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1.
Annals of Laboratory Medicine ; : 381-387, 2017.
Article in English | WPRIM | ID: wpr-99761

ABSTRACT

BACKGROUND: The third-generation bio-intact parathyroid hormone (PTH) (1–84) assay was designed to overcome problems associated with the detection of C-terminal fragments by the second-generation intact PTH assay. The two assays have been compared primarily among dialysis populations. The present study evaluated the correlations and differences between these two PTH assays among patients with chronic kidney disease (CKD) stages 3 to 5 not yet on dialysis. METHODS: Blood samples were collected from 98 patients with CKD stages 3 to 5. PTH concentrations were measured simultaneously by using the second-generation - PTH intact-STAT and third-generation bio-intact 1–84 PTH assays. Other serum biomarkers of bone mineral disorders were also assessed. CKD stage was calculated by using the CKD-Epidemiology Collaboration (EPI) formula. RESULTS: Serum bio-intact PTH concentrations were strongly correlated but significantly lower than the intact PTH concentrations (r=0.963, P<0.0001). This finding was consistent among CKD stages 3 to 5. PTH concentrations by both assays (intact and bio-intact PTH) positively correlated with urea (r=0.523, r=0.504; P=0.002, respectively), phosphorus (r=0.532, r=0.521; P<0.0001, respectively) and negatively correlated with blood calcium (r=−0.435, r=−0.476; P<0.0001, respectively), 25(OH) vitamin D, (r=−0.319, r=−0.353; respectively, P<0.0001) and the estimated glomerular filtration rate (r=−0.717, r=−0.688; P<0.0001, respectively). CONCLUSIONS: Among patients with CKD stages 3 to 5 not on dialysis, the bio-intact PTH assay detected significantly lower PTH concentrations compared with intact PTH assay. Additional studies that correlate the diagnosis and management of CKD mineral and bone disorders with bone histomorphometric findings are needed to determine whether bio-intact PTH assay results are better surrogate markers in these early stages of CKD.


Subject(s)
Humans , Biomarkers , Calcium , Cooperative Behavior , Diagnosis , Dialysis , Glomerular Filtration Rate , Hyperparathyroidism, Secondary , Miners , Parathyroid Hormone , Phosphorus , Renal Insufficiency, Chronic , Urea , Vitamin D
2.
Annals of Laboratory Medicine ; : 155-158, 2017.
Article in English | WPRIM | ID: wpr-8646

ABSTRACT

Von Willebrand factor (vWF) is a glycoprotein with a crucial role in the formation of platelet thrombi, and ADAMTS13 is the main enzyme responsible for vWF cleavage. Both are important in the relationship between diabetic nephropathy, hypercoagulability, and cardiovascular disease. This study evaluated a potential relationship between vitamin D (vitD) levels, vWF, ADAMTS13 activity, and inflammation in diabetic patients on chronic hemodialysis (HD). Blood samples from 52 diabetic patients on chronic HD were obtained to determine vitD levels, vWF, and ADAMTS13 activity, and inflammatory markers. HD patients were grouped according to 25-hydroxyvitamin D [25(OH) VitD]25 nmol/L (n=36). vWF antigen and vWF activity were elevated in both groups, with an average of 214.3±82.6% and 175.8±72.6%, respectively. Average ADAMTS13 activity was within the normal range in both groups. Blood samples from the vitD <25 nmol/L group showed a positive correlation between c-reactive protein (CRP) and vWF levels (P=0.023; r=0.564; 95% confidence interval=0.095-0.828), with a negative correlation between HbA1c and 25(OH) VitD (P=0.015; r=-0.337; 95% confidence interval=-0.337-0.19). Diabetic patients on chronic HD had elevated vWF levels and activity with no significant change in ADAMTS13 activity. The correlation between CRP and vWF levels in the 25(OH) VitD<25 nmol/L group suggests inflammatory-related endothelial dysfunction in these patients.


Subject(s)
Aged , Female , Humans , Male , Middle Aged , ADAMTS13 Protein/metabolism , C-Reactive Protein/analysis , Diabetes Mellitus, Type 2/complications , Glycated Hemoglobin/analysis , Renal Dialysis , Renal Insufficiency, Chronic/complications , Vitamin D/analogs & derivatives , von Willebrand Factor/metabolism
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