Correlation between lipid profile and C-reactive protein in children with nephrotic syndrome
Abstract
Background Nephrotic syndrome (NS) causes dyslipidemia in children, which can be long term or intermittent. Dyslipidemia has long been established as a risk factor for atherosclerosis. An early sign of atherosclerosis is elevated high sensitivity C-reactive protien (hsCRP). Atherosclerosis early in life, especially in childhood, warrants an assessment for NS. Study on a correlation between lipid profile and hsCRP, as a marker of atherosclerosis, in pediatric NS patients has been limited. Objective To assess for a correlation between lipid profile and hsCRP in childhood nephrotic syndrome. Methods This cross-sectional study was undertaken on 29 children with NS in Dr. Kariadi Hospital. Serum hsCRP, total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were examined in the active phase. Spearman’s test was used to analyze a possible correlation between total cholesterol, LDL, HDL and hsCRP levels. Results Mean levels of total cholesterol (454 mg/dL) and LDL (288 mg/dL) in this study were high, while the HDL level (55 mg/dL) was normal, according to US Department of Health and Human Services classifications. The median hsCRP level was 0.33 mg/L and 9 (31%) subjects had high hsCRP levels of more than 1 mg/L. There was a positive correlation between LDL level and hsCRP (r=0.423; P<0.05). Conclusions There is a weak positive correlation between LDL and hsCRP levels in children with NS.References
Trihono PP, Alatas H, Tambunan T, Pardede SO. Konsensus tata laksana sindroma nefrotik idiopatik pada anak. 2nd edition. Jakarta: UKK Nefrologi IDAI; 2008. p.1-21.
Bagga A, Mantan M. Nephrotic syndrome in children. Indian J Med Res. 2005;122:13-28.
Data instalasi rawat inap dan rawat jalan IKA RSUP Dr. Kariadi Semarang. 2002-2006. Unpublished data.
Thabet MA, Salcedo JR, Chan JC. Hyperlipidemia in childhood nephrotic syndrome. Pediatr Nephrol. 993;7:559-66.
Chan CM. Hyperlipidemia in chronic kidney disease. Ann Acad Med Singapore. 2005;35:31-5.
Rohana E. Perbedaan kadar kolesterol darah antara penderita sindrom nefrotik awal fase remisi dengan sindrom nefrotik kambuh fase remisi. [cited November 15, 2013]. Available from: http://www.digilib.uns.ac.id/upload/dokumen/72060707200901351.pdf.
Zilleruelo G, Hsia SL, FreundLich M, Gorman HM, Strauss J. Persistence of serum lipid abnormalities in children with idiopathic nephrotic syndrome. J Pediatr. 1984;104:61-4.
Merouani A, Levy E, Mongeau J, Robitaille P, Lambert M, Delvin EE. Hyperlipidemic profiles during remission in chilhood idiopathic nephrotic syndrome. Clin Biochem. 2003;36:571-4.
Rose BD, Appel GN. Hyperlipidemia in nephrotic syndrome and renal failure. 1999. [cited November 15, 2013]. Available from: http://cmbi.bjmu.edu.cn/uptodate/lipid%20disorders/pathophysiology/Hyperlipidemia%20in%20nephrotic%20syndrome%20and%20renal%20failure.htm
Bienias B, Zajaczkowska M, Borzecka H, Sikora P, Majewski M, Ksiazek E, et al. Selected thrombosis and atherosclerosis risk factors in children with idiopathic nephrotic syndrome. J Biochem Tech. 2012;3:317-21.
Hopp H, Gilboa N, Kurland G, Weichlerl N, Orchard TJ. Acute myocardial infarction in a young boy with nephrotic syndrome: a case report and review of the literature. Pediatr Nephrol. 1994;8:290-4.
Ordonez JD, Hiatt RA, Killebrew EJ, Fireman BH. The increased risk of coronary heart disease associated with nephrotic syndrome. Kidney Int. 1993;44:638-42.
Tkaczyk M, Czupryniak A, Owczarek D, Lukamowicz J, Nowicki M. Markers of endothelial dysfunction in children with idiopathic nephrotic syndrome. Am J Nephrol. 2008;28:197-202.
Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO, Criqui M, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107:499-511.
Thakur S, Gupta S, Parchwani H, Shah V, Yadav V. HsHSCRP - a potential marker for coronary heart disease. Indian J Fundamental and Applied Life Sciences. 2011;1:1-4.
Jialal I, Devaraj S. Inflammation and atherosclerosis: the value of the high-sensitivity C-reactive protein assay as a risk marker. Am J Clin Pathol. 2001;116:S108-15.
Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005;352:1685-95.
Kronenberg F. Dyslipidemia and nephrotic syndrome: recent advances. J Ren Nutr. 2005;15:195-203.
Sreenivasa B. A clinical study of nephrotic syndrome with special reference to serum lipid profile [dissertation]. Bangalore: Mysore Medical College And Research Institute; 2008.
Prescott WA, Streetman DA, Streetman DS. The potential role of HMG-CoA reductase inhibitors in pediatric nephrotic syndrome. Ann Pharmacother. 2004;38:2105-14.
Wasilewska A, Zoch-Zwierz W, Tobolczyk J, Tenderenda E. High-sensitivity C-reactive protein (hsHSCRP) level in children with nephrotic syndrome. Pediatr Nephrol. 2007;22:403-8.
Soetadji A, Subagjo HW, Soemantri A. Hubungan kadar lipid darah dan hsHSCRP pada anak obesitas. 2007. Unpublished data.
Datta S, Iqbal Z, Prasad KR. Comparison between serum hsHSCRP and LDL cholesterol for search of a better predictor for ischemic heart disease. Indian J Clin Biochem. 2011;26:210–3.
Dandona P, Aljada A, Bandyopadhyay A. The potential therapeutic role of insulin in acute myocardial infarctionin patients admitted to intensive care and in those with unspecified hyperglycemia. Diabetes Care. 2003;26:516-9.
Esposito K, Nappo F, Marfella R, Giugliano G, Giugliano F, Ciotola M, et al. Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress. Circulation. 2002;106:2067-72.
Elboudwarej O, Hojjat H, Safarpoor S, Vazirian S, Ahmadi S. Dysfunctional HDL and cardiovascular disease risk in individuals with diabetic dyslipidemia. J Diabetes Metab S4:001. doi: 10.4172/2155-6156.S4-001.
Camont L, Chapman MJ, Kontush A. Biological activities of HDL subpopulations and their relevance to cardiovascular disease. Trends Mol Med. 2011;17:594-603.
Van Lenten BJ, Hama SY, de Beer FC, Stafforini DM, McIntyre TM, Prescott SM, et al. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J Clin Invest. 1995;96:2758-67.
Mancini GBJ, Frohlich J. Carotid ultrasound, coronary calcium, and dyslipidemia patterns in the MESA (multiethnic study of atherosclerosis) cohort. J Am Coll Cardiol. 2010;56:1042-4.
Barton M, Minotti R, Haas E. Inflammation and atherosclerosis. Circ Res. 2007;101:750-1.
Yeh ET, Anderson HV, Pasceri V, Willerson JT. C-reactive protein: linking inflammation to cardiovascular complications. Circulation. 2001;104:974-5.
Pizzi C, Kaski JC. C-reactive protein elevation and disease activity in patients with coronary artery disease. Eur Heart J. 2004;25:401-8.
Verma S, Li SH, Badiwala MV, Weisel RD, Fedak PWM, Li RK, et al. Endothelin antagonism and interleukin-6 inhibition attenuate the proatherogenic effects of C-reactive protein. Circulation. 2002;105:1890-6.
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Accepted 2016-07-12
Published 2015-03-01