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BioMed Research International
Volume 2014 (2014), Article ID 349602, 6 pages
Research Article

Urinary Angiotensinogen Is Elevated in Patients with Nephrolithiasis

1Department of Urological Surgery, Shanghai Tenth People’s Hospital, Tongji University, Shanghai 200072, China
2Department of Nephrology, Affiliated Drum Tower Hospital, Nanjing University, Nanjing, Jiangsu 210093, China

Received 4 February 2014; Accepted 19 March 2014; Published 9 April 2014

Academic Editor: John J. Gildea

Copyright © 2014 Wei Sun et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Elevated urinary angiotensinogen (UA) was identified as novel prognostic biomarker capable of predicting chronic kidney disease, and in the present study, we will investigate the diagnostic value of UA in the patients of nephrolithiasis. Methods. Urine angiotensinogen levels and α1-microglobulin were measured by enzyme-linked immunosorbent assay (ELISA) in 60 patients presenting with nephrolithiasis and 50 sex- and age-matched healthy volunteers. Estimated glomerular filtration (eGFR) was calculated and, by simple regression analysis, the correlation of UA/α1-microglobulin levels and the decline of eGFR were analyzed as well. Results. Median UA levels was significantly increased in the nephrolithiasis patients compared with normal control (1250.78 439.27 versus 219.34 45.27 pg/mL; ). The mean serum creatinine levels in patients with higher UA levels (1250 pg/mL) was significantly higher than those with lower UA levels (1250 pg/mL) [92.23 18.13 μmol/L versus 70.07 11.17 μmol/L; ]. According to the single variate analysis, UA levels were significantly and positively correlated with urinary α1-microglobulin (; ), while they were significantly and negatively correlated with eGFR (; ). Conclusion. Urinary UA is a novel biomarker for patients with nephrolithiasis, which indicates renal tubular injury. Further study on the molecular pathogenic mechanism of UA and larger scale of clinical trial is required.