title: Microalbuminuria and hypertension in pregnancy: role of aldosterone and inflammation.
abstract: Women with a history of hypertension in pregnancy are at increased risk of microalbuminuria later in life. Microalbuminuria is a marker of kidney dysfunction frequently related to an inflammatory event. Pregnancy is a dynamic process characterized by immune tolerance, angiogenesis, and hormonal regulation. Menstruation and pregnancy are associated with a physiological inflammation, which is altered in preeclampsia and probably in other hypertensive situations of pregnancy. An imbalance between pro-oxidant factors and the ability to scavenge these factors produces oxidative stress, which has been evaluated in many cells, but leukocytes are the main source of inflammatory cytokines and experimental and clinical evidence support a possible role of aldosterone as a mediator of placental and renal damage mediated by growth factors, reactive oxygen species, and cytokines. Angiotensin-converting enzyme inhibitors and aldosterone receptor blockers are frequently effective in reducing the risk of progression of cardiovascular and renal disease.
authors.affiliation: Department of Medicine - Endocrinology, University of Padua, Padua, Italy.
authors.forename: Decio
authors.initials: D
authors.lastname: Armanini
authors.forename: Guido
authors.initials: G
authors.lastname: Ambrosini
authors.forename: Chiara
authors.initials: C
authors.lastname: Sabbadin
authors.forename: Gabriella
authors.initials: G
authors.lastname: Donà
authors.forename: Giulio
authors.initials: G
authors.lastname: Clari
authors.forename: Luciana
authors.initials: L
authors.lastname: Bordin
mesh_terms: D000375:Aging / Q000502:physiology*; D000419:Albuminuria / Q000453:epidemiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*
references.citation: Arch Intern Med. 2001 Sep 10;161(16):2000-5
references.pmid: 11525702
references.citation: Hypertension. 2012 Jun;59(6):1099-100
references.pmid: 22526256
references.citation: J Immunol. 2010 Jan 1;184(1):191-202
references.pmid: 19949098
references.citation: J Clin Endocrinol Metab. 1992 Apr;74(4):946-9
references.pmid: 1312543
references.citation: Semin Fetal Neonatal Med. 2006 Oct;11(5):309-16
references.pmid: 16828580
references.citation: Clin Endocrinol (Oxf). 1985 Oct;23(4):341-7
references.pmid: 4064345
references.citation: Future Cardiol. 2006 Sep;2(5):535-41
references.pmid: 19804189
references.citation: Curr Opin Nephrol Hypertens. 2008 Sep;17(5):457-63
references.pmid: 18695385
references.citation: Am J Physiol. 1985 Mar;248(3 Pt 1):E388-90
references.pmid: 3156509
references.citation: Steroids. 2012 May;77(6):655-8
references.pmid: 22387621
references.citation: J Hypertens. 1995 Dec;13(12 Pt 2):1801-2
references.pmid: 8903655
references.citation: Hypertension. 2012 Jun;59(6):1241-8
references.pmid: 22526257
references.citation: J Immunol. 2009 Dec 1;183(11):7023-30
references.pmid: 19915051
references.citation: Acta Endocrinol (Copenh). 1988 Aug;118(4):479-82
references.pmid: 2840791
references.citation: J Clin Hypertens (Greenwich). 2013 Sep;15(9):617-23
references.pmid: 24034653
references.citation: Indian J Endocrinol Metab. 2012 Mar;16(2):277-82
references.pmid: 22470868
references.citation: J Clin Endocrinol Metab. 2004 Apr;89(4):1973-6
references.pmid: 15070972
references.citation: Am J Physiol. 1989 Aug;257(2 Pt 1):E170-4
references.pmid: 2764099
references.citation: Menopause. 2010 Sep-Oct;17(5):990-6
references.pmid: 20551845
references.citation: Mol Cell Endocrinol. 2004 Mar 31;217(1-2):53-8
references.pmid: 15134801