Eun Kyoung Lee

Background Selenium is an essential trace element, and its deficiency is associated with thyroid dysfunction, which is known as a cardiovascular risk factor. Hemodialysis (HD) patients are particularly prone to selenium deficiency, and this nutritional factor may increase the risk of thyroid dysfunction and subsequently cardiovascular disease (CVD). Therefore, we investigated selenium deficiency in HD patients and tried to analyze the effect of selenium deficiency on thyroid dysfunction and its correlation with CVD. Methods A cross-sectional study was conducted with 183 chronic HD patients. Selenium deficiency was defined as a serum selenium level below 90 µg/L. Patients were categorized into subgroups based on selenium status and/or thyroid hormone dysfunction. CVD prevalence was assessed. Results Of the 183 subjects, 79 (43.2%) had selenium deficiency, which was associated with a trend toward higher thyroid dysfunction and increased CVD. In the subgroup analysis, the group with both selenium deficiency and thyroid dysfunction showed a significantly higher CVD prevalence of 68.1% compared to other groups. Additionally, in the logistic regression analysis for CVD risk factors, selenium deficiency/thyroid dysfunction was found to have a significant odds ratio of 3.171. Conclusions This study demonstrates that selenium deficiency is associated with thyroid dysfunction and an increased CVD risk in chronic HD patients. Moreover, a negative synergistic effect on CVD was observed when both selenium deficiency and thyroid dysfunction were present.

Sweet’s syndrome (SS) is an autoimmune-mediated acute febrile neutrophilic dermatosis with a number of possible etiologies, including infection, malignancy, and drug reactions. In contrast to its original description, it can rarely involve extracutaneous organs, including the central nervous system, cardiovascular system, lung, liver, gastrointestinal tract, spleen, and bone. To our knowledge, there have been only three cases of SS accompanied by acute kidney injury worldwide, and this is the first report in which the patient recovered completely from acute kidney injury as well as cutaneous lesions with early steroid administration. Here, we report a case of SS with acute kidney injury in a patient with myelodysplastic syndrome (MDS) whose skin lesions and renal function recovered fully with early diagnosis and steroid therapy along with a review of the relevant literature.

Evidence suggests that alkaline phosphatase attenuates inflammatory response in sepsis by lipopolysaccharide detoxification and adenosine triphosphate dephosphorylation. We sought to determine changes in alkaline phosphatase (AP) activity during septic acute kidney injury (AKI) and clinical parameters associated with AP activity. In this retrospective study, we investigated baseline (when initiating CRRT) and follow-up AP activity on day 3, and associated outcomes in patients who underwent continuous renal replacement therapy (CRRT) due to septic AKI. We analyzed the baseline AP activity of 155 patients and day 3 AP activity in 123 patients. Baseline AP activity was not associated with renal or inflammatory biomarkers, or outcomes. It did not significantly differ between the 75 survivors and 80 non-survivors (p = 0.155). AP activity was higher on day 3 than at baseline (105 U/L [interquartile range, 79–156] vs 90 U/L [interquartile range, 59–133]). In particular, liver and bone isoforms increased significantly (p < 0.05), but intestine isoforms did not reach statistical significance (p = 0.367). In addition, day 3 AP activity showed a weak correlation with length of ICU stay (r = 0.213, p = 0.018) and length of hospital stay (r = 0.216, p = 0.017), but not with survival (r = − 0.035, p = 0.698). Endogenous AP activity significantly increased in patients with septic AKI. However, neither baseline nor follow-up AP activity was associated with survival.

Won Yong Suh, Eun Kyoung Lee. Kidney Res Clin Pract 2018;37:174-7. https://doi.org/10.23876/j.krcp.2018.37.2.174

Changhyun Park, So Mi Kim, Doh Hyung Kim, Eun Kyoung Lee. Kidney Res Clin Pract 2018;37:96-7. https://doi.org/10.23876/j.krcp.2018.37.1.96