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Case Report: Persistent Moderate-to-Severe Creatine Kinase Enzyme Activity Elevation in a Subclinical Dog

ABSTRACT: A 4-year-old, male-castrated, mixed breed dog was presented for a routine wellness examination at which time a moderate increase in serum creatine kinase (CK) enzyme activity (hyperCKemia) (15,137 IU/L; reference interval 10–200 IU/L), and moderate increases in alanine transaminase and aspartate aminotransferase enzyme activities were first identified. There was no history of clinical abnormalities (e.g., lethargy, lameness, anorexia, dysphagia, weakness, gait abnormalities, or exercise intolerance) and the physical examination was unremarkable. The dog was screened for several relevant potential infectious diseases known to cause inflammatory myopathies and was treated empirically with clindamycin. The serum total CK enzyme activity remained increased, which prompted recommendations for an echocardiogram, electromyogram (EMG), and muscle biopsy acquisition. The echocardiogram and electrocardiographic monitoring were unremarkable. The EMG and muscle biopsies were declined by the owner. The dog was evaluated several times in the subsequent 5 years and remained subclinical with unremarkable physical examinations despite a persistent moderate-to-severe hyperCKemia. Differential diagnoses considered most likely in this dog were an occult/latent hereditary muscular dystrophic disorder or idiopathic hyperCKemia, a phenomenon not yet reported in the veterinary literature. This report describes for the first time, clinical and diagnostic features of a subclinical dog with persistent moderate-to-severe hyperCKemia.

SUBMITTER: Gunther M

PROVIDER: S-EPMC8573117 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Chronic kidney disease (CKD) has been associated with a higher risk of cardiovascular disease (CVD). CKD patients present a decrease in the levels of the protein Klotho that accompanies the decrease in kidney function. This protein has been related to protective effects against CVD. However, it is unclear whether circulating Klotho, and its expression in peripheral blood cells (PBCs) are also associated with subclinical atherosclerosis in CKD. The present study aimed to study the relationship between Klotho and subclinical atherosclerosis in a population of patients with moderate to severe CKD. We determined the serum levels and gene expression in PBCs levels of Klotho and three inflammatory cytokines in 103 patients with CKD and investigated their relationship with two surrogate markers of subclinical atherosclerotis: ankle-brachial index (ABI) and carotid intima-media thickness (CIMT). Patients with subclinical atherosclerosis presented lower serum and PBCs expression levels of Klotho. Both variables were associated with the presence of subclinical atherosclerosis, being directly related with ABI and inversely with CIMT (P < 0.0001 for both). Multiple regression analysis demonstrated that both variables were significant determinants for ABI (adjusted R2 = 0.511, P < 0.0001) and CIMT (adjusted R2 = 0.445, P < 0.0001), independently of traditional and emergent cardiovascular risk factors. Moreover, both constituted protective factors against subclinical atherosclerosis [OR: 0.993 (P = 0.002) and 0.231 (P = 0.025), respectively]. Receiver operating characteristic analysis pointed to the utility of serum Klotho (area under the curve [AUC]: 0.817, 95% CI: 0.736-0.898, P < 0.001) and its gene expression in PBCs (AUC: 0.742, 95% CI: 0.647-0.836, P < 0.001) to distinguish subclinical atherosclerosis. The reductions in serum and PBCs expression levels of Klotho in CKD patients are independently associated with the presence of for subclinical atherosclerosis. Further research exploring whether therapeutic approaches to maintain or elevate Klotho could reduce the impact of CVD in CKD patients is warranted.

Project description:ObjectivesBody mass index (BMI) is associated with acute kidney injury (AKI) after trauma, but underlying mechanisms are unclear. Body mass index correlates with both excess adiposity and increased muscle mass. Since the latter could predispose to severe rhabdomyolysis after trauma, we hypothesized that the BMI-AKI association may be partially explained by a direct relationship of BMI with serum creatine kinase (CK).MethodsProspective cohort study of 463 critically ill patients admitted to a level I trauma center from 2005 to 2015 with Injury Severity Score of >15 and serum CK measured in the first 7 days. We defined AKI by AKI Network creatinine criteria. We used simple linear regression to determine the association of BMI with peak CK and multivariable logistic regression to adjust the BMI-AKI association for peak CK and confounders.ResultsMedian age was 43 years, 350 (76%) were male, 366 (79%) had blunt mechanism, and median Injury Severity Score was 24. Body mass index was associated with peak CK (R = 0.05, p < 0.001). Acute kidney injury developed in 148 patients (32%), and median time to peak CK was 29 hours (interquartile range, 15-56 hours) after presentation. Body mass index was significantly associated with AKI in multivariable models adjusted for age, race, sex, diabetes, injury mechanism and severity, and red blood cell transfusions (odds ratio [OR], 1.31 per 5 kg/m; 95% confidence interval [CI], 1.09-1.58; p = 0.004). Adding peak CK to the model partially attenuated the association of BMI with AKI (OR, 1.26 per 5 kg/m; 95% CI, 1.04-1.52; p = 0.018), and peak CK was also associated with AKI (OR, 1.19 per natural log; 95% CI, 1.00-1.41; p = 0.049). Peak CK remained associated with AKI when restricted to patients with values of <5,000 U/L (OR, 1.31 per natural log; 95% CI, 1.01-1.69; p = 0.043).ConclusionSerum CK correlated with BMI and partially attenuated the association of BMI with AKI after major trauma, suggesting that excess muscle injury may contribute to the BMI-AKI association.Level of evidenceEpidemiologic study, level III.

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Case Report: Persistent Moderate-to-Severe Creatine Kinase Enzyme Activity Elevation in a Subclinical Dog

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