Elevated levels of heat shock proteins (HSPs) and antibodies against them have been described in adults with atherosclerotic lesions and cardiovascular events. However, there are no investigations of these variables in children with CKD treated conservatively or on peritoneal dialysis. Therefore, we decided to evaluate the profile of HSPs and their Z-VAD-FMK mechanism of action potential role as markers of atherosclerosis in these groups of patients.

Methods: The study group consisted of 37 children with CKD treated conservatively and 19 children and young adults on

automated peritoneal dialysis (APD). The control group comprised 15 age-matched subjects with normal kidney function. HSP-60, HSP-70, HSP-90alpha, anti-HSP-60, anti-HSP-70, sE-selectin, and interleukin (IL)-4 serum concentrations were assessed by ELISA; high-sensitivity see more C-reactive protein (hs-CRP) serum levels

were assessed by nephelometry. Serum lipid profiles (total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, triglycerides) were also estimated.

Results: HSP-90 alpha alpha anti-HSP-60, and sE-selectin concentrations in the CKD and APD patients were higher than in the controls and were lower in the predialysis subjects than in the children on dialysis. Median values of anti-HSP-70 were higher in the CKD patients than in the control group. Levels of IL-4 were increased in all patients versus controls. Median values of HSP-60 were decreased in the CKD and APD children versus controls. HSP-70 and hs-CRP concentrations were comparable in all groups.

Conclusions: The altered HSP and anti-HSP concentrations may imply that the response to stress conditions in the course of CKD is disturbed in children; APD does not aggravate that dysfunction in a significant way. Relationships between HSPs, lipid profile, and markers of inflammation selleck suggest a possible role of the selected HSPs as markers

of atherosclerosis in children with CKD.”
“It is well established that there is a relationship between patterns of early growth and subsequent risk of development of metabolic diseases such as type 2 diabetes and cardiovascular disease. Studies in both humans and in animal models have provided strong evidence that the early environment plays an important role in mediating these relationships. The concept of the developmental origins of health and disease is therefore widely accepted. The mechanisms by which an event in very early life can have a permanent effect on the long-term health of an individual are still relatively poorly understood. However a growing body of evidence has implicated a number of candidate mechanisms. These include permanent changes in an organ structure, programmed changes in gene expression through epigenetic modifications and persistent effects on regulation of cellular ageing.