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논문분류	춘계학술대회 초록집
제목	Vitamin D deficiency is associated with erythropoietin deficiency and endogenous erythropoietin resistance in patients with chronic kidney disease
저자	Il Young Kim1, June Hyun Kim1, Min Jeong Kim1, Dong Won Lee1, Soo Bong Lee1, Miyeun Han2, Harin Rhee2, Sang Heon Song2, Ihm Soo Kwak2
출판정보	2018; 2018(1):
키워드	1,25 dihydroxyvitamin D \| anemia \| chronic kidney disease \| erythropoietin
초록	Objectives: Erythropoietin (EPO) deficiency and resistance to endogenous EPO is an important pathophysiological feature in anemia of chronic kidney disease (CKD). 1,25 dihydroxyvitamin D [1,25(OH)2D] deficiency is known to contribute to anemia of CKD. We aimed to investigate the associations between serum 1,25(OH)2D and anemia, EPO deficiency, and endogenous EPO resistance in patients with CKD Methods: This study included 409 patients with CKD [glomerular filtration rate (GFR) < 60 ml/min/1.73m2] who were not on dialysis therapy. Patients on exogenous EPO therapy and patients with iron deficiencies were excluded. Endogenous EPO resistance was assessed by calculating the ratio of endogenous EPO to hemoglobin (Hb) (endogenous EPO/Hb ratio). The associations of Hb level, endogenous EPO level, and the endogenous EPO/Hb ratio with clinical and laboratory variables were investigated by univariate and multivariate analyses. Results: In univariate analysis, serum 1,25(OH)2D level was correlated with the Hb level, endogenous EPO level, and the endogenous EPO/Hb ratio. Multiple regression analysis revealed that the serum 1,25(OH)2D level remained significantly associated with the Hb level (β = 0.523, P < 0.001), endogenous EPO level (β = 0.119, P = 0.034), and the endogenous EPO/Hb ratio (β = -0.106, P = 0.035), even after adjusting for other confounding factors, including the levels of parathyroid hormone and the inflammatory marker C-reactive protein. Conclusions: The serum 1,25(OH)2D level exhibited significant associations with anemia, EPO deficiency, and endogenous EPO resistance in CKD patients. These associations were independent of secondary hyperparathyroidism and inflammation status.
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