gms | German Medical Science

49. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds)
19. Jahrestagung der Schweizerischen Gesellschaft für Medizinische Informatik (SGMI)
Jahrestagung 2004 des Arbeitskreises Medizinische Informatik (ÖAKMI)

Deutsche Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie
Schweizerische Gesellschaft für Medizinische Informatik (SGMI)

26. bis 30.09.2004, Innsbruck/Tirol

Impact of the apolipoprotein(a) size polymorphism on total mortality in dialysis patients: a 10 year follow-up

Meeting Abstract (gmds2004)

  • corresponding author presenting/speaker Florian Kronenberg - Institute of Medical Biology and Human Genetics, University of Innsbruck, Austria and GSF - National Research Center for Environment and Health, Munich-Neuherberg, Germany, Innsbruck und München, Österreich
  • Ulrich Neyer - Feldkirch Hospital, Feldkirch, Österreich
  • Paul König - Innsbruck University Hospital, Department of Clinical Nephrology, Austria, Innsbruck
  • Martin Auinger - Lainz Hospital, Vienna, Austria
  • Karl Lhotta - Innsbruck University Hospital, Department of Clinical Nephrology, Austria, Innsbruck, Österreich
  • Martin Wiesholzer - St. Pölten Hospital, Austria, St. Pölten, Österreich
  • Hans Dieplinger - Institute of Medical Biology and Human Genetics, University of Innsbruck, Austria, Innsbruck, Österreich

Kooperative Versorgung - Vernetzte Forschung - Ubiquitäre Information. 49. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 19. Jahrestagung der Schweizerischen Gesellschaft für Medizinische Informatik (SGMI) und Jahrestagung 2004 des Arbeitskreises Medizinische Informatik (ÖAKMI) der Österreichischen Computer Gesellschaft (OCG) und der Österreichischen Gesellschaft für Biomedizinische Technik (ÖGBMT). Innsbruck, 26.-30.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04gmds135

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Veröffentlicht: 14. September 2004

© 2004 Kronenberg et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for atherosclerosis [1], [2]. About 30-70% of the Lp(a) plasma concentrations are determined by the apo(a) size polymorphism [3]. This polymorphism is caused by a kringle-IV repeat polymorphism in the LPA gene with more than 30 isoforms [4]. These isoforms can be grouped in low (LMW) and high molecular weight (HMW) apo(a) isoforms.

Patients with kidney disease have a 10- to 20-fold increased risk for cardiovascular complications [5] which can not be explained by traditional atherosclerosis risk factors. Lipoprotein(a) is significantly elevated in these patients [6], [7], [8]. Previous studies, however, demonstrated that the apo(a) size polymorphism is a better predictor for cardiovascular disease than Lp(a) concentrations [9], [10], [11].

We are following a group of more than 600 dialysis patients recruited between 1991 and 1996 in five Austrian dialysis centers [7]. Until fall of 2004 we will have finished the follow-up of on average 10 years in these patients. Preliminary results show that about 65% of the patients have already died. A Cox hazard regression model reveals that the following variables contributed significantly to total mortality: [Tab. 1]

From the pathogenetic standpoint the LMW apo(a) phenotype is mainly associated with atherosclerotic complication. Therefore, we conclude that the association of the apo(a) phenotype with atherosclerosis in dialysis patients is so strong that we can even observe an association with total mortality to which cardiovascular events might contribute 50%. The ongoing validation of all fatal and non-fatal cardiovascular events will be of major importance for a deepened analysis of the data.


References

1.
Kronenberg F, Utermann G: Lipoprotein(a). In: Martini, L.: Encyclopedia of Endocrine Diseases, San Diego, Academic Press, 2004, pp 188-196.
2.
Danesh J, Collins R, Peto R: Lipoprotein(a) and coronary heart disease : meta-analysis of prospective studies. Circulation 102:1082-1085, 2000.
3.
Scholtz CL, Lingenhel A, Hillermann R, Stander IA, Kriek JA, Marais MP, Odendaal HJ, Kraft HG, Utermann G, Kotze MJ: Lipoprotein(a) determination and risk of cardiovascular disease in South African patients with familial hypercholesterolaemia. S. Afr. Med. J. 90:374-378, 2000.
4.
Utermann G, Menzel HJ, Kraft HG, Duba HC, Kemmler HG, Seitz C: Lp(a) glycoprotein phenotypes: inheritance and relation to Lp(a)-lipoprotein concentrations in plasma. J. Clin. Invest. 80:458-465, 1987
5.
Foley RN, Parfrey PS, Sarnak MJ: Epidemiology of cardiovascular disease in chronic renal disease. J. Am. Soc. Nephrol. 9:S16-S23, 1998.
6.
Dieplinger H, Lackner C, Kronenberg F, Sandholzer C, Lhotta K, Hoppichler F, Graf H, König P: Elevated plasma concentrations of lipoprotein(a) in patients with end-stage renal disease are not related to the size polymorphism of apolipoprotein(a). J. Clin. Invest. 91:397-401, 1993.
7.
Kronenberg F, König P, Neyer U, Auinger M, Pribasnig A, Lang U, Reitinger J, Pinter G, Utermann G, Dieplinger H: Multicenter study of lipoprotein(a) and apolipoprotein(a) phenotypes in patients with end-stage renal disease treated by hemodialysis or continuous ambulatory peritoneal dialysis. J. Am. Soc. Nephrol. 6:110-120, 1995.
8.
Stenvinkel P, Heimbürger O, Tuck CH, Berglund L: Apo(a)-isoform size, nutritional status and inflammatory markers in chronic renal failure. Kidney Int. 53:1336-1342, 1998.
9.
Kronenberg F, Kathrein H, König P, Neyer U, Sturm W, Lhotta K, Gröchenig E, Utermann G, Dieplinger H: Apolipoprotein(a) phenotypes predict the risk for carotid atherosclerosis in patients with end-stage renal disease. Arterioscler. Thromb. 14:1405-1411, 1994.
10.
Koch M, Kutkuhn B, Trenkwalder E, Bach D, Grabensee B, Dieplinger H, Kronenberg F: Apolipoprotein B, fibrinogen, HDL cholesterol and apolipoprotein(a) phenotypes predict coronary artery disease in hemodialysis patients. J. Am. Soc. Nephrol. 8:1889-1898, 1997.
11.
Kronenberg F, Neyer U, Lhotta K, Trenkwalder E, Auinger M, Pribasnig A, Meisl T, König P, Dieplinger H: The low molecular weight apo(a) phenotype is an independent predictor for coronary artery disease in hemodialysis patients: a prospective follow-up. J. Am. Soc. Nephrol. 10:1027-1036, 1999.