BACKGROUND: Blood pressure (BP) affects hypertensive left ventricular mass (LVM), explaining 10-25% of its variation. Thus, it is plausible that other factors operate in this process. Reduced kidney function is associated with increased LVM. METHODS: We enrolled 1000 untreated hypertensives with serum creatinine ≤ 1.5mg/dL and without proteinuria. BP was measured by standard sphygmomanometer. LVM was calculated with the Devereux formula and indexed by body surface area (LVMI). Anthropometric and the following laboratory parameters were measured: plasma glucose, serum insulin, cholesterol, triglyceride, creatinine and e-GFR (CKD-EPI equation). RESULTS: On univariate analysis, both insulin (r=0.44, P<0.0001) and creatinine (r=0.37, P<0.001) were directly related to LVMI. In multivariate regression analysis insulin resulted the first factor in rank explaining the variability in LVMI (semipartial r=0.34,P<0.001), followed by creatinine. Fasting insulin interacts with creatinine in explaining LVM variability: 0.1mg/dL increase in creatinine produces an increase of 8.1g/m(2) in LVMI in patients with higher plasma insulin (upper quartiles). CONCLUSIONS: Independently of other risk factors, fasting insulin and serum creatinine contribute to explain LVM development in hypertensives with preserved renal function; insulin interacts with creatinine in explaining LVM variability in these patients.
BACKGROUND: Blood pressure (BP) affects hypertensive left ventricular mass (LVM), explaining 10-25% of its variation. Thus, it is plausible that other factors operate in this process. Reduced kidney function is associated with increased LVM. METHODS: We enrolled 1000 untreated hypertensives with serum creatinine ≤ 1.5mg/dL and without proteinuria. BP was measured by standard sphygmomanometer. LVM was calculated with the Devereux formula and indexed by body surface area (LVMI). Anthropometric and the following laboratory parameters were measured: plasma glucose, serum insulin, cholesterol, triglyceride, creatinine and e-GFR (CKD-EPI equation). RESULTS: On univariate analysis, both insulin (r=0.44, P<0.0001) and creatinine (r=0.37, P<0.001) were directly related to LVMI. In multivariate regression analysis insulin resulted the first factor in rank explaining the variability in LVMI (semipartial r=0.34,P<0.001), followed by creatinine. Fasting insulin interacts with creatinine in explaining LVM variability: 0.1mg/dL increase in creatinine produces an increase of 8.1g/m(2) in LVMI in patients with higher plasma insulin (upper quartiles). CONCLUSIONS: Independently of other risk factors, fasting insulin and serum creatinine contribute to explain LVM development in hypertensives with preserved renal function; insulin interacts with creatinine in explaining LVM variability in these patients.
Authors: Tomasz Zapolski; Jacek Furmaga; Andrzej P Wysokiński; Anna Wysocka; Sławomir Rudzki; Andrzej Jaroszyński Journal: BMC Nephrol Date: 2019-05-02 Impact factor: 2.388
Authors: Angela Sciacqua; Antonio Cimellaro; Luana Mancuso; Sofia Miceli; Velia Cassano; Maria Perticone; Teresa V Fiorentino; Francesco Andreozzi; Elena Succurro; Giorgio Sesti; Francesco Perticone Journal: Nutrients Date: 2020-02-05 Impact factor: 5.717