Urinary C-type natriuretic peptide excretion: a potential novel biomarker for renal fibrosis during aging

Sangaralingham, S. Jeson; Heublein, Denise M.; Grande, Joseph P.; Cataliotti, Alessandro; Rule, Andrew D.; McKie, Paul M.; Martín, Fernando L.; Burnett, John C.

doi:10.1152/ajprenal.00170.2011

Cited by 32 publications

(32 citation statements)

References 36 publications

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“…Here we confirm previous reports by our group and others [28, 29, 37, 38] that age-mediated cardiorenal fibrosis increases with aging in the rat. Interestingly, Col I and Col III mRNA transcripts decrease in the aging LV, renal cortex and medulla, thus suggesting the increase in fibrosis in the aged heart and kidney is not likely due to increase in collagen production.…”

Section: Discussionsupporting

confidence: 93%

“…A 24-hour urine collection was performed on ice after acclimatization for urinary protein excretion assessment as previously described [28]. Glomerular filtration rate (GFR) was also assessed by inulin clearance on anesthetized (2.0-2.5% isoflurane in oxygen) rats as described previously [28]. …”

Section: Methodsmentioning

confidence: 99%

“…Cross-sections of paraffin-embedded LV and renal tissue (4 μm) were stained with picrosirius red and quantified as previously described [28, 29]. …”

Section: Methodsmentioning

confidence: 99%

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Cardiorenal fibrosis and dysfunction in aging: Imbalance in mediators and regulators of collagen

et al. 2016

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Cardiorenal fibrosis is a biological process that increases with age and contributes to dysfunction of the heart and kidney. While numerous circulating and tissue hormones, cytokines and enzymes have been identified in the development of cardiorenal fibrosis, several reports have suggested that the anti-fibrotic natriuretic peptide system (NPS), pro-fibrotic renin-angiotensin-aldosterone system (RAAS), transforming growth factor-beta 1 (TGF-β1), matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) are fundamental regulators and mediators of this process. However, the simultaneous assessment of these components in the development of age-mediated cardiorenal fibrotic remodeling is not completely understood. Thus, we assessed cardiorenal structure and function, the circulating NPS and RAAS and the cardiorenal tissue gene expression of collagen (Col) I, Col III, TGF-β1, MMP-9 and TIMP-1 in 2 and 20 month old Fischer rats. Our studies determined that aging was characterized by an increase in cardiorenal fibrosis that was accompanied with cardiorenal dysfunction. These alterations were associated with lower circulating atrial and C-type natriuretic peptides and higher angiotensin II and aldosterone levels in the aged rats. Moreover, we observed a decrease in Col I and III, an increase in TIMP-1 and no change in MMP-9 mRNA expressions in the aged heart and kidney, while TGF-β1 expression increased only in the aged kidney. We conclude that the age-mediated alterations in these fibrotic regulator and mediator profiles favors collagen accumulation due to an imbalance between the NPS and RAAS as well as a decline in the degradative pathway, thus suggesting a therapeutic opportunity to target these components.

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Section: Discussionsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

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Cardiorenal fibrosis and dysfunction in aging: Imbalance in mediators and regulators of collagen

et al. 2016

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“…CNP molecular forms in the urine and plasma are currently assessed using proprietary radio- or sandwich immunoassays [14] [38] [44-46]. Reproducibility and a high degree of sensitivity and specificity have been reported within individual pre-clinical and clinical research studies, particularly with the use of the radioimmunoassays [14, 44, 47].…”

Section: C-type Natriuretic Peptide Biologymentioning

confidence: 99%

“…Reproducibility and a high degree of sensitivity and specificity have been reported within individual pre-clinical and clinical research studies, particularly with the use of the radioimmunoassays [14, 44, 47]. However a clinical laboratory platform for CNP measurement in clinical practice has yet to be developed.…”

Section: C-type Natriuretic Peptide Biologymentioning

confidence: 99%

Urinary C-type natriuretic peptide: An emerging biomarker for heart failure and renal remodeling

Zakeri

Burnett

Sangaralingham

2015

Clinica Chimica Acta

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The public health and economic burden of heart failure (HF) is staggering and the need for relevant pathophysiologic and clinical biomarkers to advance the field and improve HF therapy remains high. Renal dysfunction is common among HF patients and is associated with increased HF hospitalization and mortality. It is widely recognized that mechanisms contributing to HF pathogenesis include a complex bidirectional interaction between the kidney and heart, encompassed by the term cardiorenal syndrome (CRS). Among a new wave of urinary biomarkers germane to CRS, C-type natriuretic peptide (CNP) has emerged as an innovative biomarker of renal structural and functional impairment in HF and chronic renal disease states. CNP is a hormone, synthesized in the kidney, and is an important regulator of cell proliferation and organ fibrosis. Hypoxia, cytokines and fibrotic growth factors, which are inherent to both cardiac and renal remodeling processes, are among the recognized stimuli for CNP production and release. In this review we aim to highlight current knowledge regarding the biology and pathophysiologic correlates of urinary CNP, and its potential clinical utility as a diagnostic and prognostic biomarker in HF and renal disease states.

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Mechanisms of Cardiorenal Syndrome: From Molecular Pathways to Novel Therapeutics

Ichiki

Chen

BurnettJr.

2019

Cardiorenal Syndrome in Heart Failure

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Urinary C-type natriuretic peptide excretion: a potential novel biomarker for renal fibrosis during aging

Abstract: Sangaralingham SJ, Heublein DM, Grande JP, Cataliotti A, Rule AD, McKie PM, Martin FL, Burnett JC, Jr. Urinary C-type natriuretic peptide excretion: a potential novel biomarker for renal fibrosis during aging.

Cited by 32 publications

References 36 publications

Cardiorenal fibrosis and dysfunction in aging: Imbalance in mediators and regulators of collagen

Cardiorenal fibrosis and dysfunction in aging: Imbalance in mediators and regulators of collagen

Urinary C-type natriuretic peptide: An emerging biomarker for heart failure and renal remodeling

Mechanisms of Cardiorenal Syndrome: From Molecular Pathways to Novel Therapeutics

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