Assessment of urinary angiotensinogen as a marker of podocyte injury in proteinuric nephropathies

Eriguchi, Masahiro; Yotsueda, Ryusuke; Torisu, Kumiko; Kawai, Yasuhiro; Hasegawa, Shoko; Tanaka, Shigeru; Noguchi, Hideko; Masutani, Kosuke; Kitazono, Takanari; Tsuruya, Kazuhiko

doi:10.1152/ajprenal.00260.2015

Cited by 9 publications

(9 citation statements)

References 36 publications

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“…Although renal angiotensinogen is predominantly localized in the proximal tubules [ 44 , 46 , 47 ], weak expression is also detected in glomeruli. Since glomerular angiotensinogen is increased in damaged glomeruli [ 56 – 58 ], local RAAS activation in glomerulus may play a role in the pathophysiology of glomerular injury. Recently, Eriguchi et al [ 56 ] have shown that angiotensinogen is generated in injured glomerular podocytes in nephrotic rats induced by puromycin.…”

Section: Specific Role Of Angiotensinogen In the Regulation Of Ang IImentioning

confidence: 99%

“…Since glomerular angiotensinogen is increased in damaged glomeruli [ 56 – 58 ], local RAAS activation in glomerulus may play a role in the pathophysiology of glomerular injury. Recently, Eriguchi et al [ 56 ] have shown that angiotensinogen is generated in injured glomerular podocytes in nephrotic rats induced by puromycin. These data suggest the potential contribution of podocyte angiotensinogen generation in the progression of proteinuria.…”

Section: Specific Role Of Angiotensinogen In the Regulation Of Ang IImentioning

confidence: 99%

“…Matsusaka et al [ 75 , 76 ] have shown that in mice with severe podocyte injury and loss of macromolecular barrier function of the glomerular capillary wall, intrarenal Ang II generation is augmented by filtered angiotensinogen originated from the liver. Eriguchi et al [ 56 ] have shown that during the progression of podocyte injury, filtered angiotensinogen is abundantly re-absorpted by proximal tubules, leading to reduction in proximal tubular angiotensinogen generation. It has also been suggested glomerular podocyte is an important source of urinary angiotensinogen in this pathological condition [ 9 ].…”

Section: Urinary Angiotensinogen As a Biomarker Of Intrarenal Raas Anmentioning

confidence: 99%

“…Several clinical studies have shown that urinary angiotensinogen is significantly increased in patients with CKD including IgA nephropathy [ 55 ], diabetic nephropathy [ 84 , 87 , 89 ], polycystic kidneys [ 90 , 91 ], focal segmental glomerulosclerosis [ 56 ]. In these CKD patients, urinary angiotensinogen is positively correlated with urinary protein or albumin levels, while it is negatively correlated with estimated glomerular filtration rate.…”

Section: Urinary Angiotensinogen As a Biomarker Of Intrarenal Raas Anmentioning

confidence: 99%

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Independent regulation of renin–angiotensin–aldosterone system in the kidney

2018

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Renin–angiotensin–aldosterone system (RAAS) plays important roles in regulating renal hemodynamics and functions, as well as in the pathophysiology of hypertension and renal disease. In the kidney, angiotensin II (Ang II) production is controlled by independent multiple mechanisms. Ang II is compartmentalized in the renal interstitial fluid with much higher concentrations than those existing in the circulation. Inappropriate activation of the intrarenal RAAS is an important contributor to the pathogenesis of hypertension and renal injury. It has been revealed that intrarenal Ang II levels are predominantly regulated by angiotensinogen and therefore, urinary angiotensinogen could be a biomarker for intrarenal Ang II generation. In addition, recent studies have demonstrated that aldosterone contributes to the progression of renal injury via direct actions on glomerular podocytes, mesangial cells, proximal tubular cells and tubulo-interstitial fibroblasts through the activation of locally expressed mineralocorticoid receptor. Thus, it now appears that intrarenal RAAS is independently regulated and its inappropriate activation contributes to the pathogenesis of the development of hypertension and renal disease. This short review article will focus on the independent regulation of the intrarenal RAAS with an emphasis on the specific role of angiotensinogen.

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Section: Specific Role Of Angiotensinogen In the Regulation Of Ang IImentioning

confidence: 99%

Section: Specific Role Of Angiotensinogen In the Regulation Of Ang IImentioning

confidence: 99%

Section: Urinary Angiotensinogen As a Biomarker Of Intrarenal Raas Anmentioning

confidence: 99%

Section: Urinary Angiotensinogen As a Biomarker Of Intrarenal Raas Anmentioning

confidence: 99%

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Independent regulation of renin–angiotensin–aldosterone system in the kidney

2018

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“…Some have mixed origin; they can originate both in tubular cells and in podocytes, for example, angiotensinogen [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Urinary Biomarkers in the Assessment of Early Diabetic Nephropathy

Gluhovschi

Petrică

et al. 2016

Journal of Diabetes Research

118

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Diabetic nephropathy (DN) is a frequent and severe complication of diabetes mellitus (DM). Its diagnosis in incipient stages may allow prompt interventions and an improved prognosis. Towards this aim, biomarkers for detecting early DN can be used. Microalbuminuria has been proven a remarkably useful biomarker, being used for diagnosis of DN, for assessing its associated condition—mainly cardiovascular ones—and for monitoring its progression. New researches are pointing that some of these biomarkers (i.e., glomerular, tubular, inflammation markers, and biomarkers of oxidative stress) precede albuminuria in some patients. However, their usefulness is widely debated in the literature and has not yet led to the validation of a new “gold standard” biomarker for the early diagnosis of DN. Currently, microalbuminuria is an important biomarker for both glomerular and tubular injury. Other glomerular biomarkers (transferrin and ceruloplasmin) are under evaluation. Tubular biomarkers in DN seem to be of a paramount importance in the early diagnosis of DN since tubular lesions occur early. Additionally, biomarkers of inflammation, oxidative stress, podocyte biomarkers, and vascular biomarkers have been employed for assessing early DN. The purpose of this review is to provide an overview of the current biomarkers used for the diagnosis of early DN.

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Renal angiotensin I-converting enzyme-deficient mice are protected against aristolochic acid nephropathy

Juretzko

Steinbach

Witte

et al. 2022

Pflugers Arch - Eur J Physiol

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The renal renin-angiotensin system (RAS) is involved in the development of chronic kidney disease. Here, we investigated whether mice with reduced renal angiotensin I-converting enzyme (ACE−/−) are protected against aristolochic acid nephropathy (AAN). To further elucidate potential molecular mechanisms, we assessed the renal abundances of several major RAS components. AAN was induced using aristolochic acid I (AAI). Glomerular filtration rate (GFR) was determined using inulin clearance and renal protein abundances of renin, angiotensinogen, angiotensin I-converting enzyme (ACE) 2, and Mas receptor (Mas) were determined in ACE−/− and C57BL/6J control mice by Western blot analyses. Renal ACE activity was determined using a colorimetric assay and renal angiotensin (Ang) (1–7) concentration was determined by ELISA. GFR was similar in vehicle-treated mice of both strains. AAI decreased GFR in controls but not in ACE−/− mice. Furthermore, AAI decreased renal ACE activity in controls but not in ACE−/− mice. Vehicle-treated ACE−/− mice had significantly higher renal ACE2 and Mas protein abundances than controls. AAI decreased renal ACE2 protein abundance in both strains. Furthermore, AAI increased renal Mas protein abundance, although the latter effect did not reach statistical significance in the ACE−/− mice. Renal Ang(1–7) concentration was similar in vehicle-treated mice of both strains. AAI increased renal Ang(1–7) concentration in the ACE−/− mice but not in the controls. Mice with reduced renal ACE are protected against AAN. Our data suggest that in the face of renal ACE deficiency, AAI may activate the ACE2/Ang(1–7)/Mas axis, which in turn may deploy its reno-protective effects.

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Assessment of urinary angiotensinogen as a marker of podocyte injury in proteinuric nephropathies

Cited by 9 publications

References 36 publications

Independent regulation of renin–angiotensin–aldosterone system in the kidney

Independent regulation of renin–angiotensin–aldosterone system in the kidney

Urinary Biomarkers in the Assessment of Early Diabetic Nephropathy

Renal angiotensin I-converting enzyme-deficient mice are protected against aristolochic acid nephropathy

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