In the Journals

Endothelial dysfunction related to LV hypertrophy in non-dialysis patients with CKD

Inflammation may have an important role in the development of left ventricular hypertrophy through endothelial dysfunction in non-dialysis patients with chronic kidney disease, according to the results of a pilot study.

According to the researchers, the study is the first demonstration of a relationship between endothelial dysfunction and LV hypertrophy in this patient population, and more studies are needed to determine a cause-effect relationship and find appropriate therapies.

Although vascular endothelial dysfunction is common in patients with CKD, the link between dysfunction, LV hypertrophy and inflammation among those with CKD who are not on dialysis had yet to be assessed, according to the study background.

Dimitrios Poulikakos, MD, and colleagues studied 30 patients with CKD (17 pre-dialysis, 13 renal transplant recipients) and 29 controls matched for age and sex. All subjects were measured for high-sensitivity C-reactive protein levels and underwent brachial artery flow-mediated dilatation to assess endothelial dysfunction. LV hypertrophy was assessed via two-dimensional echocardiography, and LV mass index was also calculated in all subjects.

Poulikakos, of St. George’s University of London, and colleagues found that patients with CKD had higher C-reactive protein levels (3.9 mg/L vs. 1 mg/L; P<.001), reduced flow-mediated dilatation (3.2% vs. 6.1%) and reduced LV mass index (146.1 g/m vs. 105.3 g/m; P<.001) compared with controls.

Among those with CKD, LV mass index increased with decreasing flow-mediated dilatation (r=–0.371; P=.043), while and flow-mediated dilatation decreased with increasing C-reactive protein levels (r=–0.741; P<.001).

In addition, the researchers observed that patients with CKD and poorer endothelial function, defined as flow-mediated dilatation below <2.3%, had higher C-reactive protein levels (5.6 mg/L vs. 2.1 mg/L; P<.001) and LV mass index (161.9 g/m vs. 130.4 g/m; P=.033) than patients with CKD and flow-mediated dilatation ≥2.3%. Those with lower flow-mediated dilatation did not differ significantly from other patients with CKD in terms of age, BP, hemoglobin or kidney function.

The relationship between high LV mass index and low flow-mediated dilatation did not change after adjustment for age, diabetes and smoking (adjusted beta = –0.396; P=.004). However, adjustment for hypertension eliminated the significance of the correlation (adjusted beta = –0.191; P=.174).

“Traditional CV risk factors … contribute to the high CV morbidity and mortality rates seen in CKD patients, but do not explain the entire risk,” Poulikakos and colleagues wrote. “The significantly increased prevalence of CV disease in CKD patients compared with the general population needs to be explained by other non-traditional factors … Inflammation causes [endothelial dysfunction] and hence may be a common mediator for endothelial injury related to all non-traditional risk factors. As atherosclerosis is recognized as an inflammatory disease, inflammation may also be the common mediator for all traditional risk factors causing [endothelial dysfunction]. … Our findings demonstrate a linear relationship between inflammation and [endothelial dysfunction].”

Disclosure: The researchers report no relevant financial disclosures.

Inflammation may have an important role in the development of left ventricular hypertrophy through endothelial dysfunction in non-dialysis patients with chronic kidney disease, according to the results of a pilot study.

According to the researchers, the study is the first demonstration of a relationship between endothelial dysfunction and LV hypertrophy in this patient population, and more studies are needed to determine a cause-effect relationship and find appropriate therapies.

Although vascular endothelial dysfunction is common in patients with CKD, the link between dysfunction, LV hypertrophy and inflammation among those with CKD who are not on dialysis had yet to be assessed, according to the study background.

Dimitrios Poulikakos, MD, and colleagues studied 30 patients with CKD (17 pre-dialysis, 13 renal transplant recipients) and 29 controls matched for age and sex. All subjects were measured for high-sensitivity C-reactive protein levels and underwent brachial artery flow-mediated dilatation to assess endothelial dysfunction. LV hypertrophy was assessed via two-dimensional echocardiography, and LV mass index was also calculated in all subjects.

Poulikakos, of St. George’s University of London, and colleagues found that patients with CKD had higher C-reactive protein levels (3.9 mg/L vs. 1 mg/L; P<.001), reduced flow-mediated dilatation (3.2% vs. 6.1%) and reduced LV mass index (146.1 g/m vs. 105.3 g/m; P<.001) compared with controls.

Among those with CKD, LV mass index increased with decreasing flow-mediated dilatation (r=–0.371; P=.043), while and flow-mediated dilatation decreased with increasing C-reactive protein levels (r=–0.741; P<.001).

In addition, the researchers observed that patients with CKD and poorer endothelial function, defined as flow-mediated dilatation below <2.3%, had higher C-reactive protein levels (5.6 mg/L vs. 2.1 mg/L; P<.001) and LV mass index (161.9 g/m vs. 130.4 g/m; P=.033) than patients with CKD and flow-mediated dilatation ≥2.3%. Those with lower flow-mediated dilatation did not differ significantly from other patients with CKD in terms of age, BP, hemoglobin or kidney function.

The relationship between high LV mass index and low flow-mediated dilatation did not change after adjustment for age, diabetes and smoking (adjusted beta = –0.396; P=.004). However, adjustment for hypertension eliminated the significance of the correlation (adjusted beta = –0.191; P=.174).

“Traditional CV risk factors … contribute to the high CV morbidity and mortality rates seen in CKD patients, but do not explain the entire risk,” Poulikakos and colleagues wrote. “The significantly increased prevalence of CV disease in CKD patients compared with the general population needs to be explained by other non-traditional factors … Inflammation causes [endothelial dysfunction] and hence may be a common mediator for endothelial injury related to all non-traditional risk factors. As atherosclerosis is recognized as an inflammatory disease, inflammation may also be the common mediator for all traditional risk factors causing [endothelial dysfunction]. … Our findings demonstrate a linear relationship between inflammation and [endothelial dysfunction].”

Disclosure: The researchers report no relevant financial disclosures.