【Abstract】Objective To evaluate the risk factors of coronary artery calcification (CAC) in patients with chronic kidney disease (CKD) stage 3～5 and the relationship between iron metabolism indices and CAC. Methods One hundred and sixty-two patients with CKD stage 3～5 in the Department of Nephrology of the Second Hospital of Anhui Medical University were recruited. Clinical data and laboratory indices were collected. Serum iron, ferritin, transferrin and total iron binding capacity (TIBC) were examined, and transferrin saturation (TSAT) was calculated. Ferrin> 800 μg/L and/or TSAT> 50% were defined as iron overload. The coronary artery calcification score (CACs) was measured by multi-slice spiral computed tomography. According to CACs>10, patients were divided into calcification group and non-calcification group. To investigate the correlation between iron metabolism and CAC, and to explore the predictive value of risk factors on CAC. Result Ninety-two patients (56.8%) had CAC. Transferrin and TIBC were negatively correlated with CACs (r=-0.293, -0.253, P < 0.001, 0.001, respectively). Binary logistic regression analysis showed that old age(OR=1.050, 95% CI=1.013～1.088, P=0.007), diabetes (OR=4.712, 95% CI=1.445～15.371, P=0.010), higher neutrophil- lymphocyte (NLR) (OR=1.253, 95% CI=1.025～1.533, P=0.028), higher blood phosphorus (OR=3.981, 95% CI=1.791～8.849, P=0.001), and lower transferrin (OR=0.130, 95% CI=0.044～0.378, P< 0.001) were independent risk factors of CAC.ROC curve showed that the area under the curve of combined prediction of CAC by age, diabetes, NLR, blood phosphorus and transferrin was 0.828 (95% CI 0.766～0.891, P<0.001), the sensitivity was 79.3%, and the specificity was 75.7%. Conclusion The incidence of CAC was high in patients with CKD stage 3～5. Old age, diabetes, hyperphosphatemia, high NLR and decreased blood
transferrin level are independent risk factors of CAC. The combined indicator including the above risk factors has good predictive value for the occurrence of CAC.
[1] Chen J, Budoff M J, Reilly M P, et al. Coronary Artery Calcification and Risk of Cardiovascular Disease and Death Among Patients With Chronic Kidney Disease[J]. JAMA Cardiol,2017,2(6):635-643.
[2] Honda H, Hosaka N, Ganz T, et al. Iron Metabolism in Chronic Kidney Disease Patients[J]. Contrib Nephrol,2019,198:103-111.
[3] Kuscuoglu D, Janciauskiene S, Hamesch K, et al. Liver - master and servant of serum proteome[J]. J Hepatol,2018,69(2):512-524.
[4] Ruiz-Jaramillo Mde L, Guízar-Mendoza JM, Amador-Licona N, et al. Iron overload as cardiovascular risk factor inchildren and adolescents with renal disease[J]. Nephrol Dial Transplant,2011,26(10):3268-3273.
[5] Chen Y, Zhao X, Wu H. Arterial Stiffness: A Focus on Vascular Calcification and Its Link to Bone Mineralization[J]. Arterioscler Thromb Vasc Biol,2020,40(5):1078-1093.
[6] Adeney KL, Siscovick DS, Ix JH, et al. Association of serum phosphate with vascular and valvular calcification in moderate CKD[J]. J Am Soc Nephrol,2009,20(2):381-387.
[7] 吴茜茜，王德光，张森，等.慢性肾脏病 3～5 期非透析患者中性粒细胞与淋巴细胞比值与腹主动脉钙化的相关性研究[J].安徽医科大学报,2019,54(07):1141-1145.
[8] Cornelissen A, Guo L, Sakamoto A, et al. New insights into the role of iron in inflammation and atherosclerosis[J]. EBioMedicine,2019,47(9):598-606.
[9] Xu S.Iron and Atherosclerosis: The Link Revisited[J]. Trends Mol Med,2019,25(8):659-661.
[10] Kuo KL, Hung SC, Lee TS, et al. Iron sucrose accelerates early atherogenesis by increasing superoxide production and upregulating adhesion molecules in CKD[J]. J Am Soc Nephrol, 2014,25(11): 2596-2606.
[11] Shi Y, Zhou L, Huang L H, et al. Plasma ferritin levels, genetic variations in HFE gene, and coronary heart disease in Chinese: a case-control study[J]. Atherosclerosis,2011,218(2):386-390.
[12] Gkouvatsos K, Papanikolaou G, Pantopoulos K. Regulation of iron transport and the role of transferrin[J]. Biochim Biophys Acta,2012,1820(3):188-202.
[13] Kibel A, Belovari T, Drenjancevi?-Peri? I. The role of transferrin in atherosclerosis[J]. Med Hypotheses,2008,70(4):793-797.
[14] Besarab A, Coyne DW. Iron supplementation to treat anemia in patients with chronic kidney disease[J]. Nat Rev Nephrol,2010,6(12):699-710.
[15] 魏萌，魏丽敏，王萌，等.维持性血液透析患者血管钙化的危险因素分析[J]. 中国血液净化,2020,19(11):742-746.
[16] Kotur-Stevuljevic J, Simic-Ogrizovic S, Dopsaj V, et al. A hazardous link between malnutrition, inflammation and oxidative stress in renal patients[J]. Clin Biochem,2012,45(15):1202-1205.
[17] Breuer W, Hershko C, Cabantchik ZI. The importance of non-transferrin bound iron in disorders of iron metabolism[J]. Transfus Sci,2000,23(3):185-192.
[18] Vinchi F, Porto G, Simmelbauer A, et al. Atherosclerosis is aggravated by iron overload and ameliorated by dietary and pharmacological iron restriction[J]. Eur Heart J,2020,41(28):2681-2695.
[19] Hilton RJ, Seare MC, Andros ND, et al. Phosphate inhibits in vitro Fe3 loading into transferrin by forming a soluble Fe(III)-phosphate complex: a potential non-transferrin bound iron species[J]. J Inorg Biochem,2012,110:1-7.
