title: [Genetic predisposition to systemic complications of arterial hypertension in maintenance haemodialysis patients].
abstract: Cardiovascular disease is the most common cause of a high morbidity and mortality in patients on renal replacement therapy and is responsible for about 50% of deaths. Hypertension is the main risk factor for cardiovascular events in the general population as well as in haemodialysed (HD) patients. The hypertension in HD patients is caused by excess extracellular fluid volume (ECV) on the other hand hypertension resistant to normalization of ECV may result from the accelerated activity of the systemic and local--vascular renin-angiotensin-aldosteron system (RAAS). RAAS genes are potential etiological candidates for cardiovascular damage. The aim of the study was to evaluate the prevalence of hypertension, left ventricular hypertrophy, hypertensive retinopathy in patients treated with haemodialysis and to evaluate the association between the polymorphism of RAAS genes: ACE I/D, AGT M235T AT1R A1166C, CYP112 (-344) and the systemic complications of arterial hypertension such as hypertensive retinopathy, left ventricular hypertrophy and also mortality in haemodialysis patients.
  
  
  METHODS
  The studied population consisted of 302 HD patients (175 men, 127 women) age 21-87, mean 56, at four dialysis units. Patients with cardiac defect, advanced coronary artery disease and atrial fibrillation were excluded from the study. 62 patients died during 3,5 years of observation. Methods consisted of tree times repeated blood pressure measurements before and post dialysis, echocardiography, direct opthalmoscopy (Keith-Wegener-Barker classification of hypertensive retinopathy) and DNA analysis--genotypes ACE I/D, AGT M235T AT1R A1166C, CYP11B2 T(-344)C were determined through PCR or PCR-RFLP method.
  
  
  RESULTS
  Hypertension was present in 72%, LVH in 84% haemodialysed patients. Arterial pressure correlated with LVMI values and hypertension was connected with LVH. Insufficient control of blood pressure and LVH were connected with worse survival in HD patients.
  
  
  CONCLUSIONS
  It seems that I/D polymorphism ACE gene and AC AT1 gene influence the development of hypertension and LVH in HD patients. The most dangerous in the development of hypertension and LVH was DD genotype ACE gene and CC AT1 gene. ACE I/D, AGT M/T, AT1 A/C, CYP11B2 T/C polymorphism appears to have no relation to the short-term prognosis in HD patients. The mortality did not differ among groups with different genotypes of ACE I/D, AGT M/T AT1 A/C, CYP11B2 T/C polymorphisms. Direct ophtalmoscopy seems to be an insufficient method in the estimation of the systemic complications of hypertension in haemodialysed patients.
authors.affiliation: Klinika Nefrologii, Transplantologii i Chorób Wewnetrznych. bbzoma@mp.pl
authors.forename: Beata
authors.initials: B
authors.lastname: Bzoma
authors.forename: Alicja
authors.initials: A
authors.lastname: Debska-Slizień
authors.forename: Maria
authors.initials: M
authors.lastname: Dudziak
authors.forename: Krystyna
authors.initials: K
authors.lastname: Raczyńska
authors.forename: Waldemar
authors.initials: W
authors.lastname: Slizień
authors.forename: Alicja
authors.initials: A
authors.lastname: Brylowska
authors.forename: Bolesław
authors.initials: B
authors.lastname: Rutkowski
mesh_terms: D000101:Acetyl-CoA C-Acetyltransferase / Q000235:genetics*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015984:Causality; D015897:Comorbidity; D005260:Female; D006801:Humans; D006977:Hypertension, Renal / Q000453:epidemiology*; D017379:Hypertrophy, Left Ventricular / Q000453:epidemiology*; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D011110:Polymorphism, Genetic; D015995:Prevalence; D006435:Renal Dialysis / Q000706:statistics & numerical data*; D012164:Retinal Diseases / Q000453:epidemiology*; D015996:Survival Rate
chemical_list: C506639:ACAT1 protein, human; D000101:Acetyl-CoA C-Acetyltransferase; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A