title: Subclinical nephrosclerosis is linked to left ventricular hypertrophy independent of classical atherogenic factors.
abstract: Recently, cardio-renal interactions have been considered to be important and it has been demonstrated that mild renal dysfunction is associated with left ventricular hypertrophy (LVH). However, the correlation between LVH and subclinical renal damage is unclear. We investigated this association by assessing pretransplant biopsies from living kidney donors with normal renal function. We retrospectively categorized 238 living kidney donors into tertiles according to the percentage of global glomerulosclerosis (%GGS) observed in pretransplant biopsies (low, 0-3.45% (n=80); moderate, 3.46-11.76% (n=78); high, ⩾11.77% (n=80)) to analyze trends in their left ventricular mass index (LVMI) measured by echocardiography and baseline factors. LVH was defined as LVMI >110 g m(-2) in female and >125 g m(-2) in male subjects. We used a logistic regression model to evaluate any correlations between %GGS and LVH. LVMI increased significantly with increasing tertiles of %GGS, as did the prevalence of left ventricular remodeling and LVH. According to multivariate logistic regression analysis, subjects with high %GGS tertiles had a sevenfold greater risk of LVH than did those with low tertiles, even after adjusting for age, sex, systolic blood pressure, history of diabetes mellitus, total serum cholesterol and glomerular filtration rate (GFR) measured by a radioisotopic technique. There is an association between GGS and LVH in subjects with normal renal function. This association is significant after adjustment for age, sex, blood pressure, GFR and other atherogenic factors.
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Naoki
authors.initials: N
authors.lastname: Haruyama
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Akihiro
authors.initials: A
authors.lastname: Tsuchimoto
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Kosuke
authors.initials: K
authors.lastname: Masutani
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Masaharu
authors.initials: M
authors.lastname: Nagata
authors.affiliation: Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Hidehisa
authors.initials: H
authors.lastname: Kitada
authors.affiliation: Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Masao
authors.initials: M
authors.lastname: Tanaka
authors.affiliation: 1] Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan [2] Department of Integrated Therapy for Chronic Kidney Disease, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Tsuruya
authors.affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Takanari
authors.initials: T
authors.lastname: Kitazono
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009400:Nephrosclerosis / Q000150:complications* / Q000503:physiopathology; D012307:Risk Factors