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In blood, we measured NT\u2010proBNP, troponin T, C\u2010reactive protein, creatinine, cystatin C; in urine, N\u2010acetyl\u2010beta\u2010<jats:sc>d<\/jats:sc>\u2010glucosaminidase and kidney\u2010injury\u2010molecule\u20101. Angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs) were inversely associated with cardiac impairment, inflammation, and renal tubular damage, but not with glomerular dysfunction. Diuretics were associated with worse biomarker profiles and with a hazard ratio for adverse clinical outcome of 1.12 (95% confidence interval: 1.03\u20131.22) per 40 mg higher doses. ACE\u2010inhibitors\/ARBs were more frequently downtitrated and diuretics more frequently uptitrated in patients who experienced endpoints than in those who did not. In conclusion, a decrease or withholding of ACE\u2010inhibitors\/ARBs solely based on glomerular function is not justified because of the beneficial effects on the heart, inflammation, and renal tubules. Higher and increased diuretic doses mark progression towards endstage CHF.<\/jats:p>","DOI":"10.1002\/cpt.931","type":"journal-article","created":{"date-parts":[[2017,11,6]],"date-time":"2017-11-06T05:26:43Z","timestamp":1509946003000},"page":"346-355","source":"Crossref","is-referenced-by-count":2,"title":["Real\u2010Life Use of Neurohormonal Antagonists and Loop Diuretics in Chronic Heart Failure: Analysis of Serial Biomarker Measurements and Clinical Outcome"],"prefix":"10.1111","volume":"104","author":[{"given":"Milos","family":"Brankovic","sequence":"first","affiliation":[{"name":"Department of Cardiology Erasmus MC Rotterdam the Netherlands"},{"name":"School of Medicine University of Belgrade Belgrade Serbia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K. 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