dc.contributor.author | Makówka, Agnieszka | |
dc.contributor.author | Dryja, Przemysław | |
dc.contributor.author | Chwatko, Grażyna | |
dc.contributor.author | Bald, Edward | |
dc.contributor.author | Nowicki, Michał | |
dc.date.accessioned | 2015-02-03T16:34:59Z | |
dc.date.available | 2015-02-03T16:34:59Z | |
dc.date.issued | 2012 | |
dc.identifier.citation | Makówka et al.: Treatment of chronic hemodialysis patients with low-dose fenofibrate effectively reduces plasma lipids and affects plasma redox status. Lipids in Health and Disease 2012 11:47. | pl_PL |
dc.identifier.issn | 1476-511X | |
dc.identifier.uri | http://hdl.handle.net/11089/6494 | |
dc.description.abstract | Dyslipidemia is common in chronic hemodialysis patients and its underlying mechanism is complex. Hemodialysis causes
an imbalance between antioxidants and production of reactive oxygen species, which induces the oxidative stress and
thereby may lead to accelerated atherosclerosis. Statins have been found to be little effective in end-stage kidney disease
and other lipid-lowering therapies have been only scarcely studied. The study aimed to assess the effect of low-dose
fenofibrate therapy on plasma lipids and redox status in long-term hemodialysis patients with mild hypertriglyceridemia.
Twenty seven chronic hemodialysis patients without any lipid-lowering therapy were included in a double-blind
crossover, placebo-controlled study. The patients were randomized into two groups and were given a sequence of either
100 mg of fenofibrate per each hemodialysis day for 4 weeks or placebo with a week-long wash-out period between
treatment periods. Plasma lipids, high sensitive C-reactive protein (CRP), urea, creatinine, electrolytes, phosphocreatine
kinase (CK), GOT, GPT and plasma thiols (total and free glutathione, homocysteine, cysteine and cysteinylglycine) were
measured at baseline and after each of the study periods. Plasma aminothiols were measured by reversed phase HPLC
with thiol derivatization with 2-chloro-1-methylquinolinium tetrafluoroborate.
Fenofibrate therapy caused a significant decrease of total serum cholesterol, LDL cholesterol and triglycerides and an
increase of HDL cholesterol. The treatment was well tolerated with no side-effects but there was a small but significant
increase of CK not exceeding the upper limit of normal range. There were no changes of serum CRP, potassium, urea,
and creatinine and liver enzymes during the treatment. Neither total nor total free cysteinylglycine and cysteine changed
during the study but both total and free glutathione increased during the therapy with fenofibrate and the same was
observed in case of plasma homocysteine.
The study shows that a treatment with reduced fenofibrate dose is safe and effective in reducing serumtriglycerides and
cholesterol in chronic dialysis patients and may shift plasma aminothiol balance towards a more antioxidative pattern. | pl_PL |
dc.language.iso | en | pl_PL |
dc.publisher | BioMed Central | pl_PL |
dc.relation.ispartofseries | (Lipids in Health and Disease;2012, 11 | |
dc.rights | Uznanie autorstwa-Użycie niekomercyjne-Bez utworów zależnych 3.0 Polska | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/pl/ | * |
dc.subject | Dyslipidemia | pl_PL |
dc.subject | Fenofibrate | pl_PL |
dc.subject | Hemodialysis | pl_PL |
dc.subject | Inflammation | pl_PL |
dc.subject | Oxidative stress | pl_PL |
dc.title | Treatment of chronic hemodialysis patients with low-dose fenofibrate effectively reduces plasma lipids and affects plasma redox status | pl_PL |
dc.type | Article | pl_PL |
dc.page.number | 1-7 | pl_PL |
dc.contributor.authorAffiliation | Agnieszka Makówka- Department of Nephrology, Hypertension and Kidney Transplantation, Medical University of Łódź | pl_PL |
dc.contributor.authorAffiliation | Przemysław Dryja, Department of Nephrology, Hypertension and Kidney Transplantation, Medical University of Łódź | pl_PL |
dc.contributor.authorAffiliation | Grażyna Chwatko, Department of Environmental Chemistry, University of Łódź | pl_PL |
dc.contributor.authorAffiliation | Edward Bald, Department of Environmental Chemistry, University of Łódź | pl_PL |
dc.contributor.authorAffiliation | Michał Nowicki, Department of Nephrology, Hypertension and Kidney Transplantation, Medical University of Łódź, University Hospita | pl_PL |
dc.references | Amann K, Tyralla K, Gross ML, Eifert T, Adamczak M, Ritz E: Special characteristics of atherosclerosis in chronic renal failure. Clin Nephrol 2003, 60(Suppl.1):S13–S21. | pl_PL |
dc.references | Drüeke TB, Massy ZA: Atherosclerosis in CKD: differences from the general population. Nat Rev Nephrol 2010, 6:723–735. | pl_PL |
dc.references | Roberts MA, Hare DL, Ratnaike S, Lerino FL: Cardiovascular biomarkers in CKD: pathophysiology and implications for clinical management of cardiac disease. Am J Kidney Dis 2006, 48:341–360. | pl_PL |
dc.references | Badimon L, Torey RF, Vilahur G: Update on lipids, inflammation and atherothrombosis. Thromb Haemost 2011, 105(Suppl.1):S34–S42. | pl_PL |
dc.references | Keech A, Simes RJ, Barter P, Best J, Scott R, Taskinen MR, Forder P, Pillai A, Davis T, Glasziou P, Drury P, Kesäniemi YA, Sullivan D, Hunt D, Colman P, d’Emden M, Whiting M, Ehnholm C, Laakso M, FIELD study investigators: Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD Study): randomized controlled trial. Lancet 2005, 366:1849–1861. | pl_PL |
dc.references | Ansquer JC, Foucher C, Rattier S, Taskinen MR, Steiner G, DAIS Investigators: Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS). Am J Kidney Dis 2005, 45:485–493. | pl_PL |
dc.references | Wu J, Song Y, Li H, Chen J: Rhabdomyolysis associated with fibrate therapy: review of 76 published cases and a new case report. Eur J Clin Pharmacol 2009, 65:1169–1174. | pl_PL |
dc.references | Attridge RL, Linn WD, Ryan L, Koeller J, Frei CR: Evaluation of the incidence and risk factors for development of fenofibrate-associated nephrotoxicity. J Clin Lipidol 2012, 6:19–26. | pl_PL |
dc.references | Ansquer JC, Dalton RN, Caussé E, Crimet D, Le Malicot K, Foucher C: Effect of fenofibrate on kidney function: a 6-week randomized crossover trial in healthy people. Am J Kidney Dis 2008, 51:904–913. | pl_PL |
dc.references | Molitch ME: Management of dyslipidemias in patients with diabetes and chronic kidney disease. Clin J Am Soc Nephrol 2006, 1:1090–1099. | pl_PL |
dc.references | Arora MK, Reddy K, Balakumar P: The low dose combination of fenofibrate and rosiglitazone halts the progression of diabetes-induced experimental nephropathy. Eur J Pharmacol 2010, 636:137–144. | pl_PL |
dc.references | Hou X, Shen YH, Li C, Wang F, Zhang C, Bu P, Zhang Y: PPARalpha agonist fenofibrate protects the kidney from hypertensive injury in spontaneously hypertensive rats via inhibition of oxidative stress and MAPK activity. Biochem Biophys Res Commun 2010, 394:653–659. | pl_PL |
dc.references | Shin SJ, Lim JH, Chung S, Youn DY, Chung HW, Kim HW, Lee JH, Chang YS, Park CW: Peroxisome proliferator-activated receptor-alpha activator fenofibrate prevents high-fat diet-induced renal lipotoxicity in spontaneously hypertensive rats. Hypertens Res 2009, 32:835–845. | pl_PL |
dc.references | Liang CC, Wang IK, Kuo HL, Yeh HC, Lin HH, Liu YL, Hsu WM, Huang CC, Chang CT: Long-term use of fenofibrate is associated with increased prevalence of gallstone disease among patients undergoing maintenance hemodialysis. Ren Fail 2011, 33:489–493. | pl_PL |
dc.references | Desager JP, Costermans J, Verberckmoes R, Harvengt C: Effect of hemodialysis on plasma kinetics of fenofibrate in chronic renal failure. Nephron 1982, 31:51–54. | pl_PL |
dc.references | Harvengt C, Desager JP: Pharmacokinetics of fenofibrate in man. Nouv Presse Med 1980, 49:3725–3737. | pl_PL |
dc.references | Presse Med 1980, 49:3725–3737. 17. Okopień B, Haberka M, Madej A, Belowski D, Labuzek K, Krysiak R, Zieliński M, Basiak M, Herman ZS: Extralipid effects of micronized fenofibrate in dyslipidemic patients. Pharmacol Rep 2006, 58:729–735 | pl_PL |
dc.references | Himmelfarb J, McMenamin E, McMonagle E: Plasma aminothiol oxidation in chronic hemodialysis patients. Kidney Int 2002, 61:705–716 | pl_PL |
dc.references | Bald E, Chwatko G, Głowacki R, Kuśmierek K: Analysis of plasma thiols by high-performance liquid chromatography with ultraviolet detection. J Chromatogr A 2004, 1032:109–115. | pl_PL |
dc.references | Yao Q, Pecoits-Filho R, Lindholm B, Stenvinkel P: Traditional and nontraditional risk factors as contributors to atherosclerotic cardiovascular disease in end-stage renal disease. Scand J Urol Nephrol 2004, 38:405–416 | pl_PL |
dc.references | Yeun JY, Kaysen GA: C-reactive protein, oxidative stress, homocysteine, and troponin as inflammatory and metabolic predictors of atherosclerosis in ESRD. Curr Opin Nephrol Hypertens 2000, 9:621–630. | pl_PL |
dc.references | Kurnatowska I, Grzelak P, Stefańczyk L, Nowicki M: Tight relations between coronary calcification and atherosclerotic lesions in the carotid artery in chronic dialysis patients. Nephrology 2010, 15:184–189. | pl_PL |
dc.references | Kaysen GA: Biochemistry and biomarkers of inflamed patients: why look, what to assess. Clin J Am Soc Nephrol 2009, 4(Suppl.1):S56–S63. | pl_PL |
dc.references | Wu TJ, Ou HY, Chou CW, Hsiao SH, Lin CY, Kao PC: Decrease in inflammatory cardiovascular risk markers in hyperlipidemic diabetic patients treated with fenofibrate. Ann Clin Lab Sci 2007, 37:158–166 | pl_PL |
dc.references | Hermans MP: Non-invited review: prevention of microvascular diabetic complications by fenofibrate: lessons from FIELD and ACCORD. Diab Vasc Dis Res 2011, 8:180–189. | pl_PL |
dc.references | Genuth S, Ismail-Beigi F: Clinical Implications of the ACCORD Trial. J Clin Endocrinol Metab 2012, 97:41–48. | pl_PL |
dc.references | Watanabe H, Miyamoto Y, Otagiri M, Maruyama T: Update on the pharmacokinetics and redox properties of protein-bound uremic toxins. J Pharm Sci 2011, 100:3682–3695. | pl_PL |
dc.references | Bostom AG, Shemin D, Verhoef P, Nadeau MR, Jacques PF, Selhub J, Dworkin L, Rosenberg IH: Elevated fasting total plasma homocysteine levels and cardiovascular disease outcomes in maintenance dialysis patients: A prospective study. Arteriosclerosis Thromb Vasc Biol 1997, 17:2554–2558. | pl_PL |
dc.references | Suliman ME, Divino-Filho JC, Barany P, Anderstam B, Lindholm B, Bergström J: Effects of high-dose folic acid and pyridoxine on plasma and erythrocyte sulfur amino acids in hemodialysis patients. J Am Soc Nephrol 1999, 10:1287–1296. | pl_PL |
dc.references | Caussé E, Ribes D, Longlune N, Kamar N, Durand D, Salvayre R, Rostaing L: Aminothiols and allantoin in chronic dialysis patients: effects of hemodialysis sessions. Clin Nephrol 2010, 73:51–57. | pl_PL |
dc.references | Sauls DL, Arnold EK, Bell CW, Allen JC, Hoffman M: Pro-thrombotic and pro-oxidant effects of diet-induced hyperhomocysteinemia. Thromb Res 2007, 120:117–126 | pl_PL |
dc.references | Hofmann MA, Lalla E, Lu Y: Hyperhomocysteinemia enhances vascular inflammation and accelerates atherosclerosis in a murine model. J Clin Invest 2001, 107:675–683. | pl_PL |
dc.references | Graham LM, Daly LE, Refsum HM, Robinson K, Brattström LE, Ueland PM, Palma-Reis RJ, Boers GH, Sheahan RG, Israelsson B, Uiterwaal CS, Meleady R, McMaster D, Verhoef P, Witteman J, Rubba P, Bellet H, Wautrecht JC, de Valk HW, Sales Lúis AC, Parrot-Rouland FM, Tan KS, Higgins I, Garcon D, Andria G: Plasma homocysteine as a risk factor for vascular disease: The European Concerted Action Project. JAMA 1997, 277:1775–1781. | pl_PL |
dc.references | Boushey CJ, Beresford SA, Omenn GS, Motulsky AG: A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. JAMA 1995, 274:1049–1057. | pl_PL |
dc.references | Kugiyama K, Ohgushi M, Motoyama T, Hirashima O, Soejima H, Misumi K, Yoshimura M, Ogawa H, Sugiyama S, Yasue H: Intracoronary infusion of reduced glutathione improves endothelial vasomotor response to acetylcholine in human coronary circulation. Circulation 1998, 97:2299– 2301. | pl_PL |
dc.references | Morrison JA, Jacobsen DW, Sprecher DL, Robinson K, Khoury P, Daniels SR: Serum glutathione in adolescent males predicts parental coronary heart disease. Circulation 1999, 100:2244–2247. | pl_PL |
dc.references | Lapenna D, de Gioia S, Ciofani G, Mezzetti A, Ucchino S, Calafiore AM, Napolitano AM, Di Ilio C, Cuccurullo F: Glutathione-related antioxidant defenses in human atherosclerotic plaques. Circulation 1998, 97:1930– 1934. | pl_PL |
dc.references | Ueland PM, Mansoor MA, Guttormsen AB, Müller F, Aukrust P, Refsum H, Svardal AM: Reduced, oxidized and protein-bound forms of homocysteine and other aminothiols in plasma comprise the redox thiol status–a possible element of the extracellular antioxidant defense system. J Nutr 1996, 126(4 Suppl):1281S–1284S. | pl_PL |
dc.references | Kasiske BL: Hyperlipidemia in patients with chronic renal disease. Am J Kidney Dis 1998, 32:S142–S156. | pl_PL |
dc.references | Brunzell JD, Albers JJ, Haas LB, Goldberg AP, Agadoa L, Sherrard DJ: Prevalence of serum lipid abnormalities in chronic hemodialysis. Metabolism 1977, 26:903–910 | pl_PL |
dc.references | Attman PO, Samuelsson O: Dyslipidemia of kidney disease. Curr Opin Lipidol 2009, 20:293–299. | pl_PL |
dc.references | Chauhan V, Vaid M: Dyslipidemia in chronic kidney disease: managing a high-risk combination. Postgrad Med 2009, 121:54–61. | pl_PL |
dc.references | Ritz E, Nowicki M, Więcek A: Organ and metabolic complications: Lipids/ atherosclerosis. In Replacement of renal function by dialysis. Edition 4. Edited by Jacobs C, Kjellstrand CM, Koch KM, Winchester JF. The Netherlands: Kluwer Academic Publishers; 1996:1003–1013. | pl_PL |
dc.references | Ting RD, Keech AC, Drury PL, Donoghoe MW, Hedley J, Jenkins AJ, Davis TM, Lehto S, Celermajer D, Simes RJ, Rajamani K, Stanton K: on behalf of the FIELD Study Investigators. Benefits and safety of long-term fenofibrate therapy in people with type 2 diabetes and renal impairment: The FIELD Study. Diabetes Care 2012, 35:218–225 | pl_PL |
dc.references | Kalaitzidis RG, Elisaf MS: The role of statins in chronic kidney disease. Am J Nephrol 2011, 34:195–202. | pl_PL |
dc.references | Epstein M, Vaziri ND: Statins in the management of dyslipidemia associated with chronic kidney disease. Nat Rev Nephrol 2012, 8:214–223. | pl_PL |
dc.identifier.doi | 10.1186/1476-511X-11-47 | |