Vnitřní lékařství 5/2020

PŘEHLEDOVÉ ČLÁNKY Etiologie a management dyslipidemie u pacientů s chronickým onemocněním ledvin | 281  / Vnitř Lék 2020; 66(5): 275–281 /  VNITŘNÍ LÉKAŘSTVÍ www.casopisvnitrnilekarstvi.cz „ IDL – intermediate density lipoprotein „ ICHDK – ischemická choroba dolních končetin „ KDIGO – Kidney disease: Imporving Global Outcomes „ LDL – low density lipoprotein „ Lp(a) – lipoprotein(a) „ MDA – malondialdehyd „ MIA syndrom – malnutrition, inflammation, atherosclerosis syndrom „ MIAC syndrom – malnutrition, inflammation, atherosclerosis, cal- cification syndrome „ NADPH – nikotinaadenindinukleotidfosfát „ NPC1L1 – Niemann‑Pick C1- like protein 1 „ Ox‑LDL – oxidované LDL „ PCSK9 – proprotein konvertázy subtilisin/kexin typu 9 (proprotein convertase subtilisin/kexin type 9) „ PD – peritoneální dialýza „ PON – paraoxonáza „ sd‑LDL – small density lipoprotein „ TC – celkový cholesterol „ TxL – transplantace ledviny „ VLDL – very low density lipoprotein LITERATURA 1. Wanner C, Tonelli M. Kidney Disease: Improving Global Outcomes (KDIGO) Lipid Work Group. KDIGO Clinical Practice Guideline for Lipid Management in Chronic Kidney Disea- se. Kidney Int 2014; 85: 1303–1309. 2. Vostalová J, Galandaková A, Štrebl P, et al. Oxidační stres u pacientů s náhradou funkce ledvin hemodialýzou a peritoneální dialýzou. Vnitř Lék 2012; 58: 466–472. 3. Ellis RJ, Small DM, Ng KL, et al. Indoxyl Sulfate Induces Apoptosis and Hypertrophy in Human Kidney Proximal Tubular Cells. Toxicol Pathol 2018; 46: 449–459. 4. Atamer A, Kocyigit Y, Ecder SA, et al. Effect of oxidative stress on antioxidant en- zyme activities, homocysteine and lipoproteins in chronic kidney disease. J Nephrol 2008; 21: 924–930. 5. Tribble DL, Rizzo M, Chait A, et al. Enhanced oxidative susceptibility and reduced antioxi- dant content of metabolic precursors of small, dense low‑density lipoproteins. Am J Med 2001; 110: 103–110. 6. Kwiterovich jr. PO. Clinical relevance of the biochemical, metabolic, and genetic factors that influence low‑density lipoprotein heterogeneity. Am J Cardiol 2002; 90: 30i–47i. 7. Chait A, Brazg RL, Tribble DL, et al. Susceptibility of small, dense, low‑density lipopro- teins to oxidative modification in subjects with the atherogenic lipoprotein phenotype, pattern B. Am J Med 1993; 94: 350–356. 8. Kotani K, Tsuzaki K, Traniguchi N, et al. LDL particle size and reactive oxygen metaboli- ties in dyslipidemic patients. Int J Prev Med 2012; 3: 160–166. 9. Gardner CD, Fortmann SP, Krauss RM. Association of small low‑density lipoprotein particles with the incidence of coronary artery disease inmen and women. JAMA 1996; 276: 875–881. 10. 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 me- chanism for increased atherogenicity. J Lipid Res 1998; 39: 1263–1273. 11. Milionis HJ, Elisaf MS, Tselepis A, et al. Apolipoprotein(a) phenotypes and lipopro- tein(a) concentrations in patients with renal failure. Am J Kidney Dis 1999; 33: 1100–1106. 12. Loscalzo J. Lipoprotein(a): a unique risk factor for atherothrombotic disease. Arteriosc- lerosis 1990; 10: 672–679. 13. Kronenberg F, Kuen E, Ritz E, et al. Lipoprotein(a) serum concentrations and apolipopro- tein(a) phenotypes in mild and moderate renal failure. J Am Soc Nephrol 2000; 11: 105–115. 14. Žák A, Zeman M. Sekundární dyslipidémie. In: Svačina Š (ed.) Poruchy metabolismu a výživy. Praha: Galén 2010, 271–288. 15. Fielding CJ, Fielding PE. Molecular physiology of reverse cholesterol transport. J Li- pid Res 1995; 36: 211–228. 16. Dodani S, Grice DG, Joshi S. Is HDL function as important as HDL quantity in the coro- nary artery disease risk assessment? J Clin Lipidol 2009; 3: 70–77. 17. Dantoine TF, Debord J, Charmes JP, et al. Decrease of serum paraoxonase activity in chronic renal failure. J Am Soc Nephrol 1998; 9: 2082–2088. 18. Weichhart T, Kopecky C, Kubicek M, et al. Serum amyloid A in uremic HDL promotes inflammation. J Am Soc Nephrol 2012; 23: 934–947. 19. Dušejovská M, Staňková B, Vecka M, et al. Lipid Metabolism in Patients with End­ ‑Stage Renal Disease: A Five‑Year Follow‑up Study. Curr Vasc Pharmacol 2018; 16: 298–305. 20. Movva R, Rader DJ. Laboratory assement of HDL heterogenity and function. Clin Chem 2008; 54: 788–800. 21. Feig JE, Shamir R, Fisher EA. Atheroprotective effects of HDL: beyond reverse choles- terol transport. Curr Drug Targets 2008; 9: 196–203. 22. Tesař V Metabolické aspekty nemoci ledvin. In: Svačina Š (ed.) Poruchy metabolismu a výživy. Praha: Galén 2010, 137–150. 23. de Zeeuw D, Anzalone DA, Cain VA, et al. Renal effects of atorvastatin and rosuvasta- tin in patients with diabetes who have progressive renal disease (PLANET I): a randomi- sed clinical trial. Lancet Diabetes Endocrinol 2015; 3: 181–190. 24. 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 METE- OR trial. JAMA 2007; 297: 1344–1353. 25. 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: 881–892. 26. Kim S, Ko K, Park S, et al. Effect of Fenofibrate Medication on Renal Function. Korean J Fam Med 2017; 38: 192–198. 27. Broeders N, Knoop C, Antoine M, et al. Fibrate‑induced increase in blood urea and crea- tinine: is gemfibrozil the only innocuous agent. Nephrol Dial Transplant 2000; 15: 1993–1999. 28. Paul S, Mohan V. Fenofibrate can increase serum creatinine levels in renal insufficien- cy. J Assoc Physicians India 2006; 54: 337. 29. McQuade CR, Griego J, Anderson J, et al. Elevated serum creatinine levels associated with fenofibrate therapy. Am J Health Syst Pharm 2008; 65: 138–141. 30. Lipscombe J, Lewis GF, Cattran D, et al. Deterioration in renal function associated with fibrate therapy. Clin Nephrol 2001; 55: 39–44. 31. Ritter JL, Nabulsi S. Fenofibrate‑induced elevation in serum creatinine. Pharmacothe- rapy 2001; 21: 1145–1149. 32. 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: 904–913. 33. Hottelart C, El Esper N, Rose F, et al. Fenofibrate increases creatininemia by increasing metabolic production of creatinine. Nephron 2002; 92: 536–541. 34. 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 lipope- roxidation of LDL. Ann N Y Acad Sci 2002; 967: 336–341. 35. Kremer AE, Mettang T. Pruritus in systemic diseases: Common and rare etiologies. Hautarzt 2016; 67: 606–614. 36. Toth PP, Dwyer JP, Cannon CP, et al. Efficacy and safety of lipid lowering by alirocumab in chronic kidney disease. Kidney Int 2018; 93: 1397–1408. 37. Bláha V, Bláha M, Lánská M, et al. LDL‑aferéza v léčbě familiárních hyperlipoproteine- mií. Vnitř Lék 2014; 60: 970–976. 38. Coresh J, Selvin E, Stevens LA, et al. Prevalence of chronic kidney disease in the United States. JAMA 2007; 298: 2038–2047. 39. Dron JS, Hegele RA. Genetics and lipoprotein Disorders and Traits. Curr. Genet. Med. Rep. 2016; 4: 130–141.