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Clin Sci (Lond). 2018 Apr 6;132(7):739-758. doi: 10.1042/CS20180097. Print 2018 Apr 16.

Translational science in albuminuria: a new view of de novo albuminuria under chronic RAS suppression.

Author information

1
Department of Vascular Physiopathology, Hospital Nacional de Paraplejicos (HNP), SESCAM, Toledo, Spain.
2
Cardiorenal Translational Laboratory, Instituto de Investigación i+12, Hospital Universitario 12 de Octubre, Madrid, Spain.
3
Department of Immunology, IIS-Fundacion Jimenez Diaz, Madrid, Spain.
4
Department of Preventive Medicine and Public Health, School of Medicine, Universidad Autónoma de Madrid/IdiPAZ and CIBER in Epidemiology and Public Health (CIBERESP), Madrid, Spain.
5
School of Doctoral Studies and Research, Universidad Europea de Madrid, Madrid, Spain.
6
Department of Vascular Physiopathology, Hospital Nacional de Paraplejicos (HNP), SESCAM, Toledo, Spain megonzalezb@sescam.jccm.es marucitos@hotmail.com gemaruiz@h12o.es.
7
Cardiorenal Translational Laboratory, Instituto de Investigación i+12, Hospital Universitario 12 de Octubre, Madrid, Spain megonzalezb@sescam.jccm.es marucitos@hotmail.com gemaruiz@h12o.es.

Abstract

The development of de novo albuminuria during chronic renin-angiotensin system (RAS) suppression is a clinical entity that remains poorly recognized in the biomedical literature. It represents a clear increment in global cardiovascular (CV) and renal risk that cannot be counteracted by RAS suppression. Although not specifically considered, it is clear that this entity is present in most published and ongoing trials dealing with the different forms of CV and renal disease. In this review, we focus on the mechanisms promoting albuminuria, and the predictors and new markers of de novo albuminuria, as well as the potential treatment options to counteract the excretion of albumin. The increase in risk that accompanies de novo albuminuria supports the search for early markers and predictors that will allow practising physicians to assess and prevent the development of de novo albuminuria in their patients.

KEYWORDS:

albuminuria; cardiovascular disease; metabolomics; proteomics; renal physiology

PMID:
29626149
DOI:
10.1042/CS20180097

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