Abstract
Background and objectives:
Left ventricular mass (LVM) is known to be related to overall and cardiovascular mortality in end stage kidney disease (ESKD) patients. The aims of the present study are 1) to determine whether LVM is associated with mortality and various cardiovascular events and 2) to identify determinants of LVM including biomarkers of inflammation and fibrosis.
Design setting participants & measurements:
Analysis was performed with data of 327 ESKD patients, a subset from the CONvective TRAnsport STudy (CONTRAST). Echocardiography was performed at baseline. Cox regression analysis was used to assess the relation of LVM tertiles with clinical events. Multivariable linear regression models were used to identify factors associated with LVM.
Results:
Median age was 65 (IQR: 54-73) years, 203 (61%) were male and median LVM was 227 (IQR: 183-279) grams. The risk of all-cause mortality (hazard ratio (HR) = 1.73, 95% CI: 1.11-2.99), cardiovascular death (HR = 3.66, 95% CI: 1.35-10.05) and sudden death (HR = 13.06; 95% CI: 6.60-107) was increased in the highest tertile (>260 grams) of LVM. In the multivariable analysis positive relations with LVM were found for male gender (B = 38.8±10.3), residual renal function (B = 17.9±8.0), phosphate binder therapy (B = 16.9±8.5), and an inverse relation for a previous kidney transplantation (B = -41.1±7.6) and albumin (B = -2.9±1.1). Interleukin-6 (Il-6), high-sensitivity C-reactive protein (hsCRP), hepcidin-25 and connective tissue growth factor (CTGF) were not related to LVM.
Conclusion:
We confirm the relation between a high LVM and outcome and expand the evidence for increased risk of sudden death. No relationship was found between LVM and markers of inflammation and fibrosis.
Trial registration:
Controlled-Trials.com ISRCTN38365125.
Publication types
-
Multicenter Study
-
Randomized Controlled Trial
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Aged
-
Cardiovascular Diseases* / diagnostic imaging
-
Cardiovascular Diseases* / mortality
-
Cardiovascular Diseases* / physiopathology
-
Cardiovascular Diseases* / therapy
-
Female
-
Follow-Up Studies
-
Heart Ventricles* / diagnostic imaging
-
Heart Ventricles* / physiopathology
-
Humans
-
Kidney Failure, Chronic* / diagnostic imaging
-
Kidney Failure, Chronic* / mortality
-
Kidney Failure, Chronic* / physiopathology
-
Kidney Failure, Chronic* / therapy
-
Male
-
Middle Aged
-
Models, Biological*
-
Renal Dialysis*
-
Ultrasonography
-
Ventricular Function, Left*
Grants and funding
CONTRAST is partly supported by unrestricted grants from Fresenius Medical Care (The Netherlands) and Gambro Lundia AB (Sweden). Additional support for CONTRAST was also received from Roche, the Netherlands. There are no patents, products in development or marketed products to declare. IM Mostovaya, CH den Hoedt, O Kamp, ML Bots, NC van der Weerd, EL Penne and AHA Mazairac report receiving no lecture fees, no consulting support, or grant support. MPC Grooteman reports research funded by Fresenius, Gambro, and Baxter. PJ Blankestijn reports research funded by Fresenius, Gambro, Roche, Amgen and Novartis, consultant fee and honoraria for lectures from Fresenius, Gambro, Solvay, Medtronic, and Novartis. R Lévesque reports research funded by Amgen Canada. PM ter Wee reports research funded by Abbott, Baxter, Gambro, Fresenius, and Roche; honoraria for lectures received from Amgen, Roche, Genzyme, Fresenius. MJ Nubé reports research funded by Baxter and Fresenius; honoraria for lectures received from Fresenius and Baxter. MA van den Dorpel reports research funded by Amgen. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.