Important abnormalities of bone mineral metabolism are present in patients with coronary artery disease with a mild decrease of the estimated glomerular filtration rate

被引:0
作者
Emilio González-Parra
Álvaro Aceña
Óscar Lorenzo
Nieves Tarín
María Luisa González-Casaus
Carmen Cristóbal
Ana Huelmos
Ignacio Mahíllo-Fernández
Ana María Pello
Rocío Carda
Ignacio Hernández-González
Joaquín Alonso
Fernando Rodríguez-Artalejo
Lorenzo López-Bescós
Alberto Ortiz
Jesús Egido
José Tuñón
机构
[1] IIS-Fundación Jiménez Díaz and Autónoma University,Division of Nephrology and Hypertension
[2] IIS-Fundación Jiménez Díaz,Department of Cardiology
[3] IIS-Fundación Jiménez Díaz and Autónoma University,Renal and Vascular Research Laboratory
[4] Hospital Universitario de Móstoles,Department of Cardiology
[5] Hospital Gómez-Ulla,Laboratory of Nephrology and Mineral Metabolism
[6] Hospital de Fuenlabrada and Rey Juan Carlos University,Department of Cardiology
[7] Hospital Universitario Fundación Alcorcón,Department of Cardiology
[8] IIS-Fundación Jiménez Díaz,Department of Epidemiology
[9] Universidad Autónoma de Madrid,Department of Preventive Medicine and Public Health, School of Medicine
[10] Rey Juan Carlos University,Renal, Vascular and Diabetes Research Laboratory
[11] IIS-Fundación Jiménez Díaz,Department of Cardiology and Laboratory of Vascular Pathology
[12] Autónoma University,undefined
[13] and CIBERDEM,undefined
[14] IIS-Fundación Jiménez Díaz and Autónoma University,undefined
来源
Journal of Bone and Mineral Metabolism | 2016年 / 34卷
关键词
Glomerular filtration rate; Fibroblast growth factor 23; Parathormone; Vitamin D; Coronary artery disease;
D O I
暂无
中图分类号
学科分类号
摘要
Chronic kidney disease (CKD)–mineral and bone disorder (MBD) is characterized by increased circulating levels of parathormone (PTH) and fibroblast growth factor 23 (FGF23), bone disease, and vascular calcification, and is associated with adverse outcomes. We studied the prevalence of mineral metabolism disorders, and the potential relationship between decreased estimated glomerular filtration rate (eGFR) and CKD-MBD in coronary artery disease patients in a cross-sectional study of 704 outpatients 7.5 ± 3.0 months after an acute coronary syndrome. The mean eGFR (CKD Epidemiology Collaboration formula) was 75.8 ± 19.1 ml/min/1.73 m2. Our patients showed lower calcidiol plasma levels than a healthy cohort from the same geographical area. In the case of men, this finding was present despite similar creatinine levels in both groups and older age of the healthy subjects. Most patients (75.6 %) had an eGFR below 90 ml/min/1.73 m2 (eGFR categories G2–G5), with 55.3 % of patients exhibiting values of 60–89 ml/min/1.73 m2 (G2). PTH (r = −0.3329, p < 0.0001) and FGF23 (r = −0.3641, p < 0.0001) levels inversely correlated with eGFR, whereas calcidiol levels and serum phosphate levels did not. Overall, PTH levels were above normal in 34.9 % of patients. This proportion increased from 19.4 % in G1 category patients, to 33.7 % in G2 category patients and 56.6 % in G3–G5 category patients (p < 0.001). In multivariate analysis, eGFR and calcidiol levels were the main independent determinants of serum PTH. The mean FGF23 levels were 69.9 (54.6–96.2) relative units (RU)/ml, and 33.2 % of patients had FGF23 levels above 85.5 RU/ml (18.4 % in G1 category patients, 30.0 % in G2 category patients, and 59.2 % in G3–G5 category patients; p < 0.001). In multivariate analysis, eGFR was the main predictor of FGF23 levels. Increased phosphate levels were present in 0.7 % of the whole sample: 0 % in G1 category patients, 0.3 % in G2 category patients, and 2.8 % in G3–G5 category patients (p = 0.011). Almost 90 % of patients had calcidiol insufficiency without significant differences among the different degrees of eGFR. In conclusion, in patients with coronary artery disease there is a large prevalence of increased FGF23 and PTH levels. These findings have an independent relationship with decreased eGFR, and are evident at an eGFR of 60–89 ml/min/1.73 m2. Then, mild decreases in eGFR must be taken in consideration by the clinician because they are associated with progressive abnormalities of mineral metabolism.
引用
收藏
页码:587 / 598
页数:11
相关论文
共 386 条
  • [1] Stevens LA(2013)KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease Kidney Int Suppl 3 1-150
  • [2] Li S(2011)Comparison of the CKD epidemiology collaboration (CKD-EPI) and modification of diet in renal disease (MDRD) study equations: risk factors for and complications of CKD and mortality in the kidney early evaluation program (KEEP) Am J Kidney Dis 57 S9-S16
  • [3] Kurella Tamura M(2013)A comparison of the CKD-EPI, MDRD-4, and Cockcroft-Gault equations to assess renal function in predicting all-cause mortality in acute coronary syndrome patients Int J Cardiol 167 2325-2326
  • [4] Chen SC(2002)K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification Am J Kidney Dis 39 S1-S266
  • [5] Vassalotti JA(2009)KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD) Kidney Int 76 1-130
  • [6] Norris KC(2011)FGF23 induces left ventricular hypertrophy J Clin Invest 121 4393-4408
  • [7] Whaley-Connell AT(1997)Mutation of the mouse klotho gene leads to a syndrome resembling ageing Nature 390 45-51
  • [8] Bakris GL(2011)Klotho deficiency causes vascular calcification in chronic kidney disease J Am Soc Nephrol 22 124-136
  • [9] McCullough PA(2014)The kidney is the principal organ mediating klotho effects J Am Soc Nephrol 25 2169-2175
  • [10] Abu-Assi E(2014)Coexistence of low vitamin D and high fibroblast growth factor-23 plasma levels predicts an adverse outcome in patients with coronary artery disease PLoS One 9 e95402-612