2011
Pharmacogenetics of diabetic nephropathy
BARTÁKOVÁ, VendulaZákladní údaje
Originální název
Pharmacogenetics of diabetic nephropathy
Název česky
Farmakogenetika diabetické nefropatie
Autoři
Vydání
13th Annual Meeting YARE - Young Active Research in Endocrinology, October 7th-9th, Stockholm, Sweden, 2011
Další údaje
Jazyk
angličtina
Typ výsledku
Konferenční abstrakt
Obor
30202 Endocrinology and metabolism
Stát vydavatele
Česká republika
Utajení
není předmětem státního či obchodního tajemství
Odkazy
Označené pro přenos do RIV
Ne
Organizační jednotka
Lékařská fakulta
Klíčová slova česky
diabetes mellitus, diabetická nefropatie, renin-angiotenzin-aldosteronový systém, farmakogenetika
Klíčová slova anglicky
diabetes mellitus, diabetic nephropathy, renin-angiotenzin-aldosterone system, pharmacogenetics
Změněno: 21. 10. 2011 11:36, MUDr. Vendula Bartáková, Ph.D.
Anotace
V originále
DN is one of the most common and serious complications of diabetes mellitus with pathological activation of renin-angiotensin-aldosterone system (RAAS) as the key pathogenetic mechanism. Pharmacological blockade of RAAS represents the main renoprotective treatment of DN. Genes coding for RAAS components show genetic variability. Several single nucleotide polymorphisms (SNPs) were shown to influence interindividual variability of RAAS (e.g circulating levels of RAAS compounds and enzyme activities). These functional genetic variants are supposed to modify therapeutic effect of RAAS blockers. Genetic variability together with other factors, which are objects of therapeutical compensation (e.g. glycaemia, blood pressure, proteinuria, lipidaemia and body weight) can affect progression of kidney damage in diabetics. In my research I study the effect of genetic variability in the selected components of RAAS on the progression of kidney disease in diabetic patients. I perform genetic analyses in approx. 370 patients with a different degree of DN with aim to evaluate for 11 pharmacogenetically important candidate loci. I have mapped a pharmacotherapy, especially RAAS blockers. As quantify of pharmacotherapy I will use a calculation of cumulative given dose. The results will demonstrate if there should be any difference in progression of diabetic nephropathy in connection with different pharmacotherapy and chosen SNP. My research area is pharmacogenetics of diabetic nephropathy (DN). DN is one of the most common and serious complications of diabetes mellitus with pathological activation of renin-angiotensin-aldosterone system (RAAS) as the key pathogenetic mechanism. Pharmacological blockade of RAAS represents the main renoprotective treatment of DN. Genes coding for RAAS components show genetic variability. Several single nucleotide polymorphisms (SNPs) were shown to influence interindividual variability of RAAS (e.g circulating levels of RAAS compounds and enzyme activities). These functional genetic variants are supposed to modify therapeutic effect of RAAS blockers. Genetic variability together with other factors, which are objects of therapeutical compensation (e.g. glycaemia, blood pressure, proteinuria, lipidaemia and body weight) can affect progression of kidney damage in diabetics. In my research I study the effect of genetic variability in the selected components of RAAS on the progression of kidney disease in diabetic patients. I perform genetic analyses in approx. 370 patients with a different degree of DN with aim to evaluate for 11 pharmacogenetically important candidate loci. I have mapped a pharmacotherapy, especially RAAS blockers. As quantify of pharmacotherapy I will use a calculation of cumulative given dose. The results will demonstrate if there should be any difference in progression of diabetic nephropathy in connection with different pharmacotherapy and chosen SNP.