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Mechanisms underlying renoprotection during renin-angiotensin system blockade

M W Taal1, G M Chertow, H G Rennke

  • 1Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. mtaal@rics.bwh.harvard.edu

American Journal of Physiology. Renal Physiology
|February 24, 2001
PubMed

Insights

Both candesartan and enalapril equally protect kidneys in rats with chronic renal disease (CRD). Effective renoprotection requires controlling systolic blood pressure and urinary protein excretion.

Area of Science:

  • Nephrology
  • Pharmacology

Background:

  • Chronic renal disease (CRD) progression is a significant health concern.
  • Understanding the determinants of CRD progression is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the renoprotective effects of candesartan (Csn) and enalapril (Ena) in a rat model of CRD.
  • To identify potential determinants of CRD progression during renin-angiotensin system inhibition.

Main Methods:

  • Male Munich-Wistar rats underwent 5/6 nephrectomy and were treated with Csn or Ena.
  • Systolic blood pressure (SBP), urinary protein excretion (UprV), and glomerulosclerosis scores (GS) were measured.
  • Renal cortex mRNA levels for TGF-beta1 and MCP-1 were determined using RT-PCR.

Main Results:

  • Both Csn and Ena controlled SBP but UprV increased over 24 weeks.
  • GS scores were similar between Csn and Ena groups and correlated strongly with SBP and UprV.
  • Elevated renal TGF-beta1 and MCP-1 mRNA levels correlated with renal injury.

Conclusions:

  • Csn and Ena are equally effective renoprotective agents in this CRD model.
  • Renoprotection during renin-angiotensin system inhibition depends on controlling both SBP and UprV.
  • Incomplete suppression of renal cytokine gene expression may contribute to CRD progression.

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