The Roles of Heat Shock Protein-60 and 70 and Inflammation in Obesity-Related Kidney Disease

Abstract

Introduction The exact mechanisms of obesity-related kidney disease (ORKD) are not fully known. Heat shock proteins (HSPs) may play a role in ORKD mechanisms because of their role in cell apoptosis, cytoprotection, and inflammatory processes. We aimed to determine the role of circulating serum HSP-60 and HSP-70 levels as a biomarker for ORKD. Materials and methods This study included 40 ORKD patients, 40 obese age-matched and sex-matched controls with similar body mass index (BMI), and 40 healthy controls. Their serum biochemical and hemogram parameters as well as HSP-60 and HSP-70 levels were evaluated and compared. Their neutrophil-to-lymphocyte ratio (NLR) and C-reactive protein levels were assessed to define inflammation.  Results The patients had significantly higher HSP-60 levels than the obese and healthy controls (537.58 ± 170.35, 430.80 ± 110.61, and 371.85 ± 76.34, respectively; p<0.00). The results revealed that the 24-hour urinary protein levels had a positive correlation (r= 0.544), whereas the glomerular filtration rate had a negative correlation (r = 0.38) with the serum HSP-60 level. According to the regression analysis performed on the HSP-60 and 24-hour urinary protein excretion levels, an increase in the HSP-60 level significantly increased the 24-hour urinary protein excretion rate (r=0.15; p<0.005). The HSP-60 levels were correlated with inflammatory markers Conclusion The serum HSP-60 levels increased in patients with ORKD. This increase was correlated with 24-hour urinary protein excretion. Increased circulating levels of HSP-60 may play a role in the initiation and/or progression of renal damage and inflammation. HSP-60 is a potential biomarker for ORKD. However, additional information and studies are required to further elucidate this finding.