Urinary Angiotensinogen Is Elevated in Patients with Nephrolithiasis

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-micr...

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Bibliographic Details
Main Authors: Sun, Wei, Feng, Yuan, Yao, Xu-Dong, Xu, Yun-Fei, Peng, Bo, Liu, Min, Zheng, Jun-Hua
Format: Online
Language:English
Published: Hindawi Publishing Corporation 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4000960/
Description
Summary: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; P < 0.01). 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; P < 0.05]. According to the single variate analysis, UA levels were significantly and positively correlated with urinary α1-microglobulin (r = 0.733; P = 1.33 × 10−15), while they were significantly and negatively correlated with eGFR (r = −0.343; P = 1.03 × 10−4). 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.