BACKGROUND: Cardiovascular disease (CVD) is the main cause of death in end-stage renal disease (ESRD) patients. It has been suggested that inflammation plays a key role in the development of both atherosclerosis and malnutrition (MIA), a combination of complications associated with poor outcome. Although plasma levels of adiponectin, a recently discovered anti-inflammatory and antiatherogenic adipocytokine, are markedly elevated in ESRD, gene expression of adiponectin (ApM1) has not been analyzed in ESRD patients. METHODS: We analyzed the ApM1 gene expression in adipose tissue from 18 ESRD patients of whom 9 (7 males, 60 +/- 8 years, BMI 24 +/- 6 kg/m(2)) had a high prevalence of MIA complications, and 9 age- (55 +/- 9 years), gender- (7 males) and BMI- (24 +/- 2 kg/m(2)) matched ESRD patients had few MIA complications. The results were compared with age- (59 +/- 11 years), gender- (7 males), and BMI- (24 +/- 6 kg/m(2)) matched healthy control patients. Information on CVD was obtained at the recruitment based on a detailed medical history. Malnutrition was defined as a subjective global assessment (SGA) score >1. Inflammation was defined as CRP >/=10 mg/L. Gene expression analysis was performed using the in situ hybridization technique. RESULTS: Gene expression of ApM1 was lower in ESRD patients compared with healthy control patients (P= 0.001). On the other hand, when comparing the gene expression between ESRD patients with and without MIA complications, respectively, no difference in the ApM1 gene expression was detected. CONCLUSION: Adiponectin gene expression is significantly down-regulated in ESRD patients compared with healthy control patients. We propose that the decrease in expression may be the result of a negative feedback regulation, as a result of elevated levels of circulating adiponectin caused by renal failure.
BACKGROUND:Cardiovascular disease (CVD) is the main cause of death in end-stage renal disease (ESRD) patients. It has been suggested that inflammation plays a key role in the development of both atherosclerosis and malnutrition (MIA), a combination of complications associated with poor outcome. Although plasma levels of adiponectin, a recently discovered anti-inflammatory and antiatherogenic adipocytokine, are markedly elevated in ESRD, gene expression of adiponectin (ApM1) has not been analyzed in ESRDpatients. METHODS: We analyzed the ApM1 gene expression in adipose tissue from 18 ESRDpatients of whom 9 (7 males, 60 +/- 8 years, BMI 24 +/- 6 kg/m(2)) had a high prevalence of MIA complications, and 9 age- (55 +/- 9 years), gender- (7 males) and BMI- (24 +/- 2 kg/m(2)) matched ESRDpatients had few MIA complications. The results were compared with age- (59 +/- 11 years), gender- (7 males), and BMI- (24 +/- 6 kg/m(2)) matched healthy control patients. Information on CVD was obtained at the recruitment based on a detailed medical history. Malnutrition was defined as a subjective global assessment (SGA) score >1. Inflammation was defined as CRP >/=10 mg/L. Gene expression analysis was performed using the in situ hybridization technique. RESULTS: Gene expression of ApM1 was lower in ESRDpatients compared with healthy control patients (P= 0.001). On the other hand, when comparing the gene expression between ESRDpatients with and without MIA complications, respectively, no difference in the ApM1 gene expression was detected. CONCLUSION:Adiponectin gene expression is significantly down-regulated in ESRDpatients compared with healthy control patients. We propose that the decrease in expression may be the result of a negative feedback regulation, as a result of elevated levels of circulating adiponectin caused by renal failure.
Authors: Maria P Martinez Cantarin; Scott A Waldman; Cataldo Doria; Adam M Frank; Warren R Maley; Carlo B Ramirez; Scott W Keith; Bonita Falkner Journal: Kidney Int Date: 2013-01-02 Impact factor: 10.612