OBJECTIVE: Expression of heat shock protein (Hsp) 72 is one of the major mechanisms acting against cellular injury. It displays a plethora of functions, including a considerable impact on inflammation. The aim of this study was to investigate Hsp72 expression in blood monocytes of patients with chronic kidney disease (CKD). MATERIAL AND METHODS: Hsp72 protein level was assessed by flow cytometry in blood monocytes of predialysis, haemodialysis (HD) and continuous peritoneal dialysis patients, and controls. It was followed by evaluation of Hsp72 gene expression in the same cohorts by reverse transcription-polymerase chain reaction. RESULTS: The level of Hsp72 protein was significantly lower in the predialysis (359+/-83 AU) and HD groups (293+/-62 AU) than in controls (405+/-51 AU) (p<0.01 and p<0.001, respectively). The amount of mRNA was significantly lower only in the HD group, compared with controls (0.39+/-0.10 vs 0.48+/-0.10, p<0.01). In the predialysis group, there were negative correlations between Hsp72 protein level and serum creatinine concentration, blood urea nitrogen and C-reactive protein. CONCLUSIONS: This study demonstrates that uraemic toxicity decreases expression of Hsp72. Attenuation of Hsp 72 expression in uraemia, found in the present study, could contribute to the inflammatory state, a common complication in CKD patients.
OBJECTIVE: Expression of heat shock protein (Hsp) 72 is one of the major mechanisms acting against cellular injury. It displays a plethora of functions, including a considerable impact on inflammation. The aim of this study was to investigate Hsp72 expression in blood monocytes of patients with chronic kidney disease (CKD). MATERIAL AND METHODS:Hsp72 protein level was assessed by flow cytometry in blood monocytes of predialysis, haemodialysis (HD) and continuous peritoneal dialysis patients, and controls. It was followed by evaluation of Hsp72 gene expression in the same cohorts by reverse transcription-polymerase chain reaction. RESULTS: The level of Hsp72 protein was significantly lower in the predialysis (359+/-83 AU) and HD groups (293+/-62 AU) than in controls (405+/-51 AU) (p<0.01 and p<0.001, respectively). The amount of mRNA was significantly lower only in the HD group, compared with controls (0.39+/-0.10 vs 0.48+/-0.10, p<0.01). In the predialysis group, there were negative correlations between Hsp72 protein level and serum creatinine concentration, blood ureanitrogen and C-reactive protein. CONCLUSIONS: This study demonstrates that uraemic toxicity decreases expression of Hsp72. Attenuation of Hsp 72 expression in uraemia, found in the present study, could contribute to the inflammatory state, a common complication in CKDpatients.