Urinary angiotensinogen levels reflect the severity of renal histopathology in patients with chronic kidney disease

Kim, Seon Mee; Hr, Jang; Yj, Lee; Lee, Je; Ws, Huh; Dj, Kim; Hy, Oh; Kim, Yong‐Gil

doi:10.5414/cn107045

Cited by 22 publications

(24 citation statements)

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“…Urinary AGT has been reported to significantly correlate with urinary protein in patients with CKD, including IgAN (17,18). Consequently, its decrease is expected to associate with a decrease in daily proteinuria.…”

Section: Discussionmentioning

confidence: 99%

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Altered urinary excretion of aquaporin 2 in IgA nephropathy

Rocchetti

Tamma

Lasorsa

et al. 2011

European Journal of Endocrinology

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Objective: The intrarenal renin-angiotensin system (RAS) activation plays a pivotal role in immunoglobulin A nephropathy (IgAN) pathogenesis, which is still largely undefined. Recently, vasopressin (AVP) has been advocated to contribute to the genesis and progression of chronic kidney diseases (CKD) directly, and indirectly, via RAS activation. Our aim is to explore the intrarenal activity of AVP, its relationship with RAS activity, as well as its modulation by therapies in IgAN. Design: In this observational study, we measured plasma copeptin, a surrogate marker of AVP, the urine excretion of aquaporin 2 (AQP2), a protein reflecting renal AVP action, and angiotensinogen (AGT), a parameter of renal RAS activation, and their relationship with renal function in 44 IgAN patients at the time of renal biopsy, without any drug therapy, and after 6-month treatment with ACEi or steroidCACEi. Twenty-one patients with other CKD and 40 healthy subjects were recruited as controls. Methods: ELISAs were used to measure all variables of interest. Results: At baseline, IgAN patients showed higher urinary levels of AQP2, compared with controls and patients with other CKD. Urinary AQP2 and AGT levels strongly correlated with the presence of arterial hypertension. SteroidsCACEi caused the decrease of all the variables examined. The fall of urinary AQP2 and AGT following drug treatments was associated with the decrease of daily proteinuria. Conclusion: Our findings would support the involvement of AVP-AQP2 axis, interacting with the RAS, in the progression of IgAN and candidate AQP2 as a possible novel marker of the disease.

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Section: Discussionmentioning

confidence: 99%

“…Recently, uAGT has been proposed as a reliable marker of activated intrarenal RAS in IgAN: increases in uAGT levels were correlated with augmented intrarenal AGT gene expression and Ang II levels (16). Then, uAGT concentration is deemed to reflect the extension of renal damage in patients with CKD, including IgA nephropathy (17,18).…”

Section: Discussionmentioning

confidence: 99%

Altered urinary excretion of aquaporin 2 in IgA nephropathy

Rocchetti

Tamma

Lasorsa

et al. 2011

European Journal of Endocrinology

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“…Circulating ACE plays little, if any, role, and, thus, renal Ang II generation will depend entirely on locally expressed, membrane-bound ACE in the kidney [7]. Indeed, in human kidney, ACE is abundant in the brush border of the proximal tubule and, remarkably, usually absent in endothelial cells of any vessel type [8]. Endothelial neoexpression of ACE comes into play in different diseases, for example, diabetes mellitus and chronic arterial hypertension [9].…”

Section: Introductionmentioning

confidence: 99%

Urinary Angiotensinogen Is Elevated in Patients with Nephrolithiasis

Sun

Feng

Yao

et al. 2014

BioMed Research International

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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.

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“…In other studies, urinary level of AGT has been linked to severity of chronic kidney disease. It has been found with human patients that urinary AGT levels correlate to kidney function and increased levels correlate to tubular atrophy, glomeruloscerosis and tubular fibrosis [37] . Studies with animals demonstrate that urimic toxins, indoxyl sulphate and p-cresol sulphate activate intrarenal renin-angiotensin-aldosterone system causing increased angiotensinogen expression including other fibrogenic markers [38].…”

Section: Pathophysiologymentioning

confidence: 99%

Role of Angiotensin Peptides Precursor in Ethanol Mediated Hepato toxicity: Perspective on Angiotensinogen

Ansari¹

2012

TOGASJ

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Alcohol usage poses serious social and economical challenges. Its overuse is responsible for loss of billions of dollars due to fatal accidents and causes multiple diseases. Chronic alcoholism leads to liver disorders, including steatosis, hepatitis, fibrosis and cirrhosis. Both binge and chronic alcohol drinking result in blood pressure elevation and hypertension. As a significant mechanism, changes in the levels of angiotensinogen-released peptides play an important role in advanced alcohol liver disease. This review summarizes some of the studies that have demonstrated their role in liver fibrosis, cirrhosis and hypertension. Further, the individual variants and polymorphic sites may play a role in alcoholmediated regulation of angiotensinogen. Possible role of human angiotensinogen on alcohol hepatotoxicity is also discussed.

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Urinary angiotensinogen levels reflect the severity of renal histopathology in patients with chronic kidney disease

Cited by 22 publications

References 0 publications

Altered urinary excretion of aquaporin 2 in IgA nephropathy

Altered urinary excretion of aquaporin 2 in IgA nephropathy

Urinary Angiotensinogen Is Elevated in Patients with Nephrolithiasis

Role of Angiotensin Peptides Precursor in Ethanol Mediated Hepato toxicity: Perspective on Angiotensinogen

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