The degree of natriuretic peptide system activation in stable and high risk CHF characterized by increased cystatin C is not reflected in cGMP activation

Background Cardiorenal syndrome (CRS) is characterized by neurohumoral activation, sodium retention, ventricular dysfunction and congestion, and renal insufficiency (RI). The congestive heart failure (CHF) component evolves from asymptomatic, to stable symptomatic to overt symptomatic CHF. The natriuretic peptide system (NPS), including atrial (ANP) and brain (BNP) natriuretic peptides is progressively activated during progression of CHF. Less is known about the second messenger, cGMP, of the NPS across the spectrum of CHF. RI in CHF remains an important clinical challenge and Cystatin C is emerging as an important marker of RI. Further work is needed in characterizing Cystatin C across the spectrum of CHF and CRS.