Autumn Harris' collaborative team of basic and clinical scientists from the College of Medicine and Veterinary Medicine applies interrelated translational science to develop a wide variety of approaches, including animal models directed at understanding the mechanisms through which the kidneys maintain the correct acid-base balance in the body. The team currently has an NIH K08 career development grant from the NIDDK to explore sex differences in renal ammonia metabolism and determine the underlying mechanisms. The team is also particularly interested in acid-base balance during chronic kidney disease (CKD), in which abnormalities in acid-balance result in increased progression and mortality of chronic kidney disease.
Areas of Expertise (9)
Chronic Kidney Disease
Sex Steroid Hormone Receptors
Small Animal Internal Medicine
Media Appearances (1)
Hope for better management of chronic kidney disease in dogs
UF Vet Med Voice online
Researchers at UF are investigating the potential of a novel biomarker as a tool for identifying animals at high risk of developing end-stage renal failure and hope their findings will lead to improved therapies for chronic kidney disease. Autumn Harris DVM discusses hope for better management of chronic kidney disease in dogs.
Case report: septic pericarditis with achromobacter xyloxidans in an immunosuppressed dog.Frontiers in veterinary science
Kristina M. Pascutti, et. al
A 5-year-old female spayed French Bulldog presented for anorexia and increased respiratory rate. On presentation, she was dyspneic with stridor and increased bronchovesicular sounds. Point-of-care ultrasound identified pericardial effusion. Thoracic radiographs identified pleural effusion, a wide cranial mediastinum and multifocal unstructured interstitial pulmonary opacities.
Acid-base effects of combined renal deletion of NBCe1-A and NBCe1-BAmerican Journal of Physiology-Renal Physiology
Hyun-Wook Lee, et. al
The molecular mechanisms regulating ammonia metabolism are fundamental to acid-base homeostasis. Deletion of the A splice variant of Na+-bicarbonate cotransporter, electrogenic, isoform 1 (NBCe1-A) partially blocks the effect of acidosis to increase urinary ammonia excretion, and this appears to involve the dysregulated expression of ammoniagenic enzymes in the proximal tubule (PT) in the cortex but not in the outer medulla (OM).
The proximal tubule through an NBCe1-dependent mechanism regulates collecting duct phenotypic and remodeling responses to acidosisAmerican Journal of Physiology-Renal Physiology
Jill W. Verlander, et. al
The renal response to acid-base disturbances involves phenotypic and remodeling changes in the collecting duct. This study examines whether the proximal tubule controls these responses. We examined mice with genetic deletion of proteins present only in the proximal tubule, either the A variant or both A and B variants of isoform 1 of the electrogenic Na+-bicarbonate cotransporter (NBCe1). Both knockout (KO) mice have spontaneous metabolic acidosis.