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  • 1
    Online Resource
    Online Resource
    Walter de Gruyter GmbH ; 2021
    In:  Clinical Chemistry and Laboratory Medicine (CCLM) Vol. 59, No. 7 ( 2021-06-25), p. 1231-1237
    In: Clinical Chemistry and Laboratory Medicine (CCLM), Walter de Gruyter GmbH, Vol. 59, No. 7 ( 2021-06-25), p. 1231-1237
    Abstract: Severe hyperkalemia can cause life-threatening arrhythmia, cardiac arrest, or death. This study aimed to investigate the incidence and the associated factors relevant to critical hyperkalemia (≥6 mmol/L) among inpatients, outpatients, and emergency department. Their clinical outcomes were also analyzed. Methods All patients whose high serum potassium values had been reported as critical laboratory values in 2016 were enrolled. Their demographic data, comorbidities, clinical symptoms, biochemical data, and outcomes were reviewed and collected. The Charlson comorbidity score (CCS) and glomerular filtration rate (GFR) were computed to assess the comorbidity burden and renal function. Patients were divided into groups according to different settings, potassium and GFR levels, and their survival. Results Of the 293,830 total serum potassium tests, 1,382 (0.47%) reports were listed as critical laboratory values. The average reply time was 6.3 min. Their mean age was 67.2 years, while the average GFR was 12.2 mL/min/1.73 m 2 . The overall mortality rate was 34%. Patients in the emergency department had the highest incidence (0.92%), while inpatients had the worst outcome (51% mortality). The leading cause of mortality was septic shock. The fatal group had higher rates of clinical symptoms, higher potassium values, CCS, and eGFR (all p 〈 0.05). Conclusions Most of the responses for the reports were obtained within a short period of time. Patients with reported high critical serum potassium values were characterized by high rates of comorbidity, reduced eGFR, and mortality. The incidence, clinical manifestations, and outcomes varied in the different clinical settings.
    Type of Medium: Online Resource
    ISSN: 1437-4331 , 1434-6621
    Language: English
    Publisher: Walter de Gruyter GmbH
    Publication Date: 2021
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    detail.hit.zdb_id: 1492732-9
    SSG: 15,3
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  • 2
    In: Antioxidants, MDPI AG, Vol. 10, No. 8 ( 2021-07-22), p. 1166-
    Abstract: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of oral glucose-lowering agents. Apart from their glucose-lowering effects, large clinical trials assessing certain SGLT2 inhibitors have revealed cardiac and renal protective effects in non-diabetic patients. These excellent outcomes motivated scientists and clinical professionals to revisit their underlying mechanisms. In addition to the heart and kidney, redox homeostasis is crucial in several human diseases, including liver diseases, neural disorders, and cancers, with accumulating preclinical studies demonstrating the therapeutic benefits of SGLT2 inhibitors. In the present review, we aimed to update recent advances in the antioxidant roles of SGLT2 inhibitors in common but debilitating human diseases. We anticipate that this review will guide new research directions and novel therapeutic strategies for diabetes, cardiovascular diseases, nephropathies, liver diseases, neural disorders, and cancers in the era of SGLT2 inhibitors.
    Type of Medium: Online Resource
    ISSN: 2076-3921
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2704216-9
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Wiley ; 2015
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 42, No. 3 ( 2015-03), p. 287-292
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 42, No. 3 ( 2015-03), p. 287-292
    Abstract: Indoxyl sulphate is a protein‐bound uraemic toxin that has deleterious effects on the cardiovascular system. Rosiglitazone ( RGZ ) is an insulin sensitizer used for glycaemic control in type 2 diabetes. Rosiglitazone has been shown to be beneficial for cardiovascular disease because of its pleiotropic effects. Whether RGZ can improve indoxyl sulphate‐induced endothelial damage has not been investigated. In the present in vitro study, we examined the effects of RGZ on indoxyl sulphate‐induced endothelial injury. Endothelial cells were exposed to RGZ (5 and 10  μ mol/L) and then treated with indoxyl sulphate (100 and 1000  μ mol/L) for 48 h. Indoxyl sulphate upregulated intracellular cell adhesion molecule‐1, vascular cell adhesion molecule‐1 and monocyte chemotactic protein‐1 expression. Indoxyl sulphate also increased the abundance of NADPH oxidase 4 ( NOX 4) and nuclear factor ( NF )‐ κ B. Both extracellular signal‐regulated kinase ( ERK ) 1/2 and p38 mitogen‐activated protein kinase ( MAPK ) signalling pathways were activated after 48 h treatment with indoxyl sulphate. Pretreatment of cells with both concentrations of RGZ improved indices of endothelial injury. In addition, RGZ attenuated the increase in NOX 4 and NF ‐ κ B and prevented the activation of the ERK 1/2 and p38 MAPK signalling pathways. We conclude that RGZ ameliorates indoxyl sulphate‐induced endothelial injury.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 189277-0
    detail.hit.zdb_id: 2020033-X
    SSG: 15,3
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