title: Patients with nephrolithiasis had lower fetuin-A protein level in urine and renal tissue.
abstract: Fetuin-A acts as an inhibitor of systemic and local ectopic calcification and inflammatory response, but the role of fetuin-A in the etiology of urolithiasis is still unclear. We aim to investigate the expression of fetuin-A in the serum, urine and renal tissue of patients with or without nephrolithiasis. 48 patients with nephrolithiasis (group A) and 32 individuals without urolithiasis (group B, control group) were enrolled into our study. Level of fetuin-A in serum and urine was measured by ELISA, and expression of fetuin-A in renal tissue was localized and assessed by immunohistochemistry, real-time polymerase chain reaction, and Western blotting, respectively. Indexes of oxidative stress in kidney were evaluated. Other routine serum and urine chemistries for inpatients were measured biochemically. The results showed that fetuin-A expressed widely in the proximal and distal renal tubule, the thin segment of Henle's loop and the collecting duct epithelium. There were no differences in serum fetuin-A level between the two groups. Compared with control group, cellular expression of P47phox and fetuin-A mRNAs in the renal tissue of patients with nephrolithiasis increased, the level of MDA in renal tissue and the level of urinary calcium also increased, but urinary and renal fetuin-A protein and the activities of SOD in renal tissue decreased. Correlation analysis showed that there was a negative correlation between the level of renal fetuin-A protein and the expression of P47phox mRNA and MDA. These results revealed that nephrolithiasis patients had lower fetuin-A protein level in urine and renal tissue.
authors.affiliation: Department of Urology, The First Affiliated Hospital of Guangxi Medical University, 530021, Nanning, China.
authors.forename: Yong Xian
authors.initials: YX
authors.lastname: Wu
authors.forename: Cheng Yang
authors.initials: CY
authors.lastname: Li
authors.forename: Yao Liang
authors.initials: YL
authors.lastname: Deng
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood / Q000378:metabolism / Q000652:urine; D015153:Blotting, Western; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008875:Middle Aged; D019255:NADPH Oxidases / Q000235:genetics; D053040:Nephrolithiasis / Q000235:genetics / Q000378:metabolism* / Q000652:urine*; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D013482:Superoxide Dismutase / Q000378:metabolism; D060749:alpha-2-HS-Glycoprotein / Q000235:genetics / Q000378:metabolism* / Q000652:urine*
chemical_list: C556354:AHSG protein, human; D015415:Biomarkers; D012333:RNA, Messenger; D060749:alpha-2-HS-Glycoprotein; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1