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Renin‐Angiotensin System Components Profile in Chronic Renal Failure Patients
Author(s) -
ARITA DANIELLE YURI,
Cunha Tatiana Sousa,
Perez Juliana Dinéia,
Sakata Maísa Mayumi,
Morais Luciene,
Watanabe Ingrid Kazue Mizuno,
Nogueira Marie Doki,
Arita Lilian Saemi,
Sousa Nádia Karina Guimarães,
Casarini Dulce Elena
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.824.1
Diabetes and hypertension are the major causes of chronic kidney disease (CKD). The local increase activity of Renin‐Angiotensin System has been implied in hypertension, heart failure, CKD and other pathogenesis. Our group has already described differences in N‐domain ACE isoforms profile between urine of healthy and hypertensive patients, suggesting that the 90 kDa ACE isoform could be a possible genetic marker of hypertension. The aim is to associate dysfunctions of the renal system with possible alterations in ACE isoforms profile in CKD patients. Patients were divided into 3 groups: (I) DM ‐ normotensive patients with type 1 DM and normoalbuminuria (n=37); (II) DMH ‐ hypertensive patients with type 1 DM and microalbuminuria (n=29); (III) DMHCR ‐ patients with DM type 1 and CKD (n=19). The ratio between specific substrates for N‐ and C‐domain activity (ZhePhe/HHL) showed a high N‐domain activity in DMH and DMHCR patients. ACE isoforms were significantly over‐expressed in urine of DMHCR group as compared with the other two groups, corroborating with the activity alterations. Bradykinin levels were statistically decreased in both DMH and DMHCR groups compared to only diabetes group. Our results suggest that pathophysiological changes could lead to an increased activity and expression of N‐domain ACE isoform. Therefore, it possibly may be one of the most important targets on the treatment of diabetic nephropathy, besides early detecting and preventing CKD (Supported by Fapesp and CNPq).