Publication details
Pharmacogenetics of diabetic nephropathy
| Authors | |
|---|---|
| Year of publication | 2011 |
| Type | Conference abstract |
| MU Faculty or unit | |
| Citation | |
| Description | 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. |