Premium
N‐DOMAIN ACE ACTIVITIES AND EXPRESSION PROFILES IN CHRONIC RENAL FAILURE PATIENTS
Author(s) -
ARITA DANIELLE YURI,
SAKATA MAISA MAYUMI,
WATANABE INGRID KAZUE,
PEREZ JULIANA DINEIA,
COLUCCI JULIANA ALMADA,
MORAIS LUCIENE,
CASARINI DULCE ELENA
Publication year - 2009
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.23.1_supplement.930.10
Subject(s) - microalbuminuria , medicine , endocrinology , pathogenesis , diabetic nephropathy , urine , renin–angiotensin system , gene isoform , diabetes mellitus , nephropathy , angiotensin converting enzyme , kidney disease , kidney , chemistry , blood pressure , gene , biochemistry
Diabetes mellitus (DM) is recognized as a leading cause of chronic kidney disease and end‐stage renal failure. The local increase of components of Renin‐Angiotensin System has been implied in different hypertension pathogenesis. In our laboratory, we observed N‐domain ACEs isoforms with 190 and 65 kDa in urine of healthy subjects, and 90 and 65 kDa isoforms were detected in urine of hypertensive patients, suggesting that the 90 kDa ACE could be a possible genetic marker of hypertension. The aim is to associate dysfunctions of the renal system with possible alterations in protein expression and/or ACE isoforms enzymatic activity and in angiotensin (ang) levels in chronic renal failure (CRF) patients. Patients were divided into three groups: (I) DM ‐ normotensive patients with type 1 DM and normoalbuminuria (n=30); (II) DMH ‐ hypertensive patients with type 1 DM and microalbuminuria (n=18); (III) DMCR ‐ patients with DM type 1 and CRF (n=11). ACE activity was slightly decreased in serum of DMH and DMCR (DM=124.1±6.4; DMH=98.4±9.8; DMCR=95.2±7.8 nmol/min/mL). ACE isoforms were significantly over‐expressed in urine of DMH group compared with other two groups by Western blotting. High AngII levels were detected in patient serum of DMCR (DMCR=3.32±0.54; DM=0.41±0.04; DMH= 0.58±0.43 nmol/mL) group, therefore, AngI and Ang1‐7 did not present significant alterations. Our results suggest that somatic and N‐domain ACEs expressions could be associated with renal damage. High levels of AngII in DMCR patients suggest this peptide is resulted by alternative pathways. Supported by FAPESP.