Accurate serum creatinine (Cr) concentration measurement is essential for evaluating kidney function. In 2011, the Korean Association of External Quality Assessment Service (KEQAS) launched an accuracy-based Cr proficiency testing (ABCr PT) survey. We analyzed long-term data of the KEQAS ABCr PT survey collected between 2011 and 2019 to assess recent trends in Cr assays in Korea.

The ABCr PT survey including three commutable fresh-frozen serum samples was performed twice a year. The target Cr concentration was assigned using isotope-dilution mass spectrometry. We analyzed data obtained from the participating laboratories, calculated the yearly bias, and evaluated bias trends for the major reagents and instruments. Outliers were excluded from all analysis.

The mean percentage bias based on the total data of all participating laboratories was 10.8% in the 2011-A survey and 0.2% in 2019-B survey. Bias for the major reagents and instruments differed depending on the manufacturer. Enzymatic assays generally showed desirable bias ranging from -3.9% to 3.2% at all Cr concentrations and lower interlaboratory variability than non-enzymatic assays (enzymatic vs. non-enzymatic, 3.3%-7.2% vs. 6.3%-9.1%).

Although the mean percentage bias of Cr assays tends to decrease over time, it is necessary to continuously strive to improve Cr assay accuracy, especially at low concentrations.

Although the mean percentage bias of Cr assays tends to decrease over time, it is necessary to continuously strive to improve Cr assay accuracy, especially at low concentrations.

Total cholesterol concentration measurement is important in the diagnosis of dyslipidemia and evaluation of cardiovascular disease risk factors. Measurement reliability for obtaining an accurate total cholesterol concentration requires procedure standardization. We evaluated the standardization status for total cholesterol concentration measurement through Korean external quality assessment (EQA) data analysis.

This study involved 1,670 laboratories that participated in the EQA of total cholesterol concentration measurements in 2019 for 32 products from different manufacturers. The target concentrations of three quality control (QC) materials (samples A, B, and C) were measured using the reference method and compared with EQA data. The performance criteria for total cholesterol concentration measurement were based on the National Cholesterol Education Program guidelines, with ±3% inaccuracy.

The target values and inaccuracies of the QC material based on the reference method measurements were 254.65±7.64cts from these manufacturers.

Neutrophil gelatinase-associated lipocalin (NGAL) and hepcidin-25 are involved in catalytic iron-related kidney injury after cardiac surgery with cardiopulmonary bypass. We explored the predictive value of plasma NGAL, plasma hepcidin-25, and the plasma NGALhepcidin-25 ratio for major adverse kidney events (MAKE) after cardiac surgery.

We compared the predictive value of plasma NGAL, hepcidin-25, and plasma NGALhepcidin-25 with that of serum creatinine (Cr) and urinary output and protein for primary-endpoint MAKE (acute kidney injury [AKI] stages 2 and 3, persistent AKI >48 hours, acute dialysis, and in-hospital mortality) and secondary-endpoint AKI in 100 cardiac surgery patients at intensive care unit (ICU) admission. We performed ROC curve, logistic regression, and reclassification analyses.

At ICU admission, plasma NGAL, plasma NGALhepcidin-25, plasma interleukin-6, and Cr predicted MAKE (area under the ROC curve [AUC] 0.77, 0.79, 0.74, and 0.74, respectively) and AKI (0.73, 0.89, 0.70, and 0.69). For AKI prediction, plasma NGALhepcidin-25 had a higher discriminatory power than Cr (AUC difference 0.26 [95% CI 0.00-0.53]). Urinary output and protein, plasma lactate, C-reactive protein, creatine kinase myocardial band, and brain natriuretic peptide did not predict MAKE or AKI (AUC <0.70). Only plasma NGALhepcidin-25 correctly reclassified patients according to their MAKE and AKI status (category-free net reclassification improvement 0.82 [95% CI 0.12-1.52], 1.03 [0.29-1.77]). After adjustment to the Cleveland risk score, plasma NGALhepcidin-25 ≥0.9 independently predicted MAKE (adjusted odds ratio 16.34 [95% CI 1.77-150.49],

=0.014).

Plasma NGALhepcidin-25 is a promising marker for predicting postoperative MAKE.

Plasma NGALhepcidin-25 is a promising marker for predicting postoperative MAKE.Understanding anatomic variations in neurovascular structure inside the femoral triangle is crucial for regional anesthesiologists performing femoral nerve block. During routine dissection of a cadaver, an ascending branch of the lateral circumflex femoral artery with an anomalous course passing through the femoral nerve, specifically the posterior division, was identified inside the femoral triangle on the left thigh. The novel variation identified in this study occurred in an early stage of prenatal development. Recognition of this anatomic variation will be helpful for reducing unexpected complications during the femoral nerve block and the tensor fascia latae flap. Penetration of the posterior division of the femoral nerve by the arterial branch might cause pain or paresthesia of the medial aspect of the leg in the distribution of the saphenous nerve.Diabetes-induced oxidative stress is vital in initiating neuronal damage in the diabetic retina, leading to diabetic retinopathy (DR). selleck chemicals This study investigates the possible effects of coumestrol (CMS) on streptozotocin (STZ)-induced DR. First, we established a rat model of DR by STZ injection and a cell model involving high-glucose (HG) exposure of human retinal microvascular endothelial cells (hRMECs). We characterized the expression patterns of oxidative stress indicators, pro-inflammatory cytokines, and pro-apoptotic proteins in hRMECs. Polymerase chain reaction showed sirtuin 1 (SIRT1) to be poorly expressed in the retinal tissues of STZ-treated rats and HG-exposed hRMECs, but its expression was upregulated upon treatment with CMS treatment. Furthermore, CMS treatment attenuated the STZ-induced pathologies such as oxidative stress, inflammation, and cell apoptosis. Consistent with the in vivo results, CMS activated the expression of SIRT1, thereby inhibiting oxidative stress, inflammation, and apoptosis of HG-treated hRMECs.