Open AccessImpact of renin-angiotensin system polymorphisms on renal haemodynamic responsiveness to acute angiotensin-converting enzyme inhibition in type 2 diabetes mellitus
Author(s) -
Bilge Volkan Salancı,
Selçuk Dağdelen,
Mehmet Alikaşifoĝlu,
Tomris Erbaş,
Mutlu Hayran,
Belkıs Erbaş
Publication year - 2009
Publication title -
jraas. journal of the renin-angiotensin-aldosterone system/journal of the renin-angiotensin-aldosterone system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 46
eISSN - 1752-8976
pISSN - 1470-3203
DOI - 10.1177/1470320309102326
Subject(s) - captopril , medicine , endocrinology , angiotensin converting enzyme , renin–angiotensin system , diabetes mellitus , hemodynamics , ace inhibitor , microalbuminuria , blood pressure
.The aim of this study was to document the impact of renin-angiotensin system (RAS) polymorphisms on renal haemodynamics and renal hormones in type 2 diabetes mellitus. Materials and methods. Fifty-nine adult patients were studied. Renal haemodynamics were evaluated using 99mTc-MAG3 clearance (MAG3 Cle ) using Bubeck's method and captopril renogram. RAS hormones and angiotensin-converting enzyme (ACE) levels were measured before and after captopril.ACE, angiotensin II type 1 receptor and angiotensinogen gene polymorphisms were analysed. Results. Post-captopril MAG3 Cle values were significantly lower in patients with microalbuminuria compared to nonproteinuric patients. Statistically significant negative correlation was found between clearance percentage change values and HbA 1c levels (r: —0.42, p=0.009). MAG3 Cle was relatively lower following captopril administration in DD patients, while a relative increment was observed in I allele carriers (p=0.02).TheAC-CC group had significantly higher mean post-captopril clearance value compared to the AA genotype (480.9±56.1 ml/min/1.73 m 2 vs. 428.4±74.8 ml/min/1.73 m 2 , p=0.022). Conclusions. Our data indicate that the heterogeneity of patients' response to ACE inhibition is, at least partly, genetically determined, and the genetic polymorphisms in RAS might predict the acute responsiveness to ACE inhibitors.