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Tytuł pozycji:

Cystatin C predicts the risk of incident cerebrovascular disease in the elderly: A meta-analysis on survival date studies.

Tytuł:
Cystatin C predicts the risk of incident cerebrovascular disease in the elderly: A meta-analysis on survival date studies.
Autorzy:
Zheng X; Department of Neurology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong.
She HD; Department of Neurology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong.
Zhang QX; Department of Neurology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong.
Si T; Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing.
Wu KS; Department of Public and preventive medicine, Shantou University Medical College, Shantou, Guangdong, China.
Xiao YX; Department of Neurology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong.
Źródło:
Medicine [Medicine (Baltimore)] 2021 Jul 16; Vol. 100 (28), pp. e26617.
Typ publikacji:
Journal Article; Meta-Analysis
Język:
English
Imprint Name(s):
Original Publication: Hagerstown, Md : Lippincott Williams & Wilkins
MeSH Terms:
Atherosclerosis/*epidemiology
Carotid Artery Diseases/*epidemiology
Cystatin C/*blood
Stroke/*epidemiology
Aged ; Atherosclerosis/blood ; Carotid Artery Diseases/blood ; Causality ; Cerebrovascular Disorders/blood ; Cerebrovascular Disorders/epidemiology ; Humans ; Proportional Hazards Models ; Risk Factors ; Stroke/blood
References:
GBD 2017 Causes of Death Collaborators. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 2018;392:1736–88.
GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet 2020;396:1204–22.
Feigin VL, Norrving B, Mensah GA. Global burden of stroke. Circ Res 2017;120:439–48.
Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med 2004;351:1296–305.
Jha V, Garcia-Garcia G, Iseki K, et al. Chronic kidney disease: global dimension and perspectives. Lancet 2013;382:260–72.
National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. AM J Kidney Dis 2002;39: (2 suppl 1): S1–266.
Yahalom G, Schwartz R, Schwammenthal Y, et al. Chronic kidney disease and clinical outcome in patients with acute stroke. Stroke 2009;40:1296–303.
Lee M, Saver JL, Chang KH, Liao HW, Chang SC, Ovbiagele B. Low glomerular filtration rate and risk of stroke: meta-analysis. BMJ (Clinical research ed) 2010;341:c4249.
Ninomiya T. Risk of stroke in kidney disease. Contrib Nephrol 2013;179:58–66.
O’Rourke MF, Safar ME. Relationship between aortic stiffening and microvascular disease in brain and kidney: cause and logic of therapy. Hypertension 2005;46:200–4.
Hsu CY, Chertow GM, Curhan GC. Methodological issues in studying the epidemiology of mild to moderate chronic renal insufficiency. Kidney Int 2002;61:1567–76.
Coll E, Botey A, Alvarez L, et al. Serum cystatin C as a new marker for noninvasive estimation of glomerular filtration rate and as a marker for early renal impairment. Am J Kidney Dis 2000;36:29–34.
Jacobsson B, Lignelid H, Bergerheim US. Transthyretin and cystatin C are catabolized in proximal tubular epithelial cells and the proteins are not useful as markers for renal cell carcinomas. Histopathology 1995;26:559–64.
Shi GP, Sukhova GK, Grubb A, et al. Cystatin C deficiency in human atherosclerosis and aortic aneurysms. J Clin Invest 1999;104:1191–7.
Li W, Sultana N, Siraj N, et al. Autophagy dysfunction and regulatory cystatin C in macrophage death of atherosclerosis. J Cell Mol Med 2016;20:1664–72.
Liu J, Sukhova GK, Yang JT, et al. Cathepsin L expression and regulation in human abdominal aortic aneurysm, atherosclerosis, and vascular cells. Atherosclerosis 2006;184:302–11.
Wu H, Du Q, Dai Q, Ge J, Cheng X. Cysteine protease cathepsins in atherosclerotic cardiovascular diseases. J Atheroscler Thromb 2018;25:111–23.
Ix JH, Shlipak MG, Chertow GM, Whooley MA. Association of cystatin C with mortality, cardiovascular events, and incident heart failure among persons with coronary heart disease: data from the Heart and Soul Study. Circulation 2007;115:173–9.
Yang B, Zhu J, Miao Z, et al. Cystatin C is an independent risk factor and therapeutic target for acute ischemic stroke. Neurotox Res 2015;28:01–7.
Guoxiang H, Hui L, Yong Z, Xunming J, Zhuo C. Association between Cystatin C and SVD in Chinese population. Neurol Sci 2018;39:2197–202.
Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation 2012;125:e2–20.
Erlandsen EJ, Randers E, Kristensen JH. Evaluation of the Dade Behring N Latex Cystatin C assay on the Dade Behring Nephelometer II System. Scand J Clin Lab Invest 1999;59:01–8.
Sharrief A, Grotta JC. Stroke in the elderly. Handb Clin Neurol 2019;167:393–418.
Shlipak MG, Sarnak MJ, Katz R, et al. Cystatin C and the risk of death and cardiovascular events among elderly persons. N Engl J Med 2005;352:2049–60.
Shlipak MG, Katz R, Sarnak MJ, et al. Cystatin C and prognosis for cardiovascular and kidney outcomes in elderly persons without chronic kidney disease. Ann Intern Med 2006;145:237–46.
Deo R, Fyr CL, Fried LF, et al. Kidney dysfunction and fatal cardiovascular disease--an association independent of atherosclerotic events: results from the Health, Aging, and Body Composition (Health ABC) study. Am Heart J 2008;155:62–8.
Aguilar MI, O’Meara ES, Seliger S, et al. Albuminuria and the risk of incident stroke and stroke types in older adults. Neurology 2010;75:1343–50.
Agarwala A, Virani S, Couper D, et al. Biomarkers and degree of atherosclerosis are independently associated with incident atherosclerotic cardiovascular disease in a primary prevention cohort: The ARIC study. Atherosclerosis 2016;253:156–63.
Garcia-Carretero R, Vigil-Medina L, Barquero-Perez O, et al. Cystatin C as a predictor of cardiovascular outcomes in a hypertensive population. J Hum Hypertens 2017;31:801–7.
Hoke M, Amighi J, Mlekusch W, et al. Cystatin C and the risk for cardiovascular events in patients with asymptomatic carotid atherosclerosis. Stroke 2010;41:674–9.
Crippa A, Khudyakov P, Wang M, Orsini N, Spiegelman D. A new measure of between-studies heterogeneity in meta-analysis. Stat Med 2016;35:3661–75.
Higgins JP, Thompson SG, Deeks JJ, Altman DG. Measuring inconsistency in meta-analyses. BMJ (Clinical research ed) 2003;327:557–60.
Kestenbaum B, Rudser KD, de Boer IH, et al. Differences in kidney function and incident hypertension: the multi-ethnic study of atherosclerosis. Ann Intern Med 2008;148:501–8.
Loew M, Hoffmann MM, Koenig W, Brenner H, Rothenbacher D. Genotype and plasma concentration of cystatin C in patients with coronary heart disease and risk for secondary cardiovascular events. Arterioscler Thromb Vasc Biol 2005;25:1470–4.
Evangelopoulos AA, Vallianou NG, Bountziouka V, et al. Association between serum cystatin C, monocytes and other inflammatory markers. Intern Med J 2012;42:517–22.
Schulte S, Sun J, Libby P, et al. Cystatin C deficiency promotes inflammation in angiotensin II-induced abdominal aortic aneurisms in atherosclerotic mice. Am J Pathol 2010;177:456–63.
Shlipak MG, Katz R, Cushman M, et al. Cystatin-C and inflammatory markers in the ambulatory elderly. Am J Med 2005;118:1416.
Knight EL, Verhave JC, Spiegelman D, et al. Factors influencing serum cystatin C levels other than renal function and the impact on renal function measurement. Kidney Int 2004;65:1416–21.
Salgado JV, Souza FL, Salgado BJ. How to understand the association between cystatin C levels and cardiovascular disease: Imbalance, counterbalance, or consequence? J Cardiol 2013;62:331–5.
Ferri KF, Kroemer G. Organelle-specific initiation of cell death pathways. Nat Cell Biol 2001;3:E255–263.
Fu J, Deng HY, Hu ML, Liao LY, Li YK. [Relationships between serum cystatin C, chemerin levels and subclinical atherosclerosis in type 2 diabetes mellitus patients]. Zhonghua Yi Xue Za Zhi 2019;99:307–11.
Bild DE, Bluemke DA, Burke GL, et al. Multi-ethnic study of atherosclerosis: objectives and design. Am J Epidemiol 2002;156:871–81.
Liu J, Sukhova GK, Sun JS, Xu WH, Libby P, Shi GP. Lysosomal cysteine proteases in atherosclerosis. Arterioscler Thromb Vasc Biol 2004;24:1359–66.
Kim HJ, Byun DW, Suh K, Yoo MH, Park HK. Association between Serum Cystatin C and Vascular Complications in Type 2 Diabetes Mellitus without Nephropathy. Diabetes Metab J 2018;42:513–8.
O’Hare AM, Newman AB, Katz R, et al. Cystatin C and incident peripheral arterial disease events in the elderly: results from the Cardiovascular Health Study. Arch Intern Med 2005;165:2666–70.
Pardell H, Armario P, Hernandez R. [Pathogenesis and epidemiology of arterial hypertension]. Drugs 1998;56: (suppl 2): 01–10.
Kusano E. Mechanism by which chronic kidney disease causes cardiovascular disease and the measures to manage this phenomenon. Clin Exp Nephrol 2011;15:627–33.
Chi L, Cheng X, He X, et al. Increased cortical infarction and neuroinflammation in ischemic stroke mice with experimental periodontitis. Neuroreport 2019;30:428–33.
Vallon V, Grahammer F, Volkl H, et al. KCNQ1-dependent transport in renal and gastrointestinal epithelia. Proc Natl Acad Sci U S A 2005;102:17864–9.
Dixit G, Dabney-Smith C, Lorigan GA. The membrane protein KCNQ1 potassium ion channel: Functional diversity and current structural insights. Biochim Biophys Acta Biomembr 2020;1862:183148.
Glisic S, Arrigo P, Alavantic D, Perovic V, Prljic J, Veljkovic N. Lipoprotein lipase: A bioinformatics criterion for assessment of mutations as a risk factor for cardiovascular disease. Proteins 2008;70:855–62.
Dwivedi P, Rodriguez J, Ibe NU, Weers PM. Deletion of the N- or C-Terminal Helix of Apolipophorin III To Create a Four-Helix Bundle Protein. Biochemistry 2016;55:3607–15.
Zeng Q, Huang Z, Wei L, Fang J, Lin K. Correlations of serum cystatin C level and gene polymorphism with vascular cognitive impairment after acute cerebral infarction. Neurol Sci 2019;40:1049–54.
Nagai A, Murakawa Y, Terashima M, et al. Cystatin C and cathepsin B in CSF from patients with inflammatory neurologic diseases. Neurology 2000;55:1828–32.
Nagai A, Ryu JK, Terashima M, et al. Neuronal cell death induced by cystatin C in vivo and in cultured human CNS neurons is inhibited with cathepsin B. Brain Res 2005;1066:120–8.
Nagai A, Ryu JK, Kobayash S, Kim SU. Cystatin C induces neuronal cell death in vivo. Ann N Y Acad Sci 2002;977:315–21.
Zou J, Chen Z, Wei X, et al. Cystatin C as a potential therapeutic mediator against Parkinson's disease via VEGF-induced angiogenesis and enhanced neuronal autophagy in neurovascular units. Cell Death Dis 2017;8:e2854.
Nishiyama K, Konishi A, Nishio C, et al. Expression of cystatin C prevents oxidative stress-induced death in PC12 cells. Brain Res Bull 2005;67:94–9.
Pérez-González R, Sahoo S, Gauthier SA, et al. Neuroprotection mediated by cystatin C-loaded extracellular vesicles. Sci Rep 2019;9:11104.
Dong X, Nao J. Cystatin C as an index of acute cerebral infraction recurrence: one-year follow-up study. Int J Neurosci 2019;129:36–41.
Substance Nomenclature:
0 (Cystatin C)
Entry Date(s):
Date Created: 20210714 Date Completed: 20210729 Latest Revision: 20230103
Update Code:
20240105
PubMed Central ID:
PMC8284707
DOI:
10.1097/MD.0000000000026617
PMID:
34260548
Czasopismo naukowe
Background: Stroke is the third leading cause of global year of life lost in all-age and second-ranked cause of disability adjusted life years in middle-aged and elder population. Therefore, it is critical to study the relationship between vascular-related risk factors and cerebrovascular diseases. Several cross-sectional studies have shown that Cystatin C (Cys C) is an independent risk factor for cerebrovascular diseases and levels of Cys C are significantly higher in stroke patients than in healthy individuals. In this meta-analysis, we introduce a Cox proportional hazards model to evaluate the causality between Cys C and the risk of cerebrovascular accident in the elderly.
Methods: We searched PubMed, EMBASE, the Web of Science, and the Cochrane Library from 1985 to 2019 for studies on the relationship between serum Cys C and incidence stroke with Cox proportional hazards models. We conducted a subgroup analysis of the selected studies to determine a connection between atherosclerosis and stroke. Finally, 7 research studies, including 26,768 patients without a history of cerebrovascular, were studied.
Results: After comparing the maximum and minimum Cys C levels, the hazard ratio for all types of stroke, including ischemic and hemorrhagic stroke, was 1.18 (95% confidence interval 1.04-1.31) with moderate heterogeneity (I2 = 43.0%; P = .119) in a fixed-effect model after pooled adjustment for other potential risk factors. In the subgroup analysis, the hazard ratio and 95% confidence interval for Cys C stratified by atherosclerosis was 1.85 (0.97-2.72). As shown in Egger linear regression test, there was no distinct publication bias (P = .153).
Conclusion: Increased serum Cys C is significantly associated with future stroke events in the elderly, especially in patients with carotid atherosclerosis. Thus, serum levels of Cys C could serve as a predicted biomarker for stroke attack.
Competing Interests: The authors report no conflicts of interest.
(Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

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