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

Abstract

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.

Renal papillary tip extract stimulates BNP production and excretion from cardiomyocytes

“…Additionally it is not clear which type of cells in the renal papilla can induce BNP production. Specific receptors for angiotensin II and natriuretic peptides have been found in tubular and interstitial cells [ 25 , 26 ], although we observed no change in the expression of these peptides between the papillary tip and other portions of the kidneys.…”

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

“…The heart and kidney are hormonally linked via the natriuretic peptide system (NPS), where the cardiac and reno-endothelium derived atrial natriuretic peptide (ANP) and c-type natriuretic peptide (CNP) respectively, mediates the inhibition of cardiorenal fibrosis and adverse remodeling through the particulate guanylyl cyclase receptors [1, 2]. The NPS is counter-regulated by the renin-angiotensin-aldosterone system (RAAS) of which angiotensin II (ANG II) via the angiotensin receptor 1 (AT1) and aldosterone through the mineralocorticoid receptor contribute to adverse cardiac and renal remodeling and fibrosis [3].…”

Biomarkers in Heart Failure

“…Given the prominent role of natriuretic peptides in chronic HF, the increasing interest in urinary C-type natriuretic peptides (CNPs) for HF and AKI should be no surprise. Zakeri et al [14] will go into the details.…”