Retrospective evaluation of risk factors for development of kidney injury after parenteral furosemide treatment of left-sided congestive heart failure in dogs

Background Kidney injury (KI) has been documented in dogs treated with furosemide for left-sided congestive heart failure (CHF). Hypothesis/Objectives Determine risk factors for development of KI in furosemide-treated dogs and determine the effect of KI on survival. Animals Seventy-nine client-owned dogs receiving parenteral furosemide for CHF. Methods Serum creatinine (sCr) and electrolyte concentrations were determined during hospitalization and at first outpatient reevaluation to detect and stage KI (increase in sCr ≥0.3 mg/dL). Furosemide dosage administered between timepoints was calculated. Multivariable modeling was performed to identify predictors of KI and percent change in serum biochemistry results over time. Results Kidney injury was identified in 38/79 (48%) dogs and mostly occurred during hospitalization. Kidney injury was Grade I in 25 dogs, Grade II in 9 dogs, and Grade III in 4 dogs. Higher blood pressure was associated with acute KI during hospitalization (odds ratio, 1.03; 95% confidence interval [95% CI] 1.01-1.07; P = .03) whereas PO furosemide dosage was associated with KI after hospital discharge (odds ratio, 7.77; 95% CI, 2.05-68.6; P = .02). Baseline sCr and use of a furosemide continuous rate infusion were not associated with increased risk of KI. Kidney injury was not associated with long-term outcome. Of 13 dogs with Grade II-III KI, azotemia was reversible in 9 dogs, and 6 dogs survived >1 year after KI. Conclusions and Clinical Importance In this cohort of dogs receiving parenteral furosemide for CHF, KI was common, mostly nonazotemic (Grade I), and did not impact survival.This is the published version of the following article: Giorgi, Maria E., Jonathan P. Mochel, Lingnan Yuan, Darcy B. Adin, and Jessica L. Ward. "Retrospective evaluation of risk factors for development of kidney injury after parenteral furosemide treatment of left‐sided congestive heart failure in dogs." Journal of Veterinary Internal Medicine 36, no. 6 (2022). DOI: 10.1111/jvim.16571. Copyright 2022 The Authors. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. Posted with permission

Metabolomic profiling in dogs with dilated cardiomyopathy eating non-traditional or traditional diets and in healthy controls

Abstract Dilated cardiomyopathy (DCM), caused by genetic and environmental factors, usually progresses to heart failure, a major cause of death in elderly people. A diet-associated form of DCM was recently identified in pet dogs eating non-traditional (NT) diets. To identify potential dietary causes, we analyzed metabolomic signatures and gene set/pathway enrichment in (1) all dogs based on disease, diet, and their interactions and (2) dogs with DCM based on diet. Metabolomic analysis was performed in 38 dogs with DCM eating NT diets (DCM-NT), 8 dogs with DCM eating traditional diets, 12 healthy controls eating NT diets, and 17 healthy controls eating traditional diets. Overall, 153 and 63 metabolites differed significantly between dogs with DCM versus healthy controls and dogs eating NT versus traditional diets, respectively, with 12 metabolites overlapping both analyses. Protein–protein interaction networks and gene set enrichment analysis identified 105 significant pathways and gene sets including aging-related pathways (e.g., nuclear factor-kappa B, oxidative damage, inflammation). Seventeen metabolites differed significantly in dogs with DCM eating NT versus traditional diets (e.g., fatty acids, amino acids, legume biomarkers), suggesting different mechanisms for primary versus diet-associated DCM. Our multifaceted metabolomic assessment of DCM in dogs highlighted diet’s role in some forms of DCM