title: Involvement of aldosterone in left ventricular hypertrophy of patients with end-stage renal failure treated with hemodialysis.
abstract: There is increasing evidence about important cardiovascular effects of aldosterone through classic mineralocorticoid receptors in the heart. It is now clear that aldosterone/excess salt administration has been shown to produce both cardiac hypertrophy and interstitial cardiac fibrosis in rats. In clinical studies, it has been reported that aldosterone seems to play an important role in cardiac hypertrophy. However, it has still not been established whether aldosterone is involved in cardiac hypertrophy in patients with end-stage renal failure treated with hemodialysis. In the present study, we have analyzed the association between cardiac hypertrophy and aldosterone in 29 patients (18 patients with nondiabetic nephropathy and 11 patients with diabetic nephropathy) who developed end-stage renal disease and received hemodialysis. Among the nondiabetic patients, left ventricular mass index correlated significantly with plasma aldosterone concentrations during both before and after hemodialysis, but it did not correlate with plasma renin activity. Furthermore, left ventricular mass index also correlated with mean blood pressure. In contrast, these correlations were not seen in the diabetic patients, despite similar age distribution, duration of hemodialysis, and several echocardiographic parameters between two groups. In conclusion, our study provides new evidence for a relation between left ventricular hypertrophy and plasma aldosterone concentrations that seems to be independent of blood pressure in nondiabetic patients with end-stage renal failure treated with hemodialysis.
authors.affiliation: Department of Internal Medicine, Mito Red Cross Hospital, Mito City, Ibaraki, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Sato
authors.forename: J W
authors.initials: JW
authors.lastname: Funder
authors.forename: T
authors.initials: T
authors.lastname: Saruta
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use; D000450:Aldosterone / Q000097:blood*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D006977:Hypertension, Renal / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D018161:Receptors, Mineralocorticoid / Q000097:blood; D006435:Renal Dialysis; D012083:Renin / Q000097:blood
chemical_list: D000317:Adrenergic alpha-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D002121:Calcium Channel Blockers; D018161:Receptors, Mineralocorticoid; D000450:Aldosterone; D012083:Renin