Gastric pH and serum gastrin concentration in age-matched healthy dogs and dogs with chronic kidney disease.

BACKGROUND: Gastric hyperacidity and hypergastrinemia are purported to cause gastric ulceration in dogs with chronic kidney disease (CKD); however, no published studies have evaluated gastric pH with serum gastrin concentrations in dogs with CKD. HYPOTHESIS: To compare mean intragastric pH, mean percent pH distribution, and serum gastrin concentrations in dogs with CKD to age-matched, healthy dogs. We hypothesized there would be no difference in mean gastric pH or serum gastrin between groups. ANIMALS: Thirteen dogs with CKD; 10 aged-matched healthy dogs. METHODS: Prospective, case-control study. Serum chemistry, complete blood count, urinalysis, and serum gastrin concentrations were evaluated in all dogs before radiographic-assisted gastric placement of a pH capsule. Forty-eight-hour continuous gastric pH monitoring was performed in all dogs. Serum gastrin concentration, mean pH, and mean percentage time that gastric pH was strongly acidic (pH <1 and pH <2) were compared between groups using a repeated measures mixed-model ANOVA. RESULTS: No significant differences were observed between groups for any pH measurements, including mean ± SD gastric pH (CKD, 2.37 ± 0.87; healthy, 2.39 ± 0.99; P > .05). Serum gastrin concentrations were not significantly different between groups (median [range]: CKD, 10.5 ng/dL [<10-17.1]; healthy, 10.9 ng/dL [<10-15]; P > .05). CONCLUSIONS AND CLINICAL IMPORTANCE: Our client-owned dogs with CKD did not have lower gastric pH or higher serum gastrin concentrations compared to healthy dogs. Our results suggest that prophylactic gastric acid suppression in dogs with CKD is not warranted unless other clinical indications for use are present.

Prevalence of dental disorders among people with mental illness: An umbrella review.

OBJECTIVE: Psychiatric patients have increased rates of comorbid physical illness. There are less data on dental disease, especially decay, despite risk factors including lifestyle and psychotropic side effects such as xerostomia. We therefore undertook an umbrella review of all meta-analyses on the association between mental illness and oral health. METHODS: We searched PubMed, MEDLINE, PsycINFO, the Cochrane Central Register of Controlled Trials, Embase and CINAHL. Articles were independently assessed. Outcomes were caries, periodontal disease, erosion, and partial or total tooth loss (edentulism), measured where possible with standardised measures such as the mean number of decayed, missing and filled teeth or surfaces. Quality was assessed in line with National Institutes of Health guidelines. RESULTS: We identified 11 meta-analyses. The most information and strongest association was between dental decay and severe mental illness or substance use, as well as erosion and eating disorders. Depressive, anxiety and eating disorders were also associated with caries, but the datasets were small. People with severe mental illness had nearly three times the odds of having lost all their teeth than the general community (odds ratio = 2.81, 95% confidence interval = [1.73, 4.57]) and those with depression between 1.17 and 1.32. Findings for periodontal disease were more equivocal, possibly because of study heterogeneity. CONCLUSION: Mental health clinicians should screen for oral diseases when treating those with mental illness and facilitate referral to affordable dental clinics when indicated. Prevention should be a priority, including the promotion of dental care, as well as the management of xerostomia when psychopharmacologic agents are prescribed.

Appetite-stimulating effects of once-daily omeprazole in cats with chronic kidney disease: Double-blind, placebo-controlled, randomized, crossover trial.

BACKGROUND: Cats with moderate to advanced chronic kidney disease (CKD) often display clinical signs such as vomiting and decreased appetite, and frequently receive omeprazole or other acid suppressants despite a lack of evidence to support their use. HYPOTHESIS/OBJECTIVES: To evaluate the effect of once-daily PO omeprazole on appetite in cats with CKD. We hypothesized that omeprazole would improve subjective appetite assessments in cats with CKD. ANIMALS: Fourteen client-owned cats with International Renal Interest Society (IRIS) stage 2 or 3 CKD and hyporexia. METHODS: Cats were prospectively enrolled in a multi-institutional, double-blinded, randomized, crossover study to evaluate the effect of a 14-day trial of once-daily PO omeprazole (1 mg/kg) or placebo (lactose gel capsule) on vomiting frequency and appetite. A daily log was completed by the owner during all treatment and rest periods to assess appetite using a subjective, qualitative, and 5-point scoring system. Mixed model analyses of variance were performed to determine if average daily percentage food consumed or appetite score, as measured by subjective owner assessment, differed between treatments. RESULTS: Compared to placebo, a negligible but statistically significant difference in percentage of food consumed was observed between treatments (P = .04) with once-daily omeprazole treatment resulting in a 2.7% increase in food consumption compared to placebo. No significant difference, however, was found in appetite score, body weight, or serum creatinine concentration between treatments. CONCLUSIONS AND CLINICAL IMPORTANCE: Once-daily omeprazole does not markedly increase appetite in cats with CKD and should not be used as a first-line treatment in the absence of evidence of gastrointestinal ulceration.

A prospective, randomized, masked, placebo-controlled crossover study for the effect of 10 mg omeprazole capsules on gastric pH in healthy dogs.

BACKGROUND: Enteric-coated omeprazole capsules are commonly used as a gastric acid suppressant in dogs. However, the efficacy of this formulation has not been evaluated for clinical use in dogs. HYPOTHESIS/OBJECTIVES: To evaluate the efficacy of a 10 mg PO omeprazole capsule (TriviumVet) undergoing FDA approval to increase gastric pH in dogs. We hypothesized that encapsulated omeprazole would significantly increase the gastric pH compared to placebo and reach pH goals extrapolated from people for the treatment of esophagitis and duodenal ulceration. ANIMALS: Six healthy research dogs. METHODS: Randomized, blinded, 2-way crossover study. Dogs were PO administered omeprazole at 0.5 to 1.0 mg/kg or placebo (empty gelatin capsules) twice-daily for 5 days. The intragastric pH was recorded on days 2 to 5 of treatment. Mean pH and the mean percentage time (MPT) intragastric pH was ≥3 or ≥4 were compared between and within treatment groups. RESULTS: Dogs treated with omeprazole had a significantly higher MPT ± SD intragastric pH ≥3 (91.2% ± 11.0%), ≥4 (86.9% ± 13.7%) and mean ± SD pH (5.4 ± 0.8) than dogs treated with placebo (19.7% ± 15.5%, 28.3 ± 20.7, and 2.4 ± 1.0, respectively) (P < .001 for all). CONCLUSIONS AND CLINICAL IMPORTANCE: The 10 mg enteric-coated omeprazole capsule PO administered evaluated in this study is an effective gastric acid suppressant in healthy dogs.

Comparative analysis of the effect of PO administered acid suppressants on gastric pH in healthy cats.

BACKGROUND: Proton pump inhibitors (PPIs) are among the most commonly prescribed medications for esophagitis and upper gastrointestinal erosion and ulceration in cats. Newer PPIs such as lansoprazole and esomeprazole are believed to be effective in cats, but the effect of many of these PPIs on gastric pH in cats has not been explored. HYPOTHESIS/OBJECTIVES: To evaluate the efficacy of PO esomeprazole, dexlansoprazole, and lansoprazole on intragastric pH in healthy cats. We hypothesized that esomeprazole and lansoprazole would provide superior acid suppression compared to dexlansoprazole and reach pH goals extrapolated from people for the treatment of esophagitis and duodenal ulceration. ANIMALS: Twelve healthy research cats. METHODS: Randomized, 3-way crossover study. Cats were given esomeprazole and lansoprazole at a dosage of 1 mg/kg PO q12h or dexlansoprazole at 6 mg/kg PO q12h. Intragastric pH was recorded at baseline and for 4 days of treatment. Mean pH and the mean percentage time (MPT) intragastric pH was ≥3 or ≥4 were compared among and within treatment groups. RESULTS: Cats treated with lansoprazole had a lower MPT ± SD of intragastric pH ≥3 (8.8 ± 6.8%) and mean ± SD pH (1.6 ± 0.5) than did cats treated with dexlansoprazole (41.2 ± 34.6% and 3.11 ± 1.6, respectively) or esomeprazole (54 ± 33.8% and 4.1 ± 3.9, respectively;P ≤ .04). Esomeprazole was the only treatment that achieved the goals defined for people for the treatment of duodenal ulceration by Day 4 of treatment (MPT ± SD of intragastric pH ≥4 of 77.1 ± 29.2%). CONCLUSIONS AND CLINICAL IMPORTANCE: Orally administered esomeprazole might be a superior acid suppressant in cats compared to PO lansoprazole or dexlansoprazole.

The effect of combined carprofen and omeprazole administration on gastrointestinal permeability and inflammation in dogs.

BACKGROUND: Proton pump inhibitors (eg, omeprazole) commonly are administered concurrently with nonsteroidal anti-inflammatory drugs (NSAIDs; eg, carprofen) as prophylaxis to decrease the risk of gastrointestinal (GI) injury. However, evidence to support this practice is weak, and it might exacerbate dysbiosis and inflammation. HYPOTHESIS/OBJECTIVES: To evaluate the effect of carprofen alone or combined with omeprazole in dogs. We hypothesized that coadministration of omeprazole and carprofen would significantly increase GI permeability and dysbiosis index (DI) compared to no treatment or carprofen alone. ANIMALS: Six healthy adult colony beagle dogs. METHODS: Gastrointestinal permeability and inflammation were assessed by serum lipopolysaccharide (LPS) concentration, plasma iohexol concentration, fecal DI, and fecal calprotectin concentration in a prospective, 3-period design. In the first 7-day period, dogs received no intervention (baseline). During the 2nd period, dogs received 4 mg/kg of carprofen q24h PO for 7 days. In the 3rd period, dogs received 4 mg/kg of carprofen q24h and 1 mg/kg of omeprazole q12h PO for 7 days. Gastrointestinal permeability testing was performed at the end of each period. Data were analyzed using repeated measures mixed model analysis of variance with Tukey-Kramer post hoc tests (P < .05). RESULTS: Serum LPS and plasma iohexol concentrations did not differ between treatments. Fecal calprotectin concentrations differed between treatments (P = .03). The DI varied over time based on the treatment received (P = .03). Coadministration of omeprazole and carprofen significantly increased fecal calprotectin concentration and DI compared to baseline and carprofen alone. CONCLUSIONS AND CLINICAL IMPORTANCE: Omeprazole prophylaxis induces fecal dysbiosis and increases intestinal inflammatory markers when coadministered with carprofen to otherwise healthy dogs with no other risk factors for GI bleeding.

Comparative analysis of the effect of IV administered acid suppressants on gastric pH in dogs.

BACKGROUND: Upper gastrointestinal (GI) ulceration and bleeding in critically ill dogs can cause severe anemia and increase morbidity. Acid suppressants using proton pump inhibitors or histamine-2 receptor blockers administered IV is commonly recommended. HYPOTHESIS/OBJECTIVES: To evaluate the efficacy of IV administered esomeprazole, pantoprazole, and famotidine constant rate infusion (CRI) on increasing the intragastric pH of dogs. We hypothesized that esomeprazole and famotidine CRI would provide superior acid suppression compared to pantoprazole and reach pH goals for the treatment of GI bleeding. ANIMALS: Nine healthy research Beagles. METHODS: Randomized, 3-way crossover. Dogs received pantoprazole or esomeprazole at 1 mg/kg IV q12h and famotidine with a loading dose of 1 mg/kg followed by 8 mg/kg IV CRI daily for 3 consecutive days. The intragastric pH was recorded at baseline and for 72 hours of treatment. The mean pH and the mean percentage time (MPT) the intragastric pH was ≥3 or ≥4 were compared among and within treatment groups. RESULTS: Significant increases in mean pH (P < 0.0001), MPT ≥3 (P < 0.001), and MPT ≥4 (P = 0.0006) were noted over time with all 3 treatments. The time effect did not differ by treatment for mean pH, MPT ≥3, and MPT ≥4 (P = .29, .56, and .37, respectively); however, only esomeprazole and famotidine CRI achieved the goals established for the treatment of gastroduodenal ulceration in people. CONCLUSIONS AND CLINICAL IMPORTANCE: Famotidine CRI and esomeprazole might be superior acid suppressants compared to standard doses of pantoprazole for the first 72 hours of treatment.

THE EFFECTS OF PROCEDURE DURATION AND ATIPAMEZOLE ADMINISTRATION ON HYPERKALEMIA IN TIGERS (PANTHERA TIGRIS) AND LIONS (PANTHERA LEO) ANESTHETIZED WITH α-2 AGONISTS.

A retrospective analysis of 40 extended (>2 hr) anesthetic events in eight lions (Panthera leo) and 32 tigers (Panthera tigris) was performed using a hierarchical linear growth curve model to assess the effects of anesthetic time, α-2 adrenoreceptor agonist dosages, administration of atipamezole, and biochemical parameters on rising plasma K+ concentrations. Hyperkalemia was first noted at a mean time of 187 min (range: 131-226 min), with time under anesthesia as a statistically significant predictor of K+ concentration (P < 0.0001). A significant two-way interaction between time and atipamezole administration (P = 0.0082) for rising K+ concentrations was demonstrated, indicating that administration of atipamezole can mitigate the rise in K+ concentrations. Administration of atipamezole beyond 150 min of anesthetic time was less effective in reducing K+ concentrations than if administered earlier. Electrocardiographic abnormalities were noted in eight animals, including three hyperkalemic individuals. Lions developed significantly greater plasma K+ concentrations than tigers (P = 0.0009) during anesthesia. No biochemical parameter was identified as a significant indicator of which individuals will develop hyperkalemia. Clinicians anesthetizing any large nondomestic felid should monitor electrolytes regularly during anesthetic events; consider early, partial- to full-dose reversal of α-2 agonists; and be prepared to correct potentially life-threatening electrocardiographic abnormalities resulting from hyperkalemia.

Evaluation of the effect of a famotidine continuous rate infusion on intragastric pH in healthy dogs.

BACKGROUND: Famotidine is sometimes administered as a continuous rate infusion (CRI) to treat gastrointestinal ulceration in critically ill dogs. However, clinical studies have not evaluated the efficacy of a famotidine CRI in dogs. HYPOTHESIS/OBJECTIVES: To evaluate the efficacy of famotidine at raising intragastric pH when it is administered as a CRI in dogs. We hypothesized that CRI treatment with famotidine would meet clinical goals for raising intragastric pH ≥3 and 4. ANIMALS: Nine healthy Beagle dogs. METHODS: Randomized 2-way crossover. All dogs received 1.0 mg/kg IV q12h famotidine or CRI famotidine at 1.0 mg/kg IV loading dose and 8.0 mg/kg/d for 3 consecutive days. Beginning on day 0 of treatment, intragastric pH monitoring was used to continuously record intragastric pH. Mean percentage times (MPTs) for which intragastric pH was ≥3 and ≥4 were compared between groups using analysis of variance. RESULTS: There was a statistically significant difference (P < .05) in MPT ≥3 and ≥4 between the CRI and IV q12h groups on all treatment days. On days 1, 2, and 3, the MPTs ± SD for which pH was ≥3 were 92.1 ± 8.5, 96.3 ± 6.2, and 90.0 ± 15.7 for the CRI treatment group and 49.3 ± 27.3, 42.2 ± 19.6, and 45.8 ± 10.1, respectively, for the twice-daily group. CONCLUSIONS AND CLINICAL IMPORTANCE: These results suggest that a famotidine CRI, but not standard doses of famotidine, achieves the clinical goals established in people to promote healing of gastric tissue injury and offers an alternative to intravenous treatment with proton pump inhibitors in dogs.

Postmortem evaluation of renal tubular vacuolization in critically ill dogs.

OBJECTIVE: To describe the frequency of renal tubular vacuolization (RTV) as a surrogate of osmotic nephrosis and assess hyperosmolar agents as predictors of RTV severity. DESIGN: Retrospective study (February 2004-October 2014). SETTING: Veterinary teaching hospital. ANIMALS: Fifty-three client-owned, critically ill dogs that had a postmortem examination. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The frequency, severity, and location of RTV were determined in small group of critically ill dogs postmortem. Logistic regression was performed to assess cumulative 6% HES (670/0.75) and mannitol dose as predictors for RTV severity with presenting serum creatinine concentration, cumulative furosemide dose, and duration of hospitalization as covariates. RTV was noted in 45 (85%) of 53 critically ill dogs and was most commonly located to the medullary rays (68%). Cumulative 6% HES (670/0.75) dose (P = 0.009) and presenting serum creatinine concentration (P = 0.027) were significant predictors of RTV severity. For every 1 mL/kg increase in 6% HES (670/0.75) dose that a dog received, there was 1.6% increased chance of having more severe RTV (OR 1.016; 95% CI 1.004-1.029). In addition, for every 88.4 µmol/L (1 mg/dL) increase in presenting serum creatinine, there was a 22.7% increased chance of having more severe RTV (OR 1.227; 95% CI 1.023-1.472). Cumulative mannitol (P = 0.548) and furosemide (P = 0.136) doses were not significant predictors of RTV severity. CONCLUSION: In a small group of critically ill dogs, there was a high frequency of RTV identified on postmortem examination. Administration of 6% HES (670/0.75) and presenting serum creatinine concentration were significant predictors of RTV severity. Larger prospective studies are needed to determine the etiology and significance of RTV in dogs.

The frequency of oral famotidine administration influences its effect on gastric pH in cats over time.

BACKGROUND: Famotidine is commonly administered to cats. Prolonged famotidine administration results in decreased efficacy in humans, dogs, and cows, but the long-term effects in cats are unknown. OBJECTIVES: To compare the effect of 2 oral administration frequencies of famotidine, twice daily (Group 1) and twice daily every second day (Group 2), on intragastric pH and serum gastrin concentrations in cats. We hypothesized a diminished effect on intragastric pH would be observed over time in Group 1 but not Group 2. ANIMALS: Sixteen healthy cats. METHODS: Randomized, 2-factor repeated measures crossover design. Cats received 0.5-1.24 mg/kg (median, 0.87 mg/kg) famotidine twice daily or twice daily every second day for 14 consecutive days. Intragastric pH monitoring was used to record intragastric pH on treatment days 1-3 and 11-13. Mean pH and mean percentage time (MPT) intragastric pH was ≥3 and 4 were compared between and within treatment groups by analysis of variance. RESULTS: Significant treatment group by time interactions were observed for mean intragastric pH, MPT intragastric pH ≥3 and 4 (P = .009, P = .02, P = .005, respectively). Interaction post hoc tests identified significant decreases in mean intragastric pH (P = .001), MPT ≥3 (P = .001), and MPT ≥4 (P = .001) on day 13 compared to day 1 in Group 1 but not in Group 2. CONCLUSIONS AND CLINICAL IMPORTANCE: Oral famotidine administration results in a diminished effect on intragastric pH in healthy cats when given twice daily every day.

Omeprazole Minimally Alters the Fecal Microbial Community in Six Cats: A Pilot Study.

Although they have historically been thought of as safe medications, proton pump inhibitors such as omeprazole have been associated with an increased risk of enteric, particularly Clostridium difficile, infections in people. In cats, omeprazole is often the first choice acid suppressant prescribed for the treatment of upper gastrointestinal (GI) ulceration and bleeding. Despite this, no studies to date have explored the effect of omeprazole on the feline fecal microbiome and metabolome. Therefore, the purpose of this pilot study was to evaluate the effect of prolonged omeprazole administration on the fecal microbiome and metabolome in healthy cats to identify targets for analysis in a larger subset of cats with GI disease. A within-subjects, before and after, pilot study was performed whereby six healthy adult cats received 60 days of placebo (250 mg lactose PO q 12 h) followed by 5 mg (0.83-1.6 mg/kg PO q 12 h) omeprazole. On days 0, 30, and 60 of placebo and omeprazole therapy, the fecal microbiome and metabolome were characterized utilizing 16S ribosomal RNA sequencing by Illumina and untargeted mass spectrometry-based methods, respectively. Omeprazole administration resulted in no significant changes in the global microbiome structure or richness. However, transient changes were noted in select bacterial groups with omeprazole administration resulting in an increased sequence percentage of Streptococcus, Lactobacillus, Clostridium, and Faecalibacterium spp. and a decreased sequence percentage of Bifidobacterium spp. Significance was lost for all of these bacterial groups after adjustment for multiple comparisons. The fecal concentration of O-acetylserine and aminomalonate decreased with omeprazole therapy, but significance was lost after adjustment for multiple comparisons. The results of this pilot study conclude that omeprazole has a mild and transient impact on the fecal microbiome and metabolome when orally administered to healthy cats for 60 days. Based on the findings of this pilot study, evaluation of the effect of omeprazole specifically on Streptococcus, Lactobacillus, Clostridium, Faecalibacterium, and Bifidobacterium spp. is warranted in cats with primary GI disease.

Buprenorphine Depresses Respiratory Variability in Obese Mice with Altered Leptin Signaling.

BACKGROUND: Opiate-induced respiratory depression is sexually dimorphic and associated with increased risk among the obese. The mechanisms underlying these associations are unknown. The present study evaluated the two-tailed hypothesis that sex, leptin status, and obesity modulate buprenorphine-induced changes in breathing. METHODS: Mice (n = 40 male and 40 female) comprising four congenic lines that differ in leptin signaling and body weight were injected with saline and buprenorphine (0.3 mg/kg). Whole-body plethysmography was used to quantify the effects on minute ventilation. The data were evaluated using three-way analysis of variance, regression, and Poincaré analyses. RESULTS: Relative to B6 mice with normal leptin, buprenorphine decreased minute ventilation in mice with diet-induced obesity (37.2%; P < 0.0001), ob/ob mice that lack leptin (62.6%; P < 0.0001), and db/db mice with dysfunctional leptin receptors (65.9%; P < 0.0001). Poincaré analyses showed that buprenorphine caused a significant (P < 0.0001) collapse in minute ventilation variability that was greatest in mice with leptin dysfunction. There was no significant effect of sex or body weight on minute ventilation. CONCLUSIONS: The results support the interpretation that leptin status but not body weight or sex contributed to the buprenorphine-induced decrease in minute ventilation. Poincaré plots illustrate that the buprenorphine-induced decrease in minute ventilation variability was greatest in mice with impaired leptin signaling. This is relevant because normal respiratory variability is essential for martialing a compensatory response to ventilatory challenges imposed by disease, obesity, and surgical stress.

Mechlorethamine, vincristine, melphalan and prednisolone rescue chemotherapy protocol for resistant feline lymphoma.

Objectives The goals of this retrospective study were to evaluate the use of mechlorethamine, vincristine, melphalan and prednisolone (MOMP) chemotherapy for rescue of feline lymphoma, to describe the protocol's toxicity and to determine prognostic indicators for progression-free survival. Methods The medical records of 12 cats treated with MOMP chemotherapy at the University of Tennessee Veterinary Medical Center between 2007 and 2017 were evaluated. Parameters assessed included lymphoma cell size, anatomical location, number of previous chemotherapy drugs and number of previous rescue protocols received. Chemotherapy-related toxicity was also described. Results Seven of 12 cats responded to this rescue protocol. Three cats experienced complete response and four cats achieved partial response for a median duration of 39 days (range 14-345 days). Cats that achieved complete response had a significantly longer median progression-free survival than cats that did not respond to treatment. Five of 12 cats developed hematologic toxicity (neutropenia) and one cat developed gastrointestinal toxicity. Toxicity was mild in most cases; no cats needed to be hospitalized. Neutropenia was associated with increased progression-free survival. Conclusions and relevance MOMP is a safe and effective rescue chemotherapy protocol for cats with relapsing and refractory lymphoma.

Retrospective analysis of the effect of acid-suppressant therapy on clinicopathologic parameters of cats with chronic kidney disease.

Objectives The aim was to retrospectively evaluate the effects of acid-suppressant therapy in a population of cats with chronic kidney disease (CKD). The study objectives were to evaluate the effects of acid-suppressant therapy on clinicopathologic variables and progression of CKD over time. Methods The databases of two institutions were searched over an 11 year time span for cats fitting inclusion criteria for CKD. A total of 89 cats met the criteria for inclusion and were grouped according to either early (ie, stages 1-2) or advanced (ie, stages 3-4) CKD. Variables were statistically analyzed before and after treatment with either: (1) proton pump inhibitors (PPIs; n = 17), (2) histamine-2 receptor antagonists (H2RAs; n = 30), (3) combined acid-suppressant therapy (PPI + H2RA; n = 6) or (4) no acid-suppressant therapy (n = 36). Shapiro-Wilk testing and Q-Q plots were used to assess normality and variance, respectively. A complete randomized design with a mixed-effects repeated measures ANOVA was used to evaluate for differences in stage, treatment and time, as well as the interaction between these effects. Results A significant increase in blood creatinine concentration was found over time independent of severity of CKD and treatment group ( P = 0.0087). A significant increase in blood sodium concentration (change of 3.12 mmol/l) was found independent of stage in cats receiving PPI therapy ( P = 0.0109). A significant decrease in total blood magnesium (change of 0.15 mmol/l) was detected in two cats with early CKD receiving combined acid suppressants ( P = 0.0025). Conclusions and relevance Results of this retrospective study suggest that cats with CKD receiving PPI therapy may develop alterations in blood sodium concentrations but do not experience more rapid progression of CKD.