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Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115
Potential determinants of chronic renal disease (CRD)
progression were studied in male Munich-Wistar rats subjected to 5/6 nephrectomy and treated with candesartan (Csn; n = 30)
or enalapril (Ena; n = 27) from 5 wk
postsurgery. Despite control of systolic blood pressure (SBP;
24 wk: Csn = 143 ± 9; Ena = 148 ± 8 mmHg), urinary protein excretion rates (UprV) increased over 24 wk
(Csn = 92 ± 10; Ena = 99 ± 8mg/day).
Glomerulosclerosis scores (GS) at 24 wk were similar for Csn (42 ± 7%) vs. Ena (42 ± 4%), values close to those of untreated
controls at 12 wk (43 ± 4%). At 24 wk, SBP and UprV
correlated strongly with GS, together accounting for 72% of the
variance in GS. Renal cortex mRNA levels (determined by competitive
RT-PCR) for transforming growth factor (TGF)-
1 and monocyte
chemoattractant protein (MCP)-1 were elevated in Csn and Ena at 12 wk
and remained higher at 24 wk vs. sham. Strong correlations were evident
among TGF-1, MCP-1, and interleukin-1 and renal injury at 24 wk.
Cns and Ena are thus equally effective renoprotective agents in this
model. During renin-angiotensin system inhibition, renoprotection is
dependent on control of both SBP and UprV. Incomplete
suppression of renal cytokine gene expression may also contribute to
CRD progression.
angiotensin-converting enzyme inhibitor; angiotensin receptor
antagonist; glomerulosclerosis; systolic blood pressure; proteinuria; interleukin-1; monocyte chemoattractant protein-1; transforming
growth factor-
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