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Losartan retards the development of Chronic Kidney Disease (CKD) after an Acute Kidney Injury (AKI) episode
Author(s) -
Rodríguez Roxana,
BarreraChimal Jonatan,
Benítez Kenya,
PérezVillalva Rosalba,
Gamba Gerardo,
Bobadilla Norma A.
Publication year - 2013
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.27.1_supplement.705.8
Subject(s) - losartan , medicine , kidney disease , renal function , urology , creatinine , acute kidney injury , oxidative stress , kidney , inflammation , angiotensin ii , ischemia , angiotensin receptor , endocrinology , fibrosis , proteinuria , receptor
We studied if preventing AKI with Losartan (Lo) stops CKD development. Fifty rats were divided in: Sham‐operated (S), Lo‐treated group (50 mg/kg) (Lo+S), rats underwent bilateral ischemia of 45 min (I), rats receiving Lo before I (Lo+I), and rats receiving Lo, 3 h after I (I+Lo). All groups were observed 270 days. Proteinuria (Prot), creatinine clearance (CrCl), renal blood flow (RBF), tubulo‐interstitial fibrosis (TIF) and glomerular diameter were measured. In addition, interleukin 6 and monocyte chemo attracting protein mRNA levels, as well as urinary kidney injury molecule and H 2 O 2 were measured. Rats underwent ischemia developed CKD characterized by a progressive increase in Prot and a decrease in CrCl and RBF. Glomerular hypertrophy, extensive TIF, and Kim‐1 up‐regulation were also observed, all these findings were associated with an increase in oxidative stress and with greater inflammation. Losartan treatment avoided the progression of CKD evidenced by CrCl and renal architecture preservation without increased inflammation or oxidative stress. We show in this model of renal injury induced by AKI that angiotensin receptor antagonism reduced CKD progression. However, prophylactic treatment was more effective than after the ischemic insult. The mechanisms activated after AKI episode and the angiotensin II involvement could give us the knowledge for designing therapeutic strategies to prevent CKD.