scholarly journals Diabetic Nephropathy Induced by IncreasedAceGene Dosage Is Associated with High Renal Levels of Angiotensin (1–7) and Bradykinin

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Nádia Bertoncello ◽  
Roseli Peres Moreira ◽  
Danielle Yuri Arita ◽  
Danielle S. Aragão ◽  
Ingrid Kazue Mizuno Watanabe ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Nephropathy ◽  
Angiotensin Converting Enzyme ◽  
Renal Dysfunction ◽  
Population Studies ◽  
Structure And Function ◽  
Diabetic Group ◽  
Ang Ii ◽  
Converting Enzyme ◽  
And Function

Population studies have shown an association between diabetic nephropathy (DN) and insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene (ACEin humans,Acein mice). The aim was to evaluate the modulation ofAcecopies number and diabetes mellitus (DM) on renal RAS and correlate it with indicators of kidney function. Increased number of copies of theAcegene, associated with DM, induces renal dysfunction. The susceptibility to the development of DN in 3 copies of animals is associated with an imbalance in activity of RAS enzymes leading to increased synthesis of Ang II and Ang-(1–7). Increased concentration of renal Ang-(1–7) appears to potentiate the deleterious effects triggered by Ang II on kidney structure and function. Results also show increased bradykinin concentration in 3 copies diabetic group. Taken together, results indicate that the deleterious effects described in 3 copies diabetic group are, at least in part, due to a combination of factors not usually described in the literature. Thus, the data presented here show up innovative and contribute to understanding the complex mechanisms involved in the development of DN, in order to optimize the treatment of patients with this complication.

scholarly journals Prospects in the treatment of diabetic nephropathy

2019 ◽  
Vol 43 (3) ◽  
pp. 20-22
Author(s):  
M. V. Shestakova ◽  
A. V. Vorontsov ◽  
S. G. Vykhristyuk ◽  
I. I. Dedov
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Nephropathy ◽  
Angiotensin Converting Enzyme ◽  
Vascular Endothelium ◽  
Structural Changes ◽  
Vascular Complications ◽  
Converting Enzyme ◽  
Treatment And Prevention ◽  
Vasoactive Factors ◽  
Triggering Factor

The authors discuss new approaches to the treatment and prevention of diabetic nephropathy based on elimination of the pathogenetic factors of its development. Hyperglycemia, the main triggering factor of vascular complications of diabetes mellitus. induces a cascade of other pathological reactions, such as renal dysfunction, biochemical and structural changes in the basal membranes of renal capillaries, and stimulates the secretion of vasoactive factors of vascular endothelium and platelets. Blocking of these reactions by specific agents inhibits the progress of diabetic nephropathy. The authors share their experience gained in the treatment of diabetic nephropathy with inhibitors of angiotensin-converting enzyme, glycosaminoglycanes, and thromboxane synthesis inhibitors. These drugs are more effective if prescribed at the early stages of diabetic involvement of the kidneys.

Effect of 24-Week Treatment with Telmisartan on Myocardial Structure and Function: Relationship to Insertion/Deletion Polymorphism of the Angiotensin-Converting Enzyme Gene

2005 ◽  
Vol 33 (1_suppl) ◽  
pp. 30A-38A ◽  
Author(s):  
AO Conrady ◽  
IO Kiselev ◽  
NI Usachev ◽  
AN Krutikov ◽  
OI Yakovleva ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Converting Enzyme ◽  
Diastolic Function ◽  
Left Ventricular Mass ◽  
Left Ventricular ◽  
Structure And Function ◽  
Converting Enzyme ◽  
Ace Gene ◽  
Myocardial Structure ◽  
And Function

The aim of the present study was to assess the effect of treatment with the angiotensin II receptor blocker telmisartan for 24 weeks on myocardial structure and function in patients with essential hypertension, and the relationship between this effect and the structural polymorphism of the angiotensin-converting enzyme (ACE) gene. Thirty-five patients with essential hypertension and left ventricular hypertrophy (LVH) without other associated morbidity were included in an open-label, non-comparative study. The patients were treated with telmisartan 40-80 mg once daily. In the final analysis, there were 29 patients who received the full course of treatment and were evaluated echocardiographically before and after treatment by the same blinded investigator, and myocardial structure and function were analysed. The myocardial mass of the left ventricle was determined in M-mode. Assessment of diastolic function of transmitral blood flow was performed using pulsed Doppler echocardiography. All patients were genotyped for insertion/deletion (I/D) polymorphism of the ACE gene. Telmisartan produced a significant reduction in left ventricular mass index from 140.4 ± 48.6 to 128.7 ± 40.6 g/m2 that was accompanied by an improvement in characteristics of diastolic function. The decrease in LVH was more significant in the ID genotype group than in the II and DD groups. Thus, prolonged treatment with telmisartan is accompanied by an improvement in myocardial structure, expressed as a reduction in left ventricular mass and function that is more marked in patients with ID genotype of the ACE gene.

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