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

• C-type natriuretic peptide (CNP) is synthesized in the kidney.
• CNP acts as an autocrine and paracrine factor.
• CNP is an important regulator of cell proliferation and organ fibrosis.
• CNP forms appear in urine and are elevated in heart failure and renal disease.
• Urine CNP excretion may enable early diagnosis of renal congestion, injury and remodeling.
• Urine CNP excretion may predict the evolution and progression of renal fibrosis.

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 pathophysiological correlates of urinary CNP, and its potential clinical utility as a diagnostic and prognostic biomarker in HF and renal disease states.