Kidney Function and Risk Factors for Left Ventricular Hypertrophy in Untreated Uncomplicated Essential Hypertension
Received 12 October 2007; accepted 26 February 2008. published online 23 April 2008.
Background
Left ventricular (LV) hypertrophy and decreased kidney function are well-established cardiovascular risk factors in hypertensive patients.
Study Design
We investigated the relationship between creatinine level, creatinine clearance, and estimated glomerular filtration rate (eGFR) with LV mass (LVM) in a cross-sectional study.
Predictors
eGFR and serum creatinine level.
Outcome
LVM index (LVMI).
Setting & Participants
400 patients with untreated uncomplicated essential hypertension.
Measurements
LVMI, eGFR (Modification of Diet in Renal Disease Study equation), Framingham risk factors, and a series of specific risk factors, ie, endothelial function (acetylcholine [ACh]-stimulated forearm blood flow [FBF]), insulin sensitivity (Homeostatic Model Assessment for insulin resistance [HOMA-R] index), C-reactive protein (CRP), and uric acid.
Results
Both eGFR and creatinine level were significantly related to LVMI (r = −0.34 and r = 0.35; P < 0.001). In a multiple regression model adjusting for Framingham risk factors, eGFR was independently associated with LVMI. However, this association, although highly significant, lost substantial strength after adjustment for such specific risk factors as HOMA-R index, ACh-stimulated FBF, CRP level, and uric acid level. eGFR interacted with insulin resistance in explaining the variability in LVMI (P = 0.007).
Limitations
The cross-sectional nature of this study precludes cause-effect conclusions.
Conclusions
Independently of other risk factors, decreased kidney function contributes to explain the variability in LVMI in patients with untreated uncomplicated essential hypertension. This association is attributable in part to the link between eGFR and such specific risk factors as HOMA-R index, ACh-stimulated FBF, CRP level, and uric acid level. Decreased kidney function and insulin resistance interact in explaining the variability in LVMI in these patients.
1Department of Experimental and Clinical Medicine, G. Salvatore, University Magna Græcia of Catanzaro, Reggio Calabria, Italy
2Consiglio Nazionale delle Ricerche, Istituto di Biomedicina, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, Reggio Calabria, Italy
Address correspondence to Carmine Zoccali, MD, CNR-IBIM, Istituto di Biomedicina, Epidemiologia Clinica e Fisiopatologia, delle Malattie Renali e dell'Ipertensione Arteriosa, 89100 Reggio Calabria, Italy.
ABSTRACT