Dyslipidemia in patients with chronic kidney disease

Czech version

Authors: Magdaléna Dušejovská ^1,2; Marek Vecka ²; Ivan Rychlík ³; Aleš Žák ²
Authors‘ workplace: Dialyzační středisko Fresenius NephroCare, Praha Vinohrady ¹; IV. interní klinika 1. LF UK a VFN v Praze ²; I. interní klinika 3. LF UK a FNKV, Praha ³
Published in: AtheroRev 2019; 4(3): 153-158
Category:

Overview

Chronic kidney disease (CKD) is a very common complication in patients with diabetes mellitus, arterial hypertension and dyslipidemia. Worldwide prevalence of CKD reaches about 15 %. However, this estimation is biased due to frequently asymptomatic signs in early stages of the disease. Dyslipidemia is a constant metabolic complication of CKD, even from its early stages. The patients are on higher risk for death from cardiovascular disease or complications in comparison to those without present kidney disease. One of current problems represents the modalities for influencing cardiovascular risk. Hypolipidemic therapy is unequivocally indicated at early stages of kidney disease; nevertheless, with decreased glomerular filtration rate, the pharmacotherapy options change as well as the recommendations for hypolipidemic therapy, particularly in patients with end stage renal disease who are dependent on some form of renal replacement therapy (RRT).

Keywords:

familial hypercholesterolemia – LDL-cholesterol – cardiovascular risk – chronic kidney disease – renal replacement therapy

Sources

[KDIGO 2012]. Summary of Recommendation Statements. Kidney Int Suppl 2013; 3(1): 5–14. Dostupné z DOI: <http://dx.doi.org/10.1038/kisup.2012.77>.
Rychlík I, Lopot F. Statistická ročenka dialyzační léčby v ČR 2018. Dostupné z WWW: <http://www.nefrol.cz/odbornici/dialyzacni-statistika>.
Nishi H, Higashihara T, Inagi R. Lipotoxicity Kidney, Heart, and Skeletal Muscle Dysfunction. Nutrients 2019; 11(7). pii: E1664. Dostupné z DOI: <http://dx.doi.org/10.3390/nu11071664>.
Vecka M, Dušejovská M, Staňková B et al. Non-cholesterol sterols and fatty acids in chronic hemodialysis patients. Nutr Metab Cardiovasc Dis (in print).
Dupont B, Oberfield SE, Smithwick EM et al. Close genetic linkage between HLA and congenital adrenal hyperplasia (21-hydroxylase deficiency). Lancet 1977; 2(8052–8053): 1309–1312. Dostupné z DOI: <http://dx.doi.org/10.1016/s0140–6736(77)90362–2>.
Weinberg JM. Lipotoxicity. Kidney Int 2006; 70(9): 1560–1566. Dostupné z DOI: <http://dx.doi.org/10.1038/sj.ki.5001834>.
Upadhyay A, Earley A, Lamont JL et al. Lipid-lowering therapy in persons with chronic kidney disease: A systematic review and meta-analysis. Ann Intern Med 2012; 157(4): 251–262. Dostupné z DOI: <http://dx.doi.org/10.7326/0003–4819–157–4-201208210–00005>.
Kotani K, Tsuzaki K, Traniguchi N et al. LDL particle size and reactive oxygen metabolites in dyslipidemic patients. Int J Prev Med 2012; 3(3): 160–166.
Galeano NF, Al-Haideri M, Keyserman F et al. Small dense low density lipoprotein has increased affinity for LDL receptor-independent cell surface binding sites: a potential mechanism for increased atherogenicity. J Lipid Res 1998; 39(6): 1263–1273.
Kronenberg F, Kuen E, Ritz E et al. Lipoprotein(a) serum concentrations and apolipoprotein(a) phenotypes in mild and moderate renal failure. J Am Soc Nephrol 2000; 11(1): 105–115.
Žák A, Zeman M. Sekundární dyslipidémie. In: Svačina Š (ed). Poruchy metabolismu a výživy. Galén: Praha 2010: 271–288. ISBN 978–80–7262–676–2.
Dodani S, Grice DG, Joshi S. Is HDL function as important as HDL quantity in the coronary artery disease risk assessment? J Clin Lipidol 2009; 3(2): 70–77. Dostupné z DOI: <http://dx.doi.org/10.1016/j.jacl.2009.02.001>.
Weichhart T, Kopecký C, Kubíček M et al. Serum amyloid A in uremic HDL promotes inflammation. J Am Soc Nephrol 2012; 23(5): 934–947. Dostupné z DOI: <http://dx.doi.org/10.1681/ASN.2011070668>.
Dušejovská M, Rychlík I, Žák A et al. Lipid Metabolism in Patients with End-Stage Renal Disease: A Five Year Follow-up Study. Curr Vasc Pharmacol 2018; 16(3): 298–305. Dostupné z DOI: <http://dx.doi.org/10.2174/1570161115666170530104143>.
Tesař V. Metabolické aspekty nemoci ledvin. In: Svačina Š (ed). Poruchy metabolismu a výživy. Galén: Praha 2010: 137–150. ISBN 978–80–7262–676–2.
de Zeeuw D, Anzalone DA, Cain VA et al. Renal effects of atorvastatin and rosuvastatin in patients with diabetes who have progressive renal disease (PLANET I): a randomised clinical trial. Lancet Diabetes Endocrinol 2015; 3(3): 181–190. Dostupné z DOI: <http://dx.doi.org/10.1016/S2213–8587(14)70246–3>.
Crouse JR, Raichlen JS, Riley WA et al. Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis: the METEOR trial. JAMA 2007; 297(12): 1344–1353. Dostupné z DOI: <http://dx.doi.org/10.1001/jama.297.12.1344>.
Su X, Zhang L, Lv J et al. Effect of Statins on Kidney Disease Outcomes: A Systematic Review and Meta-analysis. Am J Kidney Dis 2016; 67(6): 881–892. Dostupné z DOI: <http://dx.doi.org/10.1053/j.ajkd.2016.01.016>.
[Kidney Disease: Improving Global Outcomes (KDIGO) Lipid Work Group]. KDIGO Clinical Practice Guideline for Lipid Management in Chronic Kidney Disease. Kidney Int Suppl 2013; 3(3): 259–305. Dostupné z DOI: <http://dx.doi.org/10.1038/kisup.2013.27>.
Kim S, Ko K, Park S et al. Effect of Fenofibrate Medication on Renal Function. Korean J Fam Med 2017; 38(4): 192–198. Dostupné z DOI: <http://dx.doi.org/10.4082/kjfm.2017.38.4.192>.
McQuade CR, Griego J, Anderson J et al. Elevated serum creatinine levels associated with fenofibrate therapy. Am J Health Syst Pharm 2008; 65(2): 138–141. Dostupné z DOI: <http://dx.doi.org/10.2146/ajhp070005>.
Lipscombe J, Lewis GF, Cattran G et al. Deterioration in renal function associated with fibrate therapy. Clin Nephrol 2001; 55(1): 39–44.
Ritter JL, Nabulsi S. Fenofibrate-induced elevation in serum creatinine. Pharmacotherapy 2001;21(9): 1145–1149. Dostupné z DOI: <http://dx.doi.org/10.1592/phco.21.13.1145.34623>.
Ansquer JC, Dalton RN, Caussé E et al. Effect of fenofibrate on kidney function: a 6-week randomized crossover trial in healthy people. Am J Kidney Dis 2008; 51(6): 904–913. Dostupné z DOI: <http://dx.doi.org/10.1053/j.ajkd.2008.01.014>.
Hottelart C, El Esper N, Rose F et al. Fenofibrate increases creatininemia by increasing metabolic production of creatinine. Nephron 2002; 92(3): 536–541. Dostupné z DOI: <http://dx.doi.org/10.1159/000064083>.
Zeman M, Žák A, Vecka M et al. Treatment of hypertriglyceridemia with fenofibrate, fatty acid composition of plasma and LDL, and their relations to parameters of lipoperoxidation of LDL. Ann N Y Acad Sci 2002; 967: 336–341. Dostupné z DOI: <http://dx.doi.org/10.1111/j.1749–6632.2002.tb04289.x>.
Toth PP, Dwyer JP, Cannon CP et al. Efficacy nad safety of lipid lowering by alirocumab in chronic kidney disease. Kidney Int 2018; 93(6): 1397–1408. Dostupné z DOI: <http://dx.doi.org/10.1016/j.kint.2017.12.011>.
Coresh J, Selvin E, Stevens LA et al. Prevalence of chronic kidney disease in the United States. JAMA 2007; 298(17): 2038–2047. Dostupné z DOI: <http://dx.doi.org/10.1001/jama.298.17.2038>.