic collaterals (APSCs; 15 dogs with CH, 12 dogs with PHPV), 9 dogs with EH‐CPSS, and 10 healthy dogs.MethodsRetrospective study. Plasma renin activity and PAC were measured by radioimmunoassay.ResultsPlasma renin activity was significantly higher in the CH group (median, 4.4 ng/mL/h) than in the EH‐CPSS (median, 1.0 ng/mL/h; P < .01) and the healthy (median, 1.1 ng/mL/h; P < .01) groups. No significant differences were found between the PHPV group (median, 2.2 ng/mL/h) and other groups. Plasma aldosterone concentration was significantly higher in the CH (median, 111.0 pg/mL) and PHPV (median, 89.5 pg/mL) groups than in the EH‐CPSS (median, 1.0 pg/mL; P < .001, P < .01, respectively) and healthy (median, 14.5 pg/mL; P < .001, P < .05, respectively) groups.Conclusions and Clinical ImportanceActivation of the RAAS contributes to the pathophysiology of intrahepatic PH in dogs, suggesting that spironolactone may not only be effective for the treatment of ascites but also for the suppression of intrahepatic PH.