慢性肾脏病与心血管疾病关系的研究进展
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摘要
心脏和肾脏作为控制机体有效循环和血流动力学的两个重要器官,在生理功能上互相依存、在病理状态下互相影响,在治疗上又有很多共同之处。慢性肾脏病(CKD)是一种严重危害人类健康和生命的常见疾病。CKD不仅是终末期肾病(ESRD)的高危因素,也是心血管和全因死亡的高危因素,因此防治目标不仅要减缓、控制肾功能的进行性恶化,而且要预防主要的致死性合并症——心血管疾病(cardiovascular disease,CVD)的发生及恶化。但CKD患者CVD的发病机制、危险因素及治疗预防都是非常棘手和复杂的,故本文就CKD患者CVD的发病机制、危险因素、治疗及预防等三个方面作一综述。
As two important organs controlling the effective circulation and hemodynamics of the body, heart and kidney are interdependent in physiological function and influence each other in pathological state, and have much in common in treatment. Chronic kidney disease(CKD) is a common disease that seriously endangers human health and life. CKD is not only a high risk factor of end stage renal disease(ESRD), but also a high risk factor of cardiovascular and all-cause death. Therefore, the prevention and treatment objectives should not only slow down and control the progressive deterioration of renal function, but also prevent the occurrence and deterioration of cardiovascular disease(CVD), the main fatal complication. However, the pathogenesis, risk factors and treatment and prevention of CVD in CKD patients are very difficult and complex. This article reviews the pathogenesis, risk factors, treatment and prevention of CVD in CKD patients.
As two important organs controlling the effective circulation and hemodynamics of the body, heart and kidney are interdependent in physiological function and influence each other in pathological state, and have much in common in treatment. Chronic kidney disease(CKD) is a common disease that seriously endangers human health and life. CKD is not only a high risk factor of end stage renal disease(ESRD), but also a high risk factor of cardiovascular and all-cause death. Therefore, the prevention and treatment objectives should not only slow down and control the progressive deterioration of renal function, but also prevent the occurrence and deterioration of cardiovascular disease(CVD), the main fatal complication. However, the pathogenesis, risk factors and treatment and prevention of CVD in CKD patients are very difficult and complex. This article reviews the pathogenesis, risk factors, treatment and prevention of CVD in CKD patients.
引文
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[2] Cheng ZY, Ye T, Ling QY, et al. Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal-regulated protein kinase 1/2 and nuclear factor-κB signaling pathways[J]. Exp Ther Med, 2018, 15(2):1754-1760.
[3] Duni A, Liakopoulos V, Rapsomanikis KP, et al. Chronic kidney disease and disproportionally increased cardiovascular damage: does oxidative stress explain the burden?[J]. Oxid Med Cell Longev,2017,20(17):364-378.
[4] Bozic M, Mendezbarbero N, Gutierrezmunoz C, et al. Combination of biomarkers of vascular calcification and sTWEAK to predict cardiovascular events in chronic kidney disease[J]. Atherosclerosis,2018, 270(4):13-20.
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[13] Tang M, Batty JA, Lin C, et al. Pulmonary hypertension, mortality, and cardiovascular disease in CKD and ESRD Patients:a systematic review and meta-analysis[J]. Am J Kidney Dis, 2018,72(1):75-83.
[14] Premuzic V, Jelakovic B. Sexual dysfunction as a determinant of cardiovascular outcome in patients undergoing chronic hemodialysis[J]. Int J Impot Res, 2018,30(1):14-20.
[15] Harada K, Suzuki S, Ishii H, et al. Impact of skeletal muscle mass on long-term adverse cardiovascular outcomes in patients with chronic kidney disease[J]. Am J Cardiol, 2017, 119(8):1275-1280.
[16] Poesen R, Claes K, Evenepoel P, et al. Microbiota-derived phenylacetylglutamine associates with overall mortality and cardiovascular disease in patients with CKD[J]. J Am Soc Nephrol, 2016, 27(11):3479-3487.
[17] Mills KT, Chen J, Yang W, et al. Sodium excretion and the risk of cardiovascular disease in patients with chronic kidney disease[J]. JAMA,2016, 315(20):2200-2210.
[18] Zoccali C, Mallamaci F, Benedetto FA, et al. Cardiac natriuretic peptides are related to left ventricular mass and function and predict mortality in dialysis patients[J].J Am Soc Nephrol,2001, 12(7):1508-1515.
[19] Bolignano D, Coppolino G, Lacquaniti A,et al . From kidney to cardiovascular diseases: NGAL as a biomarker beyond the confines of nephrology[J].Eur J Clin Invest,2010 ,40(3):273-276.
[20] Garofalo C, Stefano TD, Vita C, et al. Hyperuricaemia and chronic kidney disease[J]. G Ital Nefrol ,2018, 35(1):379-391.
[21] Figueiredo JL, Aikawa M, Zheng C, et al. Selective cathep-sin S inhibition attenuates atherosclerosis in apolipoprotein E-deficient mice with chronic renal disease[J].Am J Pathol,2015 ,185(4): 1156-1166.
[22] McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure[J]. N Engl J Med,2014,371(11):993-1004.
[23] Liu L, Liu Y, Zhang Y, et al . High phosphate-induced downregulation of PPARγ contributes to CKD-associated vascular calcification[J]. J Mol Cell Cardiol,2018, 114(3):264-275.
[24] Turgut F, Kanbay M, Metin MR, et al. Magnesium supple-mnentation helps to improve carotid intima media thickness in patients on hemodialysis[J]. Int Urol Nephrol,2008,40(4): 1075-1082.
[25] Mortazavi M, Moeinzadeh F, Saadatnia M, et al. Effect ofmagnesium supplementation on carotid intima-media thick-ness and flow-mediated dilatation among hemodialysispatients: a double-blind, randomized, placebo-controlled trial [J]. Eur Neurol. 2013,69(5):309-316.
[26] Bressendorff I, Hansen D, Schou M, et al. Oral magnesium supplementation in chronic kidney disease stages 3 and 4: efficacy, safety, and effect on serum calcification propensity-A prospective randomized double-blinded placebo-controlled clinical trial[J]. Kidney Int Rep, 2017, 2(3):380.
[27] Zhang Q, Zhang M, Wang H, et al. Vitamin D supplementation improves endothelial dysfunction in patients with non-dialysis chronic kidney disease[J]. Int Urol Nephrol, 2018,50(5):923-927.
[2] Cheng ZY, Ye T, Ling QY, et al. Parathyroid hormone promotes osteoblastic differentiation of endothelial cells via the extracellular signal-regulated protein kinase 1/2 and nuclear factor-κB signaling pathways[J]. Exp Ther Med, 2018, 15(2):1754-1760.
[3] Duni A, Liakopoulos V, Rapsomanikis KP, et al. Chronic kidney disease and disproportionally increased cardiovascular damage: does oxidative stress explain the burden?[J]. Oxid Med Cell Longev,2017,20(17):364-378.
[4] Bozic M, Mendezbarbero N, Gutierrezmunoz C, et al. Combination of biomarkers of vascular calcification and sTWEAK to predict cardiovascular events in chronic kidney disease[J]. Atherosclerosis,2018, 270(4):13-20.
[5] Liu J, Zhang L, Zhou Y, et al. Aberrant activation of Wnt pathways in arteries associates with vascular calcification in chronic kidney disease[J]. Int Urol Nephrol, 2016, 48(8):1313-1319.
[6] Zhang S, Xu J, Feng Y, et al. Extracellular acidosis suppresses calcification of vascular smooth muscle cells by inhibiting calcium influx via L-type calcium channels[J].Clin Exp Hypertens, 2018,40(4):370-377.
[7] Panda D, Bai X, Sabbagh Y, et al. Defective interplay between mTORC1 activity and endoplasmic reticulum stress-unfolded protein response in uremic vascular calcification.[J]. Am J Physiol Renal Physiol, 2018 ,314(6):F1046-F1061
[8] Kirkman DL, Muth BJ, Ramick MG, et al. The role of mitochondria derived reactive oxygen species in microvascular dysfunction in chronic kidney disease[J]. Am J Physiol Renal Physiol, 2018, 314(3):F423-F429.
[9] Li T, Gua C, Wu B, et al. Increased circulating trimethylamine N-oxide contributes to endothelial dysfunction in a rat model of chronic kidney disease[J].Biochem Biophys Res Commun, 2018, 495(2):2071-2077.
[10] Dou L, Poitevin S, Sallée M, et al. Aryl hydrocarbon receptor is activated in patients and mice with chronic kidney disease[J]. Kidney Int, 2018,93(4):986-999.
[11] Gertow J, Ng CZ, Mamede Branca RM, et al. Altered protein composition of subcutaneous adipose tissue in chronic kidney disease[J]. Kidney Int Rep,2017, 2(6):1208-1218.
[12] Tsai YC, Lee CS, Chiu YW, et al. Angiopoietin-2, Angiopoietin-1 and subclinical cardiovascular disease in chronic kidney disease[J]. Sci Rep,2016, 19(6):394-400.
[13] Tang M, Batty JA, Lin C, et al. Pulmonary hypertension, mortality, and cardiovascular disease in CKD and ESRD Patients:a systematic review and meta-analysis[J]. Am J Kidney Dis, 2018,72(1):75-83.
[14] Premuzic V, Jelakovic B. Sexual dysfunction as a determinant of cardiovascular outcome in patients undergoing chronic hemodialysis[J]. Int J Impot Res, 2018,30(1):14-20.
[15] Harada K, Suzuki S, Ishii H, et al. Impact of skeletal muscle mass on long-term adverse cardiovascular outcomes in patients with chronic kidney disease[J]. Am J Cardiol, 2017, 119(8):1275-1280.
[16] Poesen R, Claes K, Evenepoel P, et al. Microbiota-derived phenylacetylglutamine associates with overall mortality and cardiovascular disease in patients with CKD[J]. J Am Soc Nephrol, 2016, 27(11):3479-3487.
[17] Mills KT, Chen J, Yang W, et al. Sodium excretion and the risk of cardiovascular disease in patients with chronic kidney disease[J]. JAMA,2016, 315(20):2200-2210.
[18] Zoccali C, Mallamaci F, Benedetto FA, et al. Cardiac natriuretic peptides are related to left ventricular mass and function and predict mortality in dialysis patients[J].J Am Soc Nephrol,2001, 12(7):1508-1515.
[19] Bolignano D, Coppolino G, Lacquaniti A,et al . From kidney to cardiovascular diseases: NGAL as a biomarker beyond the confines of nephrology[J].Eur J Clin Invest,2010 ,40(3):273-276.
[20] Garofalo C, Stefano TD, Vita C, et al. Hyperuricaemia and chronic kidney disease[J]. G Ital Nefrol ,2018, 35(1):379-391.
[21] Figueiredo JL, Aikawa M, Zheng C, et al. Selective cathep-sin S inhibition attenuates atherosclerosis in apolipoprotein E-deficient mice with chronic renal disease[J].Am J Pathol,2015 ,185(4): 1156-1166.
[22] McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure[J]. N Engl J Med,2014,371(11):993-1004.
[23] Liu L, Liu Y, Zhang Y, et al . High phosphate-induced downregulation of PPARγ contributes to CKD-associated vascular calcification[J]. J Mol Cell Cardiol,2018, 114(3):264-275.
[24] Turgut F, Kanbay M, Metin MR, et al. Magnesium supple-mnentation helps to improve carotid intima media thickness in patients on hemodialysis[J]. Int Urol Nephrol,2008,40(4): 1075-1082.
[25] Mortazavi M, Moeinzadeh F, Saadatnia M, et al. Effect ofmagnesium supplementation on carotid intima-media thick-ness and flow-mediated dilatation among hemodialysispatients: a double-blind, randomized, placebo-controlled trial [J]. Eur Neurol. 2013,69(5):309-316.
[26] Bressendorff I, Hansen D, Schou M, et al. Oral magnesium supplementation in chronic kidney disease stages 3 and 4: efficacy, safety, and effect on serum calcification propensity-A prospective randomized double-blinded placebo-controlled clinical trial[J]. Kidney Int Rep, 2017, 2(3):380.
[27] Zhang Q, Zhang M, Wang H, et al. Vitamin D supplementation improves endothelial dysfunction in patients with non-dialysis chronic kidney disease[J]. Int Urol Nephrol, 2018,50(5):923-927.