Levels of NT-proBNP, markers of low-grade inflammation, and endothelial dysfunction during spironolactone treatment in patients with diabetic kidney disease.

S. E. Nielsen, K.J. Schjoedt, K. Rossing, F. Persson, C.G. Schalkwijk, C.D.A. Stehouwer, H.H. Parving, P. Rossing

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Renin-angiotensin-aldosterone system (RAAS) blockade may reduce levels of biomarkers of chronic low-grade inflammation and endothelial dysfunction. We investigated the effect of spironolactone added to standard RAAS blockade on these biomarkers in an analysis of four original studies. MATERIALS AND METHODS: The studies were double-blind, randomised, placebo-controlled studies in 46 type 1 and 23 type 2 diabetic patients with micro- or macroalbuminuria treated with angiotensin-converting enzyme inhibitor (ACE inhibitor) or angiotensin receptor blocker (ARB), and randomised to additional treatment with spironolactone 25 mg and placebo daily for 60 days.Outcome measures:Changes in inflammatory (hsCRP, s-ICAM, TNFalpha, IL-6, IL-8, Serum amyloid A, IL1beta), endothelial dysfunction (sE-selectin, s-ICAM1, s-VCAM1, VWF, p-selectin, s-thrombomodulin) and NT-proBNP after each treatment period. RESULTS: During spironolactone treatment, u-albumin excretion rate was reduced from 605 (411-890) to 433 (295-636) mg/24 h, as previously reported. Markers of inflammation and endothelial dysfunction did not change; only changes in NT-proBNP (reduced by 14%, p=0.05) and serum amyloid A (reduced by 62%, p=0.10) were borderline significant.Discussions:Our results indicate that the renoprotective effect of spironolactone when added to RAAS blockade is not mediated through anti-inflammatory pathways since markers of inflammation and endothelial dysfunction are not affected during treatment.
Original languageEnglish
Pages (from-to)161-166
Number of pages6
JournalJournal of the Renin-angiotensin-aldosterone System
Volume14
Issue number2
DOIs
Publication statusPublished - Jun 2013

Keywords

  • Diabetes
  • inflammation
  • endothelial dysfunction
  • diabetic nephropathy
  • GLOMERULAR-FILTRATION-RATE
  • ANGIOTENSIN-ALDOSTERONE SYSTEM
  • RANDOMIZED CONTROLLED-TRIAL
  • URINARY ALBUMIN EXCRETION
  • BENEFICIAL IMPACT
  • NEPHROPATHY
  • MICROALBUMINURIA
  • CROSSOVER
  • BLOCKADE
  • IRBESARTAN

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