@article{skinner_specht_cicchirillo_fox‐alvarez_harris_2024, title={Association of proteinuria at time of diagnosis with survival times in dogs with lymphoma}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/jvim.17144}, DOI={10.1111/jvim.17144}, abstractNote={Abstract Background Lymphoma has been implicated as a possible cause of proteinuria in dogs. However, information about the potential importance of proteinuria in dogs with lymphoma is limited. Hypothesis To determine if the presence of proteinuria at diagnosis was associated with median survival times in dogs with lymphoma and if lymphoma stage (I‐V) or type (B vs T) were associated with the presence of proteinuria. Animals Eighty‐six client‐owned dogs with a new diagnosis of lymphoma between 2008 and 2020. Methods This was a retrospective cross‐sectional study with dogs divided into proteinuric or nonproteinuric groups based on dipstick urine protein (protein ≥30 mg/dL classified as proteinuric) or a ratio of dipstick protein to urine specific gravity (ratio ≥1.5 classified as proteinuric). Dogs were excluded for: (1) treatment within 2 months with glucocorticoid, anti‐neoplastic, or anti‐proteinuric therapies, (2) diagnosed hypercortisolism or renal lymphoma, (3) active urine sediment, or (4) urine pH >8. Survival analysis utilized a Kaplan‐Meier estimator and log‐rank testing. Results There was a significant difference in median survival between proteinuric and nonproteinuric dogs classified by urine dipstick (245 days [91, 399] vs 335 days [214, 456]; P = .03) or UP : USG (237 days [158, 306] vs 304 days [173, 434]; P = .03). No difference in prevalence of proteinuria was identified between stages (I‐V) or types (B and T). Conclusions and Clinical Importance Proteinuria appears to be negatively associated with survival time in dogs newly diagnosed with lymphoma.}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Skinner, Stephanie M. and Specht, Andrew J. and Cicchirillo, Victoria and Fox‐Alvarez, Stacey and Harris, Autumn N.}, year={2024}, month={Jul} }
 @article{berman_specht_castro_cooke_gilor_harris_2024, title={Correlation between urine anion gap and urine ammonia‐creatinine ratio in healthy cats and cats with kidney disease}, volume={38}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/jvim.17002}, DOI={10.1111/jvim.17002}, abstractNote={Abstract Background Ammonium excretion decreases as kidney function decreases in several species, including cats, and may have predictive or prognostic value in patients with chronic kidney disease (CKD). Urine ammonia measurement is not readily available in clinical practice, and urine anion gap (UAG) has been proposed as a surrogate test. Objectives Evaluate the correlation between urine ammonia‐to‐creatinine ratio (UACR) and UAG in healthy cats and those with CKD and determine if a significant difference exists between UAG of healthy cats and cats with CKD. Animals Urine samples collected from healthy client‐owned cats (n = 59) and those with stable CKD (n = 17). Methods Urine electrolyte concentrations were measured using a commercial chemistry analyzer and UAG was calculated as ([sodium] + [potassium]) − [chloride]. Urine ammonia and creatinine concentrations had been measured previously using commercially available enzymatic assays and used to calculate UACR. Spearman's rank correlation coefficient between UAG and UACR was calculated for both groups. The UAG values of healthy cats and cats with CKD were assessed using the Mann‐Whitney test ( P < .05). Results The UAG was inversely correlated with UACR in healthy cats ( P < .002, r 0 = −0.40) but not in cats with CKD ( P = .55; r 0 = −0.15). A significant difference was found between UAG in healthy cats and those with CKD ( P < .001). Conclusions and Clinical Importance The UAG calculation cannot be used as a substitute for UACR in cats. The clinical relevance of UAG differences between healthy cats and those with CKD remains unknown.}, number={2}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Berman, Alyssa R. and Specht, Andrew J. and Castro, Rebeca A. and Cooke, Kirsten L. and Gilor, Shir and Harris, Autumn N.}, year={2024}, month={Feb}, pages={1068–1073} }
 @inproceedings{claude_harris_castro_cooke_2024, title={Determining within-individual and between-subject biological variation in urine ammonia-to-creatinine ratio in healthy adult dogs}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Claude, R.J. and Harris, A.N. and Castro, R.A. and Cooke, K.L.}, year={2024}, month={Jun} }
 @article{brown_castro_griffin_mandese_rooks_stone_wuerz_cooke_specht_harris_2024, title={Development of a reference interval for urinary ammonia‐to‐creatinine ratio in feline patients}, url={https://doi.org/10.1111/vcp.13327}, DOI={10.1111/vcp.13327}, abstractNote={Abstract Background Disruption of acid–base homeostasis can lead to many clinical problems. Ammonia excretion by the kidneys is critical to maintaining acid–base homeostasis through bicarbonate production. Measurement of ammonia excretion may help determine if the kidneys are properly functioning in maintaining acid–base balance. Reference intervals are essential tools for clinical decision‐making but do not currently exist for urinary ammonia‐to‐creatinine ratio (UACR) in feline patients. Objective This study aimed to generate a reference interval (RI) for UACR in healthy adult cats. Methods The study used samples from client‐owned adult healthy cats that presented to the University of Florida Primary Care and Dentistry service ( n = 92). Physical examination, serum biochemistry, urinalysis, urine ammonia, and creatinine concentrations were measured. Cats were excluded if there were significant abnormalities in their urinalysis or biochemistry panel. The RI for UACR was calculated according to the recommendation of the American Society for Veterinary Clinical Pathology. The UACR was evaluated for correlation with serum bicarbonate, weight, age, and sex. Results The RI for UACR was 3.4–20.7 with 90% confidence intervals for the lower and upper limits of (3.0–3.7) and (16.0–23.7), respectively. No significant correlation with age, sex, or weight was found. There was no discernable relationship between serum bicarbonate and UACR. Conclusions Establishing an RI for UACR in healthy adult cats will allow further studies to determine if changes in UACR are observed during specific disease states.}, journal={Veterinary Clinical Pathology}, author={Brown, Eleanor E. and Castro, Rebecca A. and Griffin, Francesca C. and Mandese, Wendy W. and Rooks, Jenna K. and Stone, Amy E. and Wuerz, Julia A. and Cooke, Kirsten L. and Specht, Andrew J. and Harris, Autumn N.}, year={2024}, month={Mar} }
 @inproceedings{harris_2024, title={Renal Ammonia Metabolism: Make Sure “Urine” the Know!}, booktitle={NCSU Dean’s Seminar for Excellence in Research}, author={Harris, A.N.}, year={2024}, month={Jan} }
 @article{harris_thomas_dominguez rieg_fenton_rieg_2024, title={Sex differences in renal acid-base regulation}, volume={39}, ISSN={1548-9213 1548-9221}, url={http://dx.doi.org/10.1152/physiol.2024.39.s1.1922}, DOI={10.1152/physiol.2024.39.s1.1922}, abstractNote={Transport along the renal tubule differs between female and male rodents, possibly as a consequence of varying abundance and expression of transporters along the nephron. For several aspects such as renal Na + transport and blood pressure regulation, this has been comprehensively studied; however, data on sex differences in renal acid-base regulation are less well understood. We hypothesized that there will be sex differences in transporter expression profiles in response to acid-base challenges. We used female and male C57Bl/6 mice (n=10 per sex and treatment), which were challenged by acid (NH 4 Cl, 0.28 mM) and base (NaHCO 3 , 0.28 mM) in drinking water for 8 days. Blood and urine samples were collected at baseline and at the end of the experimental period before kidneys were harvested under isoflurane anesthesia. Data were analyzed by 2-way ANOVA followed by Tukey multiple comparisons test. In response to NH 4 Cl challenge, urine pH significantly decreased in both sexes without sex differences (male baseline: 6.4±0.1 vs. NH 4 Cl: 5.7±0.1; female baseline: 6.2±0.2 vs NH 4 Cl: 5.6±0.1). In contrast to the urinary response, blood pH was not significantly affected in male mice (male baseline: 7.29±0.01 vs. NH 4 Cl: 7.26±0.02); however, significantly decreased in female mice (female baseline: 7.28±0.01 vs NH 4 Cl: 7.22±0.02). Despite differences in acid-base physiology, no differences were observed in the abundance of NHE3, pS552-NHE3, Npt2a, NKCC2, NCC, pT58-NCC or pendrin between sexes. In response to NaHCO 3 challenge, urine pH significantly increased in both sexes; however, the increase was significantly smaller in female vs. male mice (male baseline: 6.3±0.1 vs. NaHCO 3 : 7.6±0.1; female baseline: 6.3±0.1 vs NaHCO 3 : 7.0±0.3). In contrast to the urinary response, blood pH significantly increased in male mice (male baseline: 7.28±0.01 vs. NaHCO 3 : 7.40±0.01); however, was not significantly affected in female mice (female baseline: 7.29±0.01 vs NaHCO 3 : 7.31±0.01). These differences in females compared to males were associated with a significantly greater abundance of Npt2a (~1.5-fold), pendrin (~1.4-fold) and H-ATPase (~1.5-fold). No differences were observed in the abundance of NHE3, pS552-NHE3, NKCC2, NCC, pT58-NCC, between sexes. In summary, our study demonstrates that acid-base regulation shows very specific sex differences: (i) female mice seem to be more prone to a NH 4 Cl disturbance compared with male mice, (ii) acid challenges under these conditions do not result in major changes in the abundance of the tested proteins, (iii) male mice are more prone to a NaHCO 3 disturbance possibly because of (iv) lower abundances of Npt2a, pendrin and H-ATPase. This work was supported by a VA Merit Review Award IBX004968A (to Dr. Rieg) and a Pilot Project from the USF Microbiomes Institute (to T.R. and J.D.R). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.}, number={S1}, journal={Physiology}, publisher={American Physiological Society}, author={Harris, Autumn and Thomas, Linto and Dominguez Rieg, Jessica Ann and Fenton, Robert and Rieg, Timo}, year={2024}, month={May} }
 @inproceedings{panyutin_lim_saffire_harris_quimby_2024, title={The effect of feeding on urine ammonia levels in cats with and without CKD}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Panyutin, A. and Lim, L. and Saffire, A. and Harris, A.N. and Quimby, J.}, year={2024}, month={Jun} }
 @inproceedings{berg_specht_castro_gilor_cooke_harris_2024, title={Urine NGAL and GGT more correlated with proteinuria than serum creatinine in CKD study dogs}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Berg, A. and Specht, A. and Castro, R. and Gilor, S. and Cooke, K.L. and Harris, A.N.}, year={2024}, month={Jun} }
 @article{harris_shankar_melanmed_batlle_2023, title={An Update on Kidney Ammonium Transport Along the Nephron}, url={https://doi.org/10.1053/j.akdh.2022.12.005}, DOI={10.1053/j.akdh.2022.12.005}, abstractNote={Acid-base homeostasis is critical to the maintenance of normal health. The kidneys have a central role in bicarbonate generation, which occurs through the process of net acid excretion. Renal ammonia excretion is the predominant component of renal net acid excretion under basal conditions and in response to acid-base disturbances. Ammonia produced in the kidney is selectively transported into the urine or the renal vein. The amount of ammonia produced by the kidney that is excreted in the urine varies dramatically in response to physiological stimuli. Recent studies have advanced our understanding of ammonia metabolism's molecular mechanisms and regulation. Ammonia transport has been advanced by recognizing that the specific transport of NH3 and NH4+ by specific membrane proteins is critical to ammonia transport. Other studies show that proximal tubule protein, NBCe1, specifically the A variant, significantly regulates renal ammonia metabolism. This review discusses these critical aspects of the emerging features of ammonia metabolism and transport.}, journal={Advances in Kidney Disease and Health}, author={Harris, Autumn N. and Shankar, Mythri and Melanmed, Michal and Batlle, Daniel}, year={2023}, month={Mar} }
 @inproceedings{berman_specht_gilor_castro_cooke_harris_2023, title={Correlation between Urine Anion Gap and Urine Ammonia-Creatinine Ratio in Healthy and Kidney Disease Cats}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Berman, A. and Specht, A.J. and Gilor, S. and Castro, R.A. and Cooke, K.L. and Harris, A.N.}, year={2023}, month={Jun} }
 @inproceedings{brown_castro_cooke_specht_harris_2023, title={Correlation of Ammonia Excretion with Renal Function and Serum Bicarbonate in Cats with Kidney Disease}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Brown, E. and Castro, R.A. and Cooke, K.L. and Specht, A.J. and Harris, A.N.}, year={2023}, month={Jun} }
 @inproceedings{harris_2023, title={Differential Effects of Sry and Y Chromosome on Ammonia Metabolism}, booktitle={Southern Salt, Water, Kidney Society}, author={Harris, A.N.}, year={2023}, month={Dec} }
 @inproceedings{brown_castro_cooke_specht_harris_2023, title={Feline Urine Ammonia-to Creatinine Ratio Reference Interval}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Brown, E. and Castro, R.A. and Cooke, K.L. and Specht, A.J. and Harris, A.N.}, year={2023}, month={Jun} }
 @inproceedings{harris_2023, title={Metabolic Acidosis in CKD, What’s all the fuss about?}, booktitle={International Renal Interest Society (IRIS) Renal Week}, author={Harris, A.N.}, year={2023}, month={Mar} }
 @inproceedings{harris_2023, title={Role of Androgens in Acid-Base Homeostasis}, booktitle={American Physiological Society Summit}, author={Harris, A.N.}, year={2023}, month={Apr} }
 @inproceedings{harris_2023, title={Sex Steroid Hormones and Renal Acid-Base Balance: What’s All the Fuss About?}, booktitle={The Ohio State University, College of Veterinary Research Day}, author={Harris, A.N.}, year={2023}, month={Apr} }
 @article{mcdonough_harris_xiong_layton_2023, title={Sex differences in renal transporters: assessment and functional consequences}, volume={20}, ISSN={1759-5061 1759-507X}, url={http://dx.doi.org/10.1038/s41581-023-00757-2}, DOI={10.1038/s41581-023-00757-2}, abstractNote={Mammalian kidneys are specialized to maintain fluid and electrolyte homeostasis. The epithelial transport processes along the renal tubule that match output to input have long been the subject of experimental and theoretical study. However, emerging data have identified a new dimension of investigation: sex. Like most tissues, the structure and function of the kidney is regulated by sex hormones and chromosomes. Available data demonstrate sex differences in the abundance of kidney solute and electrolyte transporters, establishing that renal tubular organization and operation are distinctly different in females and males. Newer studies have provided insights into the physiological consequences of these sex differences. Computational simulations predict that sex differences in transporter abundance are likely driven to optimize reproduction, enabling adaptive responses to the nutritional requirements of serial pregnancies and lactation — normal life-cycle changes that challenge the ability of renal transporters to maintain fluid and electrolyte homeostasis. Later in life, females may also undergo menopause, which is associated with changes in disease risk. Although numerous knowledge gaps remain, ongoing studies will provide further insights into the sex-specific mechanisms of sodium, potassium, acid–base and volume physiology throughout the life cycle, which may lead to therapeutic opportunities. This Review summarizes our current understanding of sex differences in renal fluid and electrolyte transporters, based primarily on studies in rodents. The authors describe the physiological consequences of these differences, based on information from experimental studies and from model predictions, and discuss the differential impact of sex on transporter regulation by hormones, diet and acid–base status.}, number={1}, journal={Nature Reviews Nephrology}, publisher={Springer Science and Business Media LLC}, author={McDonough, Alicia A. and Harris, Autumn N. and Xiong, Lingyun and Layton, Anita T.}, year={2023}, month={Sep}, pages={21–36} }
 @inproceedings{harris_2023, title={Sexual Dimorphisms in Renal Acid-Base Balance: What’s all the Fuss About? University of Alabama Department of Medicine}, booktitle={Core Concepts in Kidney Research Series}, author={Harris, A.N.}, year={2023}, month={Jun} }
 @inproceedings{harris_2023, title={The Role of Metabolic Acidosis in Chronic Kidney Disease}, booktitle={ACVIM Forum}, author={Harris, A.N.}, year={2023}, month={Jun} }
 @article{verlander_lee_wall_harris_weiner_2023, title={The proximal tubule through an NBCe1-dependent mechanism regulates collecting duct phenotypic and remodeling responses to acidosis}, url={https://doi.org/10.1152/ajprenal.00175.2022}, DOI={10.1152/ajprenal.00175.2022}, abstractNote={This study shows that the proximal tubule regulates collecting duct phenotypic and remodeling responses to acidosis.}, journal={American Journal of Physiology-Renal Physiology}, author={Verlander, Jill W. and Lee, Hyun-Wook and Wall, Susan M. and Harris, Autumn N. and Weiner, I. David}, year={2023}, month={Jan} }
 @article{rehman_melamed_harris_shankar_rosa_batlle_2023, title={Urinary Ammonium in Clinical Medicine: Direct Measurement and the Urine Anion Gap as a Surrogate Marker During Metabolic Acidosis}, volume={30}, ISSN={2949-8139}, url={http://dx.doi.org/10.1053/j.akdh.2022.12.006}, DOI={10.1053/j.akdh.2022.12.006}, abstractNote={Ammonium is the most important component of urinary acid excretion, normally accounting for about two-third of net acid excretion. In this article, we discuss urine ammonium not only in the evaluation of metabolic acidosis but also in other clinical conditions such as chronic kidney disease. Different methods to measure urine NH4+ that have been employed over the years are discussed. The enzymatic method used by clinical laboratories in the United States to measure plasma ammonia via the glutamate dehydrogenase can be used for urine ammonium. The urine anion gap calculation can be used as a rough marker of urine ammonium in the initial bedside evaluation of metabolic acidosis such as in distal renal tubular acidosis. Urine ammonium measurements, however, should be made more available in clinical medicine for a precise evaluation of this important component of urinary acid excretion.}, number={2}, journal={Advances in Kidney Disease and Health}, publisher={Elsevier BV}, author={Rehman, Mohammed Z. and Melamed, Michal and Harris, Autumn and Shankar, Mythri and Rosa, Robert M. and Batlle, Daniel}, year={2023}, month={Mar}, pages={197–206} }
 @inproceedings{daly_harris_adin_2023, title={Use of Serum Osmolality to Identify Heart Disease Stage in Dogs and Relationship to the Degree of Mathematical Chloride Correction}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Daly, E.J. and Harris, A.N. and Adin, D.B.}, year={2023}, month={Jun} }
 @article{daly_harris_adin_2023, title={Use of serum osmolality to identify heart disease stage in dogs and relationship to mathematical chloride correction}, volume={37}, ISSN={0891-6640 1939-1676}, url={http://dx.doi.org/10.1111/jvim.16863}, DOI={10.1111/jvim.16863}, abstractNote={Heart failure-associated hypochloremia can be depletional from diuretics or dilutional from water retention. Serum osmolality reflects water balance but has not been evaluated in dogs with heart disease.To determine if serum osmolality is related to heart disease stage and amount of mathematical correction of serum chloride (Cl- ) concentrations in healthy dogs and dogs with myxomatous mitral valve degeneration (MMVD).Seventy-seven dogs (20 healthy, 25 Stage B MMVD, 32 Stage C/D MMVD).Serum Cl- concentrations were mathematically corrected. Osmolality was calculated (calOsm) and directly measured by freezing point depression (dmOsm) and compared by Bland-Altman analysis. Biochemical variables and osmolality were compared among healthy, Stage B, and Stage C/D dogs. Correlations were explored between osmolality and biochemical variables. Median and range are presented. P < .05 was considered significant.The calOsm was different among groups (P = .003), with Stage B (310 mOsm/kg; 306, 316) and C/D dogs (312 mOsm/kg; 308, 319) having higher calOsm than healthy dogs (305 mOsm/kg; 302, 308). Osmolality methods were moderately correlated (P < .0001, rs = .46) but with proportional bias and poor agreement. The amount of Cl- correction was negatively correlated with calOsm (P < .0001, rs = -.78) and dmOsm (P = .004, rs = -.33). Serum bicarbonate concentration was negatively correlated with Cl- (P < .0001, rs = -.67).Dogs with Stage B and Stage C/D heart disease had higher calOsm than healthy dogs. Osmolality was inversely related to the amount of Cl- correction, which supports its use in assessing relative body water content. Poor agreement between calOsm and dmOsm prevents methodological interchange.}, number={6}, journal={Journal of Veterinary Internal Medicine}, publisher={Wiley}, author={Daly, Edward J. and Harris, Autumn N. and Adin, Darcy B.}, year={2023}, month={Sep}, pages={2011–2020} }
 @article{lee_verlander_shull_harris_weiner_2022, title={Acid-base effects of combined renal deletion of NBCe1-A and NBCe1-B}, volume={322}, url={https://doi.org/10.1152/ajprenal.00358.2021}, DOI={10.1152/ajprenal.00358.2021}, abstractNote={The results of the present study show that combined deletion of both A and B splice variants of electrogenic Na + -bicarbonate cotransporter 1 from the proximal tubule impairs acid-base homeostasis and completely blocks changes in ammonia excretion in response to acidosis, indicating that both proteins are critical to acid-base homeostasis.}, number={2}, journal={American Journal of Physiology-Renal Physiology}, author={Lee, Hyun-Wook and Verlander, Jill W. and Shull, Gary E. and Harris, Autumn N. and Weiner, I. David}, year={2022}, month={Feb}, pages={F208–F224} }
 @inproceedings{harris_2022, title={Career Development K Awards for Veterinarians}, booktitle={CTSA One Health Alliance (COHA) Translational Research Immersion Program (TRIP) for Veterinary Faculty}, author={Harris, A.N.}, year={2022}, month={Sep} }
 @article{pascutti_dolan_porter_gilor_harris_2022, title={Case Report: Septic Pericarditis With Achromobacter xyloxidans in an Immunosuppressed Dog}, volume={9}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85131546018&partnerID=MN8TOARS}, DOI={10.3389/fvets.2022.884654}, abstractNote={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. Bloodwork revealed a moderate leukocytosis characterized by a mature neutrophilia with a left shift, hypoalbuminemia, mildly increased alkaline phosphatase activity, and moderate hypokalemia. Thoracic CT findings revealed moderate pericardial and bilateral pleural effusion, mediastinal effusion, and moderate cranial mediastinal lymphadenopathy. Diagnostic thoracocentesis and pericardiocentesis revealed septic exudates with bacilli. Two days later, a median sternotomy and pericardiectomy were performed. Aerobic cultures of the effusions grew Achromobacter xylosoxidans ss deitrificans . The patient was treated with Amoxicillin-clavulanate and enrofloxacin for 12 weeks and clinically fully recovered. Achromobacter xylosoxidans has not been reported as a cause of purulent pericarditis and pyothorax in a dog. Uniquely, this patient is suspected of developing this infection secondary to immunosuppression.}, journal={Frontiers in Veterinary Science}, author={Pascutti, K.M. and Dolan, J.K. and Porter, L.T. and Gilor, S. and Harris, A.N.}, year={2022} }
 @article{harris_brown_2022, title={Clinical Applications and Limitations of Renal Biomarkers}, journal={Today’s Veterinary Practice}, author={Harris, A.N. and Brown, E.}, year={2022}, month={Sep}, pages={66–71} }
 @inproceedings{skinner_specht_cicchirillo_fox-alvarez_harris_2022, title={Proteinuria at Time of Diagnosis is Associated with Shorter Survival Time in Dogs with Lymphoma}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Skinner, S. and Specht, A.J. and Cicchirillo, V.C. and Fox-Alvarez, S. and Harris, A.N.}, year={2022}, month={Jun} }
 @inproceedings{harris_2022, title={Role of Androgens in Acid-Base Homeostasis}, booktitle={The USF Hypertension and Kidney Research Center Special Pre-ASN Symposium}, author={Harris, A.N.}, year={2022}, month={Nov} }
 @article{ehrhardt_odunayo_pascutti_carvajal_ham_harris_2023, title={Stump pyometra in a spayed female dog secondary to tamoxifen}, volume={9}, ISSN={2053-1095 2053-1095}, url={http://dx.doi.org/10.1002/vms3.1041}, DOI={10.1002/vms3.1041}, abstractNote={To describe a complication associated with the long-term use of tamoxifen for the treatment of sclerosing encapsulating peritonitis in a dog.A 2-year-old female spayed poodle cross was evaluated for a stump pyometra. The dog was diagnosed with sclerosing encapsulating peritonitis a year prior and was treated with tamoxifen, an oestrogen receptor antagonist, for treatment of the disease. The dog developed a swollen vulva with vulvar discharge and a stump pyometra was diagnosed on ultrasound. Hormonal testing was submitted to evaluate for an ovarian remnant and the dog underwent an exploratory laparotomy, where the uterine stump was removed. No ovarian remnant tissue was identified intra-operatively, and hormonal testing (anti-Müllerian hormone, progesterone, oestradiol) and histopathology were consistent with the absence of ovarian tissue. The tamoxifen was discontinued. The dog recovered uneventfully after surgery.This report describes a complication of treatment of a rarely described clinical disease. While most cases of stump pyometra involve ovarian remnant syndrome, this case report describes a stump pyometra in a dog without remnant tissue that was undergoing treatment with tamoxifen. Tamoxifen has been reported to cause pyometra in intact female dogs. To the authors' knowledge, this is the first case report to describe a stump pyometra in a spayed female dog, secondary to the use of tamoxifen.}, number={1}, journal={Veterinary Medicine and Science}, publisher={Wiley}, author={Ehrhardt, Caryn and Odunayo, Adesola and Pascutti, Kristina and Carvajal, Jose and Ham, Kathleen and Harris, Autumn Nourse}, year={2023}, month={Jan}, pages={47–52} }
 @inproceedings{lee_verlander_wall_harris_weiner_2022, title={The Proximal Tubule (PT) Regulates Collecting Duct Phenotypic and Remodeling Responses to Acidosis}, booktitle={American Society of Nephrology, Kidney Week}, author={Lee, H.W. and Verlander, J.W. and Wall, S.M. and Harris, A.N. and Weiner, I.D.}, year={2022}, month={Nov} }
 @article{harris_castro_lee_weiner_2022, title={The Role of the Androgen Receptor in Sexual Dimorphisms in Acidosis‐Stimulated Renal Ammonia Metabolism}, volume={36}, ISSN={0892-6638 1530-6860}, url={http://dx.doi.org/10.1096/fasebj.2022.36.S1.R5808}, DOI={10.1096/fasebj.2022.36.S1.R5808}, abstractNote={Renal ammonia excretion is a critical mechanism through which the kidneys maintain acid-base homeostasis. We have previously identified that ammonia excretion is less in male mice than in female mice under basal conditions, that this correlates with differences in expression of key proteins involved in ammonia metabolism, and involves both testosterone-dependent and renal androgen receptor (AR)-dependent signaling pathways. In addition, there are sex differences in the response to acid-loading. This study's objective was to determine renal AR's role in the renal ammonia response to an exogenous acid load. To avoid the known systemic effects of AR blockade/deletion, we studied mice with kidney-specific AR deletion (KS-AR-KO) using Cre/loxP techniques and the Pax8-Cre transgene; control (C) mice were Pax8-Cre-negative littermates. Mice were acid-loaded by adding HCl to powdered chow for 7 days; control mice had equal amounts of deionized water added. Urine ammonia under basal conditions was ~2 fold greater in male KO (M-KO) than in male control (M-C) mice. After acid-loading, ammonia excretion was significantly greater in M-KO than in M-C mice on day 7 (M-KO, 852±203; M-C, 588±93 µmol/day; P < 0.05; N= 6 in each group). Basal urine pH was significantly lower in M-KO than in M-C mice, but the response to acid-loading significantly between genotypes. There was no significant difference in serum Na+ , K+ , and HCO3- after acid loading. Expression of phosphoenolpyruvate carboxykinase (PEPCK), a major proximal tubule (PT) ammonia generating protein, was greater under control conditions in M-KO, but the relative increase with acid-loading was greater in M-C mice. Expression of glutamine synthetase, which recycles ammonia, significantly decreased in response to an acid load, with no significant genotype difference. NBCe1-A expression was significantly less under control conditions in M-KO, but the relative increase with acid-loading was greater in M-KO mice. Expression of NHE3, believed to be the primary mechanism of PT ammonia secretion, increased in response to acid-loading in M-KO mice but not in M-C mice. After acid-loading, cortical NKCC2, which mediates thick ascending limb ammonia reabsorption, was significantly greater in M-KO than M-C mice. The collecting duct secretes the majority of urinary ammonia, and the Rhesus glycoproteins, Rhbg and Rhcg, are the primary collecting duct ammonia transporting proteins. Expression of Rhbg increased in response to an acid load with no significant genotype difference. Renal structural analysis showed AR deletion in male mice significantly decreased kidney size (M-C, 275±33 mg; M-KO, 225±32; P<0.05; N= 6 in each group) after acid loading. In summary, KS-AR-KO increases the urinary ammonia response to acid-loading, through coordinated effects on PEPCK, GS, NBCe1-A, NHE3 and NKCC2. Thus, in male mice renal AR activation inhibits the response to acid-loading of multiple components of ammonia metabolism and transport, which leads to less ability to increase ammonia excretion.}, number={S1}, journal={The FASEB Journal}, publisher={Wiley}, author={Harris, Autumn N. and Castro, Rebeca A. and Lee, Hyun‐Wook and Weiner, David}, year={2022}, month={May} }
 @inproceedings{adrianowycz_castro_specht_harris_2021, title={Canine Urine Ammonia-to-Creatinine Ratio Reference Interval}, booktitle={American College of Veterinary Internal Medicine Forum}, author={Adrianowycz, S.E. and Castro, R.A. and Specht, A.J. and Harris, A.N.}, year={2021}, month={Jun} }
 @article{adrianowycz_castro_specht_harris_2021, title={Establishment of an RI for the urine ammonia‐to‐creatinine ratio in dogs}, volume={50}, url={https://doi.org/10.1111/vcp.13032}, DOI={10.1111/vcp.13032}, abstractNote={Ammonia is produced and excreted by the kidney, contributing to systemic acid-base homeostasis through the production of bicarbonate. Disorders of acid-base balance can lead to many clinical problems and measuring ammonia excretion helps in determining if the kidneys are responding to acid-base challenges appropriately. Reference intervals are integral to clinical decision-making, and there is no current RI for the urine ammonia-to-creatinine ratio (UACR) in dogs.This study aimed to generate an RI for the UACR in healthy adult dogs.The study used adult, client-owned dogs that were presented to the University of Florida Primary Care and Dentistry service (n = 60). Physical examinations were performed and serum chemistry and urinalysis samples were obtained. Urine ammonia and creatinine concentrations were determined. Dogs were excluded if there were significant abnormalities in either their urinalysis or serum chemistry results. The RI for the UACR was calculated according to the recommendation of the American Society for Veterinary Clinical Pathology. Data were evaluated for correlation with serum bicarbonate, weight, age, and sex.The RIs for the UACR were 0.16-23.69 with 90% confidence intervals for the lower and upper limits of (0.13-1.17) and (20.50-23.75), respectively. No significant impact of age, sex, or weight was found. There was no discernable relationship between serum bicarbonate and UACR.Establishing an RI for UACR in healthy adult dogs will allow for further studies to determine if alterations are observed during specific disease states.}, number={4}, journal={Veterinary Clinical Pathology}, author={Adrianowycz, Sarah E. and Castro, Rebeca A. and Specht, Andrew J. and Harris, Autumn N.}, year={2021}, month={Dec}, pages={597–602} }
 @article{inman_allen-durrance_cianciolo_harris_2021, title={Familial nephropathy in Bracchi Italiani: 8 cases (2012-2019)}, volume={259}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85122449943&partnerID=MN8TOARS}, DOI={10.2460/javma.20.07.0420}, abstractNote={To characterize the signalment, clinical signs, clinical pathological and histologic findings, and outcome in 8 related Bracchi Italiani with proteinuric kidney disease.8 client-owned Bracchi Italiani.Health records submitted to the Bracco Italiano Health Foundation and the Bracco Italiano Club of America between 2012 and 2019 were reviewed for dogs with evidence of nephropathy for which histologic diagnoses were obtained. Pedigree, signalment, clinical signs, diagnostic test results (including microscopic examination of kidney tissue samples collected ante- or postmortem), and outcome were acquired. Results were presented as descriptive statistics.The most common clinical sign in affected dogs was inappetence. All dogs were proteinuric, and 4 dogs were azotemic. Seven dogs developed clinical signs of kidney disease and were euthanized a median of 75 days postdiagnosis. Six dogs had glomerular amyloidosis, and 1 dog each had nephrosclerosis and nonamyloidotic fibrillar glomerulopathy.Results indicated that the clinical presentation may vary in affected dogs, and proteinuria in young or middle-aged Bracchi Italiani should raise the concern for hereditary nephropathy. Prognosis is likely poor once clinical signs are noted.}, number={12}, journal={Journal of the American Veterinary Medical Association}, author={Inman, A.L. and Allen-Durrance, A.E. and Cianciolo, R.E. and Harris, A.N.}, year={2021}, pages={1422–1427} }
 @inproceedings{harris_2021, title={Role of Androgens in Acid-Base Homeostasis}, booktitle={Southern Salt, Water, Kidney Society}, author={Harris, A.N.}, year={2021}, month={Dec} }
 @article{harris_castro_lee_verlander_weiner_2021, title={Role of the renal androgen receptor in sex differences in ammonia metabolism}, volume={321}, url={https://doi.org/10.1152/ajprenal.00260.2021}, DOI={10.1152/ajprenal.00260.2021}, abstractNote={Sexual dimorphisms in ammonia metabolism involve androgen receptor (AR)-dependent signaling pathways in male, but not female, kidneys that lead to altered proximal tubule (PT), phosphoenolpyruvate carboxykinase, and thick ascending limb Na + -K + -2Cl − cotransporter expression. Adaptive responses in Na + /H + exchanger 3 and electrogenic Na + -bicarbonate cotransporter 1-A expression limit the magnitude of the effect on ammonia excretion. Finally, the greater kidney size and PT volume density in male mice is the result of PT androgen signaling through AR.}, number={5}, journal={American Journal of Physiology-Renal Physiology}, author={Harris, Autumn N. and Castro, Rebeca A. and Lee, Hyun-Wook and Verlander, Jill W. and Weiner, I. David}, year={2021}, month={Nov}, pages={F629–F644} }
 @article{harris_weiner_2021, title={Sex differences in renal ammonia metabolism}, volume={320}, url={https://doi.org/10.1152/ajprenal.00531.2020}, DOI={10.1152/ajprenal.00531.2020}, abstractNote={Sexual dimorphic variations are present in many aspects of biology and involve the structure and/or function of nearly every organ system. Acid-base homeostasis is critical for optimal health, and renal ammonia metabolism has a major role in the maintenance of acid-base homeostasis. Recent studies have shown sex-dependent differences in renal ammonia metabolism with regard to both basal ammonia excretion and the response to an exogenous acid load. These sexual dimorphisms are associated with structural changes in the proximal tubule and the collecting duct and variations in the expression of multiple proteins involved in ammonia metabolism and transport. Studies using orchiectomy-induced testosterone deficiency and physiological testosterone replacement have shown that testosterone underlies much of the sex-dependent differences in the proximal tubule. This parallels the finding that the canonical testosterone target receptor, androgen receptor (AR), is present exclusively in the proximal tubule. Thus testosterone, possibly acting through AR activation, regulates multiple components of renal structure and ammonia metabolism. The lack of detectable AR in the remainder of the nephron and collecting duct suggests that some dimorphisms in renal structure and ammonia transporter expression are mediated through mechanisms other than direct testosterone-dependent AR activation. A better understanding of the mechanism and biological implications of sex’s effect on renal structure and ammonia metabolism is critical for optimizing our ability to care for both men and women with acid-base disturbances.}, number={1}, journal={American Journal of Physiology-Renal Physiology}, author={Harris, Autumn N. and Weiner, I. David}, year={2021}, month={Jan}, pages={F55–F60} }
 @article{harris_castro_lee_verlander_weiner_2021, title={The Role of the Androgen Receptor in Sexual Dimorphisms of Renal Ammonia Metabolism}, volume={35}, ISSN={0892-6638 1530-6860}, url={http://dx.doi.org/10.1096/fasebj.2021.35.S1.03464}, DOI={10.1096/fasebj.2021.35.S1.03464}, abstractNote={Female mice excrete ~2x more ammonia than do male mice, and this appears to result from sex-differences in ammoniagenic enzyme expression in the proximal tubule (PT) and differences in ammonia transporter expression in the PT, TAL and collecting duct. Orchiectomy studies, with and without testosterone replacement, showed that many, but not all, of these sex-differences were mediated by testosterone. We showed recently that the androgen receptor (AR) is present in the PT in both male and female kidney, and not detectably in other renal epithelial cells. This study's objective was to determine AR's role in sexual dimorphisms in ammonia handling. To avoid known systemic effects of AR blockade/deletion, we generated mice with kidney-specific AR deletion (KS-AR-KO) using Cre/loxP techniques (AR floxed mice and Pax8-Cre mice); control (C) mice were Pax8-Cre-negative littermates. Plasma testosterone did not differ significantly between KO and C mice in either sex (M-C, 67±74 ng/dl; M-KO, 239±471; F-C, 27±10; F-KO, 29±11; P=NS; N= 8-11 in each group). In male mice, KS-AR-KO increased ammonia excretion significantly (M-C, 44±14 µmol/day; M-KO, 92±74; P < 0.05; N= 8-11 in each group); this occurred despite no significant difference in food intake, a major determinant of endogenous acid production; there was no significant difference in female mice. KS-AR-KO did not alter serum Na+, K+, or HCO3- significantly in either sex. Expression of phosphoenolpyruvate carboxykinase (PEPCK), a major proximal tubule (PT) ammonia generating protein, and NKCC2, the major mechanism of TAL ammonia reabsorption, were increased significantly by KS-AR-KO in male mice, but not in female mice. KS-AR-KO decreased expression of NHE-3, the major mechanism of PT ammonia secretion, and NBCe1-A, a basolateral PT transporter that regulates PT ammonia metabolism, in male mice, but not in female mice, and did not alter the sex-specific difference in collecting duct Rhbg and Rhcg expression in either sex. Renal structural analysis showed AR deletion decreased kidney size (M-C, 222±27 mg; M-KO, 175±23; P<0.05; N= 5-6 in each group) and cortical proximal tubule volume density (C, 61±2%; KO, 42±2; P<0.05; N= 5-6 in each group) in male mice, but did not alter either parameter in females. KS-AR-KO did not alter the sexual dimorphism of collecting duct volume density in either sex. We conclude that sex-differences in ammonia generation and excretion involve AR-dependent signaling pathways in male, but not female, kidney that lead to increased PT PEPCK and TAL NKCC2 expression. Adaptive responses in NHE-3 and NBCe1-A limit the magnitude of the effect on ammonia excretion, and the sex differences in the collecting duct are not mediated by AR. Since AR is not present in the TAL, the effect of KS-AR-KO on male NKCC2 expression likely involves PT-dependent paracrine signaling. Finally, the greater kidney size and PT volume density in male mice is the result of PT AR signaling.}, number={S1}, journal={The FASEB Journal}, publisher={Wiley}, author={Harris, Autumn and Castro, Rebeca and Lee, Hyun‐Wook and Verlander, Jill and Weiner, I.}, year={2021}, month={May} }
 @inproceedings{castro_lee_verlander_harris_2021, title={The Role of the Renal Androgen Receptor in Ammonia Metabolism}, booktitle={Southern Salt, Water, Kidney Society}, author={Castro, R.A. and Lee, H.W. and Verlander, J.W. and Harris, A.N.}, year={2021}, month={Dec} }
 @inproceedings{harris_castro_lee_verlander_weiner_2021, title={The Role of the Renal Androgen Receptor in Ammonia Metabolism}, booktitle={American Physiologic Society- New Trends in Sex and Gender Medicine}, author={Harris, A.N. and Castro, R.A. and Lee, H.W. and Verlander, J.W. and Weiner, I.D.}, year={2021}, month={Oct} }
 @inproceedings{harris_2020, title={Many Species, One Health - Sex and the Kidneys: Translational Research Opportunities}, booktitle={Southeast Regional Clinical and Translational Science Conference}, author={Harris, A.N.}, year={2020}, month={Feb} }
 @article{lee_harris_romero_welling_wingo_verlander_weiner_2020, title={NBCe1-A is required for the renal ammonia and K+response to hypokalemia}, volume={318}, url={https://doi.org/10.1152/ajprenal.00481.2019}, DOI={10.1152/ajprenal.00481.2019}, abstractNote={Hypokalemia increases ammonia excretion and decreases K + excretion. The present study examined the role of the proximal tubule protein NBCe1-A in these responses. We studied mice with Na + -bicarbonate cotransporter electrogenic, isoform 1, splice variant A (NBCe1-A) deletion [knockout (KO) mice] and their wild-type (WT) littermates were provided either K + control or K + -free diet. We also used tissue sections to determine the effect of extracellular ammonia on NaCl cotransporter (NCC) phosphorylation. The K + -free diet significantly increased proximal tubule NBCe1-A and ammonia excretion in WT mice, and NBCe1-A deletion blunted the ammonia excretion response. NBCe1-A deletion inhibited the ammoniagenic/ammonia recycling enzyme response in the cortical proximal tubule (PT), where NBCe1-A is present in WT mice. In the outer medulla, where NBCe1-A is not present, the PT ammonia metabolism response was accentuated by NBCe1-A deletion. KO mice developed more severe hypokalemia and had greater urinary K + excretion during the K + -free diet than did WT mice. This was associated with blunting of the hypokalemia-induced change in NCC phosphorylation. NBCe1-A KO mice have systemic metabolic acidosis, but experimentally induced metabolic acidosis did not alter NCC phosphorylation. Although KO mice have impaired ammonia metabolism, experiments in tissue sections showed that lack of ammonia does impair NCC phosphorylation. Finally, urinary aldosterone was greater in KO mice than in WT mice, but neither expression of epithelial Na + channel α-, β-, and γ-subunits nor of H + -K + -ATPase α 1 - or α 2 -subunits correlated with changes in urinary K + . We conclude that NBCe1-A is critical for the effect of diet-induced hypokalemia to increase cortical proximal tubule ammonia generation and for the expected decrease in urinary K + excretion.}, number={2}, journal={American Journal of Physiology-Renal Physiology}, author={Lee, Hyun-Wook and Harris, Autumn N. and Romero, Michael F. and Welling, Paul A. and Wingo, Charles S. and Verlander, Jill W. and Weiner, I. David}, year={2020}, month={Feb}, pages={F402–F421} }
 @article{harris_lee_verlander_weiner_2020, title={Testosterone modulates renal ammonia metabolism}, volume={318}, url={https://doi.org/10.1152/ajprenal.00560.2019}, DOI={10.1152/ajprenal.00560.2019}, abstractNote={There are substantial sex differences in renal structure and ammonia metabolism that correlate with differences in expression of proteins involved in ammonia generation and transport. This study determined the role of testis-derived testosterone in these differences. We studied 4-mo-old male C57BL/6 mice 4 and 8 wk after either bilateral orchiectomy (ORCH) or sham-operated control surgery and determined the effect of testosterone replacement to reverse the effects of ORCH. Finally, we determined the cellular expression of androgen receptor (AR), testosterone’s canonical target receptor. ORCH decreased kidney and proximal tubule size, and testosterone replacement reversed this effect. ORCH increased ammonia excretion in a testosterone-dependent fashion; this occurred despite similar food intake, which is the primary component of endogenous acid production. ORCH increased expression of both phospho enolpyruvate, a major ammonia-generating protein, and Na + -K + -2Cl − cotransporter, which mediates thick ascending limb ammonia reabsorption; these changes were reversed with testosterone replacement. Orchiectomy also decreased expression of Na + /H + exchanger isoform 3, which mediates proximal tubule ammonia secretion, in a testosterone-dependent pattern. Finally, ARs are expressed throughout the proximal tubule in both the male and female kidney. Testosterone, possibly acting through ARs, has dramatic effects on kidney and proximal tubule size and decreases ammonia excretion through its effects on several key proteins involved in ammonia metabolism.}, number={4}, journal={American Journal of Physiology-Renal Physiology}, author={Harris, Autumn N. and Lee, Hyun-Wook and Verlander, Jill W. and Weiner, I. David}, year={2020}, month={Apr}, pages={F922–F935} }
 @article{harris_lee_fang_verlander_weiner_2019, title={Differences in acidosis-stimulated renal ammonia metabolism in the male and female kidney}, volume={317}, url={https://doi.org/10.1152/ajprenal.00244.2019}, DOI={10.1152/ajprenal.00244.2019}, abstractNote={Renal ammonia excretion is a critical component of acid-base homeostasis, and changes in ammonia excretion are the predominant component of increased net acid excretion in response to metabolic acidosis. We recently reported substantial sex-dependent differences in basal ammonia metabolism that correlate with sex-dependent differences in renal structure and expression of key proteins involved in ammonia metabolism. The purpose of the present study was to investigate the effect of sex on the renal ammonia response to an exogenous acid load. We studied 4-mo-old C57BL/6 mice. Ammonia excretion, which was less in male mice under basal conditions, increased in response to acid loading to a greater extent in male mice, such that maximal ammonia excretion did not differ between the sexes. Fundamental structural sex differences in the nonacid-loaded kidney persisted after acid loading, with less cortical proximal tubule volume density in the female kidney than in the male kidney, whereas collecting duct volume density was greater in the female kidney. To further investigate sex-dependent differences in the response to acid loading, we examined the expression of proteins involved in ammonia metabolism. The change in expression of phosphoenolpyruvate carboxykinase and Rh family B glycoprotein with acid loading was greater in male mice than in female mice, whereas Na+-K+-2Cl- cotransporter and inner stripe of the outer medulla intercalated cell Rh family C glycoprotein expression were significantly greater in female mice than in male mice. There was no significant sex difference in glutamine synthetase, Na+/H+ exchanger isoform 3, or electrogenic Na+-bicarbonate cotransporter 1 variant A protein expression in response to acid loading. We conclude that substantial sex-dependent differences in the renal ammonia response to acid loading enable a similar maximum ammonia excretion response.}, number={4}, journal={American Journal of Physiology-Renal Physiology}, author={Harris, Autumn N. and Lee, Hyun-Wook and Fang, Lijuan and Verlander, Jill W. and Weiner, I. David}, year={2019}, month={Oct}, pages={F890–F905} }
 @article{osis_webster_harris_lee_chen_fang_romero_khattri_merritt_verlander_et al._2019, title={Regulation of renal naDC1 expression and citrate excretion by NBCe1-a}, volume={317}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85070557441&partnerID=MN8TOARS}, DOI={10.1152/ajprenal.00015.2019}, abstractNote={Citrate is critical for acid-base homeostasis and to prevent calcium nephrolithiasis. Both metabolic acidosis and hypokalemia decrease citrate excretion and increase expression of Na+-dicarboxylate cotransporter 1 (NaDC1; SLC13A2), the primary protein involved in citrate reabsorption. However, the mechanisms transducing extracellular signals and mediating these responses are incompletely understood. The purpose of the present study was to determine the role of the Na+-coupled electrogenic bicarbonate cotransporter (NBCe1) A variant (NBCe1-A) in citrate metabolism under basal conditions and in response to acid loading and hypokalemia. NBCe1-A deletion increased citrate excretion and decreased NaDC1 expression in the proximal convoluted tubules (PCT) and proximal straight tubules (PST) in the medullary ray (PST-MR) but not in the PST in the outer medulla (PST-OM). Acid loading wild-type (WT) mice decreased citrate excretion. NaDC1 expression increased only in the PCT and PST-MR and not in the PST-MR. In NBCe1-A knockout (KO) mice, the acid loading change in citrate excretion was unaffected, changes in PCT NaDC1 expression were blocked, and there was an adaptive increase in PST-MR. Hypokalemia in WT mice decreased citrate excretion; NaDC1 expression increased only in the PCT and PST-MR. NBCe1-A KO blocked both the citrate and NaDC1 changes. We conclude that 1) adaptive changes in NaDC1 expression in response to metabolic acidosis and hypokalemia occur specifically in the PCT and PST-MR, i.e., in cortical proximal tubule segments; 2) NBCe1-A is necessary for normal basal, metabolic acidosis and hypokalemia-stimulated citrate metabolism and does so by regulating NaDC1 expression in cortical proximal tubule segments; and 3) adaptive increases in PST-OM NaDC1 expression occur in NBCe1-A KO mice in response to acid loading that do not occur in WT mice.}, number={2}, journal={American Journal of Physiology - Renal Physiology}, author={Osis, G. and Webster, K.L. and Harris, A.N. and Lee, H.-W. and Chen, C. and Fang, L. and Romero, M.F. and Khattri, R.B. and Merritt, M.E. and Verlander, J.W. and et al.}, year={2019}, pages={F489–F501} }
 @inproceedings{verlander_chen_matthew_harris_lee_valero_clapp_weiner_2019, title={Renal Inflammation, Vascular Pathology, and Splenomegaly are Induced in a Mouse Model of Spontaneous Chronic Metabolic Acidosis}, booktitle={Southern, Salt Water & Kidney Club Conference}, author={Verlander, J.W. and Chen, C. and Matthew, S. and Harris, A.N. and Lee, H.W. and Valero, C.M. and Clapp, W.L. and Weiner, I.D.}, year={2019}, month={Dec} }
 @inproceedings{verlander_chen_matthew_harris_lee_valero_clapp_weiner_2019, title={Renal Inflammation, Vascular Pathology, and Splenomegaly are Induced in a Mouse Model of Spontaneous Chronic Metabolic Acidosis}, booktitle={American Society of Nephrology, Kidney Week}, author={Verlander, J.W. and Chen, C. and Matthew, S. and Harris, A.N. and Lee, H.W. and Valero, C.M. and Clapp, W.L. and Weiner, I.D.}, year={2019}, month={Nov} }
 @inproceedings{lee_harris_romero_verlander_weiner_2019, title={Role of Ammonia in the Renal Potassium Response to Dietary Potassium Deficiency}, booktitle={American Society of Nephrology, Kidney Week}, author={Lee, H.W. and Harris, A.N. and Romero, M.F. and Verlander, J.W. and Weiner, I.D.}, year={2019}, month={Nov} }
 @inproceedings{harris_lee_verlander_weiner_2019, title={Role of Testosterone in Renal Ammonia Metabolism}, booktitle={American Physiologic Society – Basic Research Forum for Emerging Kidney Physiologists; Emerging Concepts in Kidney Physiology and Disease}, author={Harris, A.N. and Lee, H.W. and Verlander, J.W. and Weiner, I.D.}, year={2019}, month={Nov} }
 @article{harris_lee_fang_verlander_weiner_2019, title={Sex Differences in Acidosis‐Stimulated Renal Ammonia Metabolism}, volume={33}, ISSN={0892-6638 1530-6860}, url={http://dx.doi.org/10.1096/fasebj.2019.33.1_supplement.544.20}, DOI={10.1096/fasebj.2019.33.1_supplement.544.20}, abstractNote={Renal ammonia excretion is a critical component in maintaining acid‐base homoeostasis and changes in ammonia excretion are the predominant component of increased net acid excretion in response to metabolic acidosis. We reported recently substantial sex‐dependent differences in basal ammonia metabolism that correlate with sex‐dependent structural differences and differences in the expression of key proteins involved in ammonia metabolism. This study's objective was to determine the effect of sex on the renal ammonia response to an exogenous acid load. We compared 4‐month old C57BL/6 male (M) and female (F) mice. Mice were acid‐loaded by adding HCl to powdered chow for 7 days, and control mice had equal amounts of deionized water added. Basal ammonia excretion, factored for body weight, was ~2‐fold greater in female than male mice, but the response to acid‐loading did not differ significantly. There was no significant sex difference in serum Na + , K + , and HCO 3 − after an acid load. The basal fundamental structural differences between the female and male kidney were maintained after an acid load. After acid‐loading, in the female kidney, proximal tubules account for a lower percentage of the cortical parenchyma than in the male kidney (F, 43±2; M, 61±3%; P < 0.001), whereas the collecting ducts account for a greater percentage of the renal parenchyma (F, 16±1; M, 11±1%; P < 0.01) which are similar to basal conditions. Cortical PCT and PST cell height increased in response to acid‐loading, and the increase was greater in M than F kidney. In the outer medulla (OM), PST cell height was similar in M and F, and sex did not alter the increase with acid‐loading. Similarly, intercalated cell (IC) size in the collecting duct in the OM was greater in F than in M kidney, and increased with acid‐loading in both sexes; sex did not alter the acid‐loading increase. Cortical expression of phospho enol pyruvate, a major proximal tubule (PT) ammonia generating protein, was greater under control conditions in F, but the relative increase with acid‐loading was greater in M. Expression of glutamine synthetase, which recycles ammonia, significantly decreased in response to an acid load, with no significant sex difference. Expression of total cortical NBCe1, but not NBCe1‐A, increased in response to acid‐loading. Expression of NHE3, believed to be the major mechanism of PT ammonia secretion, increased in response to an acid load in M, but not in F. Cortical NKCC2, which mediates thick ascending limb ammonia reabsorption, was significantly greater in F than M after an acid load. The collecting duct secretes the majority of urinary ammonia and the Rhesus glycoproteins, Rhbg and Rhcg, are the primary collecting duct ammonia transporting proteins. Acid‐loading increased cortical Rhbg expression in M, but not in F in the cortex, whereas in the OM, Rhbg expression increased similarly in both M and F. Rhcg expression in intercalated cells in the inner stripe of the outer medulla was significantly greater in F than in M mice after an acid load. We conclude that there are substantial sex‐dependent differences in the mechanism of renal ammonia response to acid‐loading that enable a similar maximum ammonia excretion response. Support or Funding Information NIH R01DK045788, R01DK107798 and 5T32DK104721 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .}, number={S1}, journal={The FASEB Journal}, publisher={Wiley}, author={Harris, Autumn N and Lee, Hyun‐Wook and Fang, Lijuan and Verlander, Jill W. and Weiner, I. David}, year={2019}, month={Apr} }
 @article{harris_lee_fang_verlander_weiner_2019, title={Testosterone Modulates Renal Ammonia Metabolism}, volume={33}, ISSN={0892-6638 1530-6860}, url={http://dx.doi.org/10.1096/fasebj.2019.33.1_supplement.864.12}, DOI={10.1096/fasebj.2019.33.1_supplement.864.12}, abstractNote={Ammonia metabolism is the primary component of net acid excretion and thus has a critical role in acid‐base homeostasis. Our recent studies show there are substantial sex‐dependent differences in ammonia metabolism that correlate with sex‐dependent differences in renal structure and in expression of proteins involved in ammonia generation and transport. This study's objective was to determine the role of testis‐derived testosterone in these differences. We used 4 month‐old C57BL/6 male mice divided into 3 groups: orchiectomy plus placebo (ORCH+P), ORCH plus testosterone (ORCH+T), and sham operated control (SOC). We replaced testosterone using time‐delayed pellets implanted subcutaneously; ORCH+P received a similar pellet that did not release testosterone. Plasma testosterone levels did not differ significantly between ORCH+T and SOC mice (ORCH+T, 159±36; SOC, 120±140; P = NS). Mice were studied four weeks after surgery. Food, and thus protein, intake, which is a major determinant of endogenous acid production, was similar in all three groups (SOC, 12.3±1.7; OCRH+P, 12.6±1.2; ORCH+T, 13.3±1.2 g/d; P=NS). Despite similar food intake, ORCH+P mice excreted more ammonia than did SOC mice; this was reversed by testosterone replacement (ORCH+P, 135±32; SOC, 55±13; ORCH+T, 48±28 μmol/day; P<0.001). Similar findings were observed in a separate set of ORCH+P and SOC mice studied at 8 weeks. ORCH decreased kidney size, and this was completely reversed by testosterone replacement (ORCH+P, 187±18; SOC, 220±16; ORCH+T, 236±19 mg; P<0.001). In parallel, proximal tubule volume density in the ORCH+P kidney was less than in the SOC kidney, and testosterone replacement completely reversed this difference (ORCH+P, 47±2; SOC, 63±1; ORCH+T, 62±1%; P<0.001). Phospho enol pyruvate (PEPCK), a major proximal tubule (PT) ammonia generating protein, was significantly greater in ORCH+P mice than SOC mice, and this effect was completely reversed by testosterone replacement. Glutamine synthetase, which recycles ammonia, and NBCe1, a basolateral PT transporter that regulates PT ammonia metabolism, did not differ significantly between the groups. Expression of NKCC2, which mediates thick ascending limb ammonia reabsorption, was significantly greater in ORCH+P mice than SOC mice, and this effect was completely reversed by testosterone replacement. Finally, renal androgen receptor (AR) mRNA and protein expression were detected by real‐time RT‐PCR and immunoblot analysis, and immunohistochemistry showed AR expression throughout the proximal tubule (PT), with no detectable expression in non‐PT epithelial cells. These findings demonstrate that the loss of testis‐derived sex steroid hormones dramatically alters ammonia excretion, proximal tubule structure, and expression of key proteins involved in ammonia metabolism and transport. Furthermore, these dramatic changes derived from the loss of testis‐derived sex steroid hormones were reversed by physiologic testosterone replacement. We conclude that testosterone, likely acting through AR, decreases ammonia excretion through its effects on proximal tubule structure and on several key proteins involved in ammonia metabolism and transport. Support or Funding Information NIH R01‐DK045788, R01‐DK107798 and 5T32‐DK‐104721. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .}, number={S1}, journal={The FASEB Journal}, publisher={Wiley}, author={Harris, Autumn N and Lee, Hyun‐Wook and Fang, Lijuan and Verlander, Jill W. and Weiner, I. David}, year={2019}, month={Apr} }
 @article{harris_lee_osis_fang_webster_verlander_weiner_2018, title={Differences in renal ammonia metabolism in male and female kidney}, volume={315}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85051297901&partnerID=MN8TOARS}, DOI={10.1152/ajprenal.00084.2018}, abstractNote={Renal ammonia metabolism has a major role in the maintenance of acid-base homeostasis. Sex differences are well recognized as an important biological variable in many aspects of renal function, including fluid and electrolyte metabolism. However, sex differences in renal ammonia metabolism have not been previously reported. Therefore, the purpose of the current study was to investigate sex differences in renal ammonia metabolism. We studied 4-mo-old wild-type C57BL/6 mice fed a normal diet. Despite similar levels of food intake, and, thus, protein intake, which is the primary determinant of endogenous acid production, female mice excreted greater amounts of ammonia, but not titratable acids, than did male mice. This difference in ammonia metabolism was associated with fundamental structural differences between the female and male kidney. In the female mouse kidney, proximal tubules account for a lower percentage of the renal cortical parenchyma compared with the male kidney, whereas collecting ducts account for a greater percentage of the renal parenchyma than in male kidneys. To further investigate the mechanism(s) behind the greater ammonia excretion in female mice, we examined differences in the expression of proteins involved in renal ammonia metabolism and transport. Greater basal ammonia excretion in females was associated with greater expression of PEPCK, glutamine synthetase, NKCC2, Rhbg, and Rhcg than was observed in male mice. We conclude that there are sex differences in basal ammonia metabolism that involve both renal structural differences and differences in expression of proteins involved in ammonia metabolism.}, number={2}, journal={American Journal of Physiology - Renal Physiology}, author={Harris, A.N. and Lee, H.-W. and Osis, G. and Fang, L. and Webster, K.L. and Verlander, J.W. and Weiner, I.D.}, year={2018}, pages={F211–F222} }
 @article{fang_lee_chen_harris_romero_verlander_weiner_2018, title={Expression of the B splice variant of NBCe1 (SLC4A4) in the mouse kidney}, volume={315}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85052931250&partnerID=MN8TOARS}, DOI={10.1152/ajprenal.00515.2017}, abstractNote={Sodium-coupled bicarbonate transporters are critical for renal electrolyte transport. The electrogenic, sodium-coupled bicarbonate cotransporter, isoform 1 (NBCe1), encoded by the SLC4A4 geneencoded by the SLC4A4 gene has five multiple splice variants; the A splice variant, NBCe1-A, is the primary basolateral bicarbonate transporter in the proximal convoluted tubule. This study's purpose was to determine if there is expression of additional NBCe1 splice variants in the mouse kidney, their cellular distribution, and their regulation by metabolic acidosis. In wild-type mice, an antibody reactive only to NBCe1-A showed basolateral immunolabel only in cortical proximal tubule (PT) segments, whereas an antibody reactive to all NBCe1 splice variants (pan-NBCe1) showed basolateral immunolabel in PT segments in both the cortex and outer medulla. In mice with NBCe1-A deletion, the pan-NBCe1 antibody showed basolateral PT immunolabel in both the renal cortex and outer stripe of the outer medulla, and immunoblot analysis showed expression of a ~121-kDa protein. RT-PCR of mRNA from NBCe1-A knockout mice directed at splice variant-specific regions showed expression of only NBCe1-B mRNA. In wild-type kidney, RT-PCR confirmed expression of mRNA for the NBCe1-B splice variant and absence of mRNA for the C, D, and E splice variants. Finally, exogenous acid loading increased expression in the proximal straight tubule in the outer stripe of the outer medulla. These studies demonstrate that the NBCe1-B splice variant is present in the PT, and its expression increases in response to exogenous acid loading, suggesting it participates in the PT contribution to acid-base homeostasis.}, number={3}, journal={American Journal of Physiology - Renal Physiology}, author={Fang, L. and Lee, H.-W. and Chen, C. and Harris, A.N. and Romero, M.F. and Verlander, J.W. and Weiner, I.D.}, year={2018}, pages={F417–F428} }
 @article{harris_grimm_lee_delpire_fang_verlander_welling_weiner_2018, title={Mechanism of Hyperkalemia-Induced Metabolic Acidosis}, volume={29}, url={https://doi.org/10.1681/ASN.2017111163}, DOI={10.1681/ASN.2017111163}, abstractNote={Background Hyperkalemia in association with metabolic acidosis that are out of proportion to changes in glomerular filtration rate defines type 4 renal tubular acidosis (RTA), the most common RTA observed, but the molecular mechanisms underlying the associated metabolic acidosis are incompletely understood. We sought to determine whether hyperkalemia directly causes metabolic acidosis and, if so, the mechanisms through which this occurs.Methods We studied a genetic model of hyperkalemia that results from early distal convoluted tubule (DCT)-specific overexpression of constitutively active Ste20/SPS1-related proline-alanine-rich kinase (DCT-CA-SPAK).Results DCT-CA-SPAK mice developed hyperkalemia in association with metabolic acidosis and suppressed ammonia excretion; however, titratable acid excretion and urine pH were unchanged compared with those in wild-type mice. Abnormal ammonia excretion in DCT-CA-SPAK mice associated with decreased proximal tubule expression of the ammonia-generating enzymes phosphate-dependent glutaminase and phosphoenolpyruvate carboxykinase and overexpression of the ammonia-recycling enzyme glutamine synthetase. These mice also had decreased expression of the ammonia transporter family member Rhcg and decreased apical polarization of H+-ATPase in the inner stripe of the outer medullary collecting duct. Correcting the hyperkalemia by treatment with hydrochlorothiazide corrected the metabolic acidosis, increased ammonia excretion, and normalized ammoniagenic enzyme and Rhcg expression in DCT-CA-SPAK mice. In wild-type mice, induction of hyperkalemia by administration of the epithelial sodium channel blocker benzamil caused hyperkalemia and suppressed ammonia excretion.Conclusions Hyperkalemia decreases proximal tubule ammonia generation and collecting duct ammonia transport, leading to impaired ammonia excretion that causes metabolic acidosis.}, number={5}, journal={Journal of the American Society of Nephrology}, author={Harris, Autumn N. and Grimm, P. Richard and Lee, Hyun-Wook and Delpire, Eric and Fang, Lijuan and Verlander, Jill W. and Welling, Paul A. and Weiner, I. David}, year={2018}, month={May}, pages={1411–1425} }
 @article{lee_osis_harris_fang_romero_handlogten_verlander_weiner_2018, title={NBCe1-A Regulates Proximal Tubule Ammonia Metabolism under Basal Conditions and in Response to Metabolic Acidosis}, volume={29}, url={https://doi.org/10.1681/ASN.2017080935}, DOI={10.1681/ASN.2017080935}, abstractNote={Renal ammonia metabolism is the primary mechanism through which the kidneys maintain acid-base homeostasis, but the molecular mechanisms regulating renal ammonia generation are unclear. In these studies, we evaluated the role of the proximal tubule basolateral plasma membrane electrogenic sodium bicarbonate cotransporter 1 variant A (NBCe1-A) in this process. Deletion of the NBCe1-A gene caused severe spontaneous metabolic acidosis in mice. Despite this metabolic acidosis, which normally causes a dramatic increase in ammonia excretion, absolute urinary ammonia concentration was unaltered. Additionally, NBCe1-A deletion almost completely blocked the ability to increase ammonia excretion after exogenous acid loading. Under basal conditions and during acid loading, urine pH was more acidic in mice with NBCe1-A deletion than in wild-type controls, indicating that the abnormal ammonia excretion was not caused by a primary failure of urine acidification. Instead, NBCe1-A deletion altered the expression levels of multiple enzymes involved in proximal tubule ammonia generation, including phosphate-dependent glutaminase, phosphoenolpyruvate carboxykinase, and glutamine synthetase, under basal conditions and after exogenous acid loading. Deletion of NBCe1-A did not impair expression of key proteins involved in collecting duct ammonia secretion. These studies demonstrate that the integral membrane protein NBCe1-A has a critical role in basal and acidosis-stimulated ammonia metabolism through the regulation of proximal tubule ammonia-metabolizing enzymes.}, number={4}, journal={Journal of the American Society of Nephrology}, author={Lee, Hyun-Wook and Osis, Gunars and Harris, Autumn N. and Fang, Lijuan and Romero, Michael F. and Handlogten, Mary E. and Verlander, Jill W. and Weiner, I. David}, year={2018}, month={Apr}, pages={1182–1197} }
 @inproceedings{webster_lee_harris_romero_verlander_weiner_2018, title={NBCe1A Regulates Citrate Excretion During Hypokalemia Through NaDC1 Expression-Dependent and Independent Mechanisms}, booktitle={American Society of Nephrology, Kidney Week}, author={Webster, K.L. and Lee, H.W. and Harris, A.N. and Romero, M.F. and Verlander, J.W. and Weiner, I.D.}, year={2018}, month={Oct} }
 @article{brooks_walton_shmalberg_harris_2018, title={Novel treatment using topical malachite green for nasal phaeohyphomycosis caused by a new Cladophialophora species in a cat}, volume={4}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85126661023&partnerID=MN8TOARS}, DOI={10.1177/2055116918771767}, abstractNote={Case summaryA 1.5-year-old castrated male domestic shorthair cat presented with a 2 month history of progressive nasal swelling and hyporexia. Minimal improvement prior to referral was achieved with a course of antibiotics and glucocorticoids. Cytology of an ulcerative lesion on the dorsal aspect of the nose was consistent with a diagnosis of phaeohyphomycosis. The cat achieved static disease for 6 weeks following initiation of itraconazole but developed epistaxis at 9 weeks. CT of the head demonstrated nasal and frontal sinus involvement. Nasal biopsy and culture identified infection with a Cladophialophora species not previously reported to cause disease. Initial response to a combination of itraconazole and terbinafine was noted, but owing to severe thrombocytopenia this combination was discontinued. Voriconazole was used but discontinued because of adverse side effects. Posaconazole treatment was offered throughout the clinical course but rejected owing to financial constraints and an uncertain response to medical therapy. Rhinotomy with debulking of diseased tissue and topical malachite green treatment was performed. Following the procedure itraconazole was continued and the cat has had no recurrence for over 1 year. Relevance and novel informationInfections by Cladophialophora species have been reported in veterinary species, including cats. The specific fungal organism isolated from this cat has not been previously reported to cause disease in humans or animals and has only been described in the mangroves of Brazil. Furthermore, this is the first report to describe the use of topical malachite green as a treatment for refractory phaeohyphomycosis.}, number={1}, journal={Journal of Feline Medicine and Surgery Open Reports}, author={Brooks, I.J. and Walton, S.A. and Shmalberg, J. and Harris, A.}, year={2018} }
 @inproceedings{lee_harris_chen_coleman_welling_romero_verlander_weiner_2018, title={Proximal Tubule NBCe1-A- Dependent Regulation of Ammonia and Potassium Metabolism During Hypokalemia}, booktitle={American Society of Nephrology, Kidney Week}, author={Lee, H.W. and Harris, A.N. and Chen, C. and Coleman, R.A. and Welling, P.A. and Romero, M.F. and Verlander, J.W. and Weiner, I.D.}, year={2018}, month={Oct} }
 @inproceedings{harris_lee_osis_webster_verlander_weiner_2018, title={Sex Differences in Renal Ammonia Metabolism}, booktitle={Southern, Salt, Water & Kidney Club Conference}, author={Harris, A.N. and Lee, H.W. and Osis, G. and Webster, K.L. and Verlander, J.W. and Weiner, I.D.}, year={2018}, month={Dec} }
 @inproceedings{harris_lee_osis_webster_verlander_weiner_2018, title={Sex Differences in Renal Ammonia Metabolism}, booktitle={American Physiological Society, Cardiovascular, Renal and Metabolic Diseases: Sex-specific Implications for Physiology}, author={Harris, A.N. and Lee, H.W. and Osis, G. and Webster, K.L. and Verlander, J.W. and Weiner, I.D.}, year={2018}, month={Oct} }
 @inproceedings{lee_osis_harris_fang_verlander_weiner_2017, title={Axial Heterogeneity of Phosphate-Dependent Glutaminase Expression and Response to Metabolic Acidosis}, booktitle={American Society of Nephrology, Kidney Week}, author={Lee, H.W. and Osis, G. and Harris, A.N. and Fang, L. and Verlander, J.W. and Weiner, I.D.}, year={2017}, month={Nov} }
 @inproceedings{harris_grimm_lee_delpire_welling_verlander_weiner_2017, title={Effect of Hyperkalemia on Renal Ammonia Metabolism}, booktitle={American Society of Nephrology, Kidney Week}, author={Harris, A.N. and Grimm, P.R. and Lee, H.W. and Delpire, E.J. and Welling, P.A. and Verlander, J.W. and Weiner, I.D.}, year={2017}, month={Nov} }
 @inproceedings{lee_osis_harris_fang_chen_romero_handlogten_verlander_weiner_2017, title={Identification of Signaling Pathway Regulating Basal Acidosis–Stimulated Renal Ammonia Metabolism}, booktitle={Department of Medicine Celebration of Research}, author={Lee, H.W. and Osis, G. and Harris, A.N. and Fang, L. and Chen, C. and Romero, M.F. and Handlogten, M.E. and Verlander, J.W. and Weiner, I.D.}, year={2017}, month={Oct} }
 @inproceedings{harris_grimm_lee_delpire_welling_verlander_weiner_2017, title={Identification of the Mechanism of Acidosis in Type IV RTA- Hyperkalemia is the Culprit}, booktitle={Department of Medicine Research Celebration}, author={Harris, A.N. and Grimm, P.R. and Lee, H.W. and Delpire, E.J. and Welling, P.A. and Verlander, J.W. and Weiner, I.D.}, year={2017}, month={Oct} }
 @article{harris_beatty_estrada_winter_bohannon_sosa_hanscom_mainville_gallagher_2017, title={Investigation of an N-Terminal Prohormone of Brain Natriuretic Peptide Point-of-Care ELISA in Clinically Normal Cats and Cats With Cardiac Disease}, volume={31}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85021288939&partnerID=MN8TOARS}, DOI={10.1111/jvim.14776}, abstractNote={N-terminal prohormone of brain natriuretic peptide (NT-proBNP) concentrations may be increased in cats with various cardiac disorders. The point-of-care (POC) ELISA assay uses the same biologic reagents as the quantitative NT-proBNP ELISA. Previous studies have evaluated the sensitivity and specificity of the POC ELISA in cats with cardiac disease.To prospectively evaluate the diagnostic utility of the POC ELISA in a select population of cats.Thirty-eight client-owned cats presented to the University of Florida Cardiology Service for cardiac evaluation. Fifteen apparently healthy cats recruited as part of another study.Physical examination and echocardiography were performed in all cats. The POC ELISA was assessed visually as either positive or negative by a reader blinded to the echocardiographic findings, and results were analyzed relative to quantitative assay results.Twenty-six cats were diagnosed with underlying cardiac disease, and 27 cats were considered free of cardiac disease. Cats with cardiac disease included: 21 with hypertrophic cardiomyopathy, 2 with unclassified cardiomyopathy, 2 with restrictive cardiomyopathy, and 1 with 3rd degree atrioventricular (AV) block. The POC ELISA differentiated cats with cardiac disease with a sensitivity of 65.4% and specificity of 100%.The POC NT-proBNP ELISA performed moderately well in a selected population of cats. A negative test result cannot exclude the presence of underlying cardiac disease, and a positive test result indicates that cardiac disease likely is present, but further diagnostic investigation would be indicated for a definitive diagnosis.}, number={4}, journal={Journal of Veterinary Internal Medicine}, author={Harris, A.N. and Beatty, S.S. and Estrada, A.H. and Winter, B. and Bohannon, M. and Sosa, I. and Hanscom, J. and Mainville, C.A. and Gallagher, A.E.}, year={2017}, pages={994–999} }
 @inproceedings{harris_osis_lee_webster_verlander_weiner_2017, title={Sex Differences in Renal Ammonia Metabolism}, booktitle={American Society of Nephrology, Kidney Week}, author={Harris, A.N. and Osis, G. and Lee, H.W. and Webster, K.L. and Verlander, J.W. and Weiner, I.D.}, year={2017}, month={Nov} }
 @inproceedings{lee_osis_harris_webster_holmes_rossano_romero_verlander_weiner_2017, title={The A-Splice Variant of NBCe1 (NBCe1-A), is Necessary for the Renal Ammonia and K Response to Hypokalemia}, booktitle={American Society of Nephrology, Kidney Week}, author={Lee, H.W. and Osis, G. and Harris, A.N. and Webster, K.L. and Holmes, H.L. and Rossano, A.J. and Romero, M.F. and Verlander, J.W. and Weiner, I.D.}, year={2017}, month={Nov} }
 @inproceedings{lee_osis_harris_fang_holmes_rossano_romero_verlander_weiner_2017, title={The A-Splice Variant of NBCe1, is Necessary for Basal and Acidosis-Stimulated Renal Ammonia Metabolism}, booktitle={American Society of Nephrology, Kidney Week}, author={Lee, H.W. and Osis, G. and Harris, A.N. and Fang, L. and Holmes, H.L. and Rossano, A.J. and Romero, M.F. and Verlander, J.W. and Weiner, I.D.}, year={2017}, month={Nov} }
 @article{harris_estrada_gallagher_winter_lamb_bohannon_hanscom_mainville_2017, title={Biologic variability of N-terminal pro-brain natriuretic peptide in adult healthy cats}, volume={19}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85011636349&partnerID=MN8TOARS}, DOI={10.1177/1098612X15623825}, abstractNote={Objectives The biologic variability of N-terminal pro-brain natriuretic peptide (NT-proBNP) and its impact on diagnostic utility is unknown in healthy cats and those with cardiac disease. The purpose of this study was to determine the biologic variation of NT-proBNP within-day and week-to-week in healthy adult cats. Methods Adult cats were prospectively evaluated by complete blood count (CBC), biochemistry, total thyroxine, echocardiography, electrocardiography and blood pressure, to exclude underlying systemic or cardiac disease. Adult healthy cats were enrolled and blood samples were obtained at 11 time points over a 6 week period (0, 2 h, 4 h, 6 h, 8 h, 10 h and at weeks 2, 3, 4, 5 and 6). The intra-individual (coefficient of variation [CV I ]) biologic variation along with index of individuality and reference change values (RCVs) were calculated. Univariate models were analyzed and included comparison of the six different time points for both daily and weekly samples. This was followed by a Tukey’s post-hoc adjustment, with a P value of <0.05 being significant. Results The median daily and weekly CV I for the population were 13.1% (range 0–28.7%) and 21.2% (range 3.9–68.1%), respectively. The index of individuality was 0.99 and 1 for daily and weekly samples, respectively. The median daily and weekly RCVs for the population were 39.8% (range 17.0–80.5%) and 60.5% (range 20.1–187.8%), respectively. Conclusions and relevance This study demonstrates high individual variability for NT-proBNP concentrations in a population of adult healthy cats. Further research is warranted to evaluate NT-proBNP variability, particularly how serial measurements of NT-proBNP may be used in the diagnosis and management of cats with cardiac disease.}, number={2}, journal={Journal of Feline Medicine and Surgery}, author={Harris, A.N. and Estrada, A.H. and Gallagher, A.E. and Winter, B. and Lamb, K.E. and Bohannon, M. and Hanscom, J. and Mainville, C.A.}, year={2017}, pages={216–223} }
 @article{harris_armentano_torres_gallagher_2016, title={Use of endoscopic-assisted argon plasma coagulation for the treatment of colonic vascular ectasia (angiodysplasia) in an adult dog}, volume={248}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84958559093&partnerID=MN8TOARS}, DOI={10.2460/javma.248.5.526}, abstractNote={Abstract CASE DESCRIPTION A 10-year-old neutered male mixed-breed dog was evaluated for a 5-year history of intermittent hematochezia and chronic anemia that were unresponsive to medical treatment. CLINICAL FINDINGS Colonoscopy revealed multifocal areas of coalescing tortuous mucosal blood vessels throughout the colon and rectum. Colonic vascular ectasia (angiodysplasia) was diagnosed on the basis of the endoscopic appearance of the lesions. TREATMENT AND OUTCOME The dog failed to respond to traditional medical treatments for colonic vascular ectasia and required multiple plasma and blood transfusions. The dog received 4 endoscopic-assisted argon plasma coagulation treatments, which resulted in long-term resolution of gastrointestinal hemorrhage. Colonic perforation occurred during the third argon plasma coagulation treatment. The perforation was surgically repaired. The dog remained free from clinical signs of colonic vascular ectasia for > 1 year after the third argon plasma coagulation treatment and was euthanized because of clinical deterioration associated with progressive heart disease. CLINICAL RELEVANCE Endoscopic-assisted argon plasma coagulation treatment is a novel treatment for dogs with colonic vascular ectasia and provided long-term resolution of clinical signs for the dog of this report. In human patients, complications associated with endoscopic-assisted argon plasma coagulation treatment include colonic perforation, which also occurred in the dog of this report.}, number={5}, journal={Journal of the American Veterinary Medical Association}, author={Harris, A.N. and Armentano, R.A. and Torres, A.R. and Gallagher, A.E.}, year={2016}, pages={526–531} }
 @inproceedings{harris_estrada_gallagher_mincey_2015, title={Biological Variability of NT-proBNP in Adult Healthy Cats}, booktitle={American College of Veterinary Internal Medicine, Forum}, author={Harris, A.N. and Estrada, A.H. and Gallagher, A.E. and Mincey, B.}, year={2015}, month={Jun} }
 @inproceedings{harris_estrada_gallagher_mincey_2015, title={Biological Variability of NT-proBNP in Adult Healthy Cats}, booktitle={Phi Zeta Proceedings, University of Florida College of Veterinary Medicine}, author={Harris, A.N. and Estrada, A.H. and Gallagher, A.E. and Mincey, B.}, year={2015}, month={Mar} }
 @article{kukanich_kukanich_harris_heinrich_2014, title={Effect of sucralfate on oral minocycline absorption in healthy dogs}, volume={37}, ISSN={0140-7783 1365-2885}, url={http://dx.doi.org/10.1111/jvp.12116}, DOI={10.1111/jvp.12116}, abstractNote={Sucralfate and minocycline may be administered concurrently to dogs. The relative bioavailability of tetracyclines may be reduced if administered with sucralfate, but studies confirming these interactions in dogs are not available. This study evaluated the pharmacokinetics of oral minocycline in dogs (M), determined the effects of concurrent administration of sucralfate and minocycline (MS) on minocycline pharmacokinetics, determined the effects of delaying sucralfate administration by 2 h (MS+2) on minocycline pharmacokinetics, and established dosing recommendations based on pharmacodynamic indices. Oral minocycline (300 mg) and sucralfate suspension (1 g) were administered to five greyhounds in a randomized crossover design. Minocycline plasma concentrations were evaluated using liquid chromatography with mass spectrometry. The maximum plasma concentration (C MAX ) and area under the curve (AUC) of minocycline were 1.15 μg/mL and 8.0 h* μg/mL, respectively. The C MAX and AUC were significantly lower ( P < 0.05) in the MS group (C MAX = 0.33 μg/mL, AUC 3.0 h*μg/mL) compared with M or MS+2 (C MAX = 0.97 μg/mL, AUC 10.3 h*μg/mL). Delaying sucralfate by 2 h did not decrease oral minocycline absorption, but concurrent administration significantly decreased minocycline absorption. A dose of 7.5 mg/kg p.o. q12 h achieves the pharmacodynamic index for a bacterial minimum inhibitory concentration (MIC) of 0.25 μg/mL (AUC:MIC≥33.9).}, number={5}, journal={Journal of Veterinary Pharmacology and Therapeutics}, publisher={Wiley}, author={KuKanich, K. and KuKanich, B. and Harris, A. and Heinrich, E.}, year={2014}, month={Mar}, pages={451–456} }
 @inproceedings{harris_estrada_gallagher_mincey_2014, title={Investigation on NT-proBNP Point-of-Care SNAP ELISA in Clinically Normal Adult Feline Patients}, booktitle={European College of Veterinary Internal Medicine Forum}, author={Harris, A.N. and Estrada, A.H. and Gallagher, A.E. and Mincey, B.}, year={2014}, month={Sep} }
 @article{ammari_harris_stokes_bailey_pinchuk_2014, title={Negative Regulatory Effects of Phosphatidylinositol 3-Kinase Pathway on Phagocytosis and Macropinocytosis in Bovine Monocytes}, volume={1}, number={2}, journal={Journal of Veterinary Medicine Research}, author={Ammari, M.G. and Harris, A.N. and Stokes, J.V. and Bailey, B.H. and Pinchuk, L.M.}, year={2014}, month={Aug}, pages={1008} }
 @inproceedings{harris_ammari_stokes_howe_hart_pinchuk_2009, title={Involvement of Phosphatidylinositol 3-Kinase Pathway in Salmonella Kentucky uptake in bovine monocytes}, booktitle={Merck Veterinary Scholars National NIH Symposium}, author={Harris, A.N. and Ammari, M. and Stokes, J. and Howe, K. and Hart, B. and Pinchuk, L.}, year={2009}, month={Aug} }