This is prospective cohort study with the purpose of improving our understanding of morbidity and mortality risk in patients with heart failure and chronic kidney disease.

The CDC reports that approximately 5.7 million adults in the U.S. have heart failure (HF), and NHANES reports that 26% of individuals 60 years-of-age and older have Chronic Kidney Disease. NHANES also reports that End-Stage Kidney Disease (ESKD) accounts for $40 billion in Medicare and Non-Medicare costs in 2009; 37% of those patients had a prior episode of HF. These figures demonstrate that the treatment of patients with HF and ESKD costs Americans almost $15 billion annually. A meta-analysis of 16 studies estimates that 63% of HF patients have some kidney impairment; a serum creatinine (Cr)>1.0mg/dL or Glomerular Filtration Rate (GFR)<90 ml/min. Among HF patients with even mildly decreased GFR, mortality increases significantly; those with none, any, and at least moderate CKD experienced a 24%, 38% and 51% 1-year mortality, respectively. In 2015, 66,713 patients were seen at our hospital. About 3% of those patients had a new diagnosis of CHF and at least 30% of those patients diagnosed with CHF had a dual diagnosis of CKD. This population alone accounted for 79,835 of visits in the same year. It is evident that there are both fiscal and ethical incentives, both locally and nationally, to understand how to mitigate disease progression in this population.

Current classification schemes for patients with HF and chronic kidney disease (CKD), cardiorenal syndrome, do not significantly alter management other than managing HF or CKD independently with respect to their individual severity. In CKD, worsening renal function often leads to poor phosphate (PO4) regulation where hyperphosphatemia is significantly associated as a predictor of mortality. Further characterizations of the factors that contribute to hyperphosphatemia implicates Fibroblast Growth Factor 23 (FGF-23) as a major hormone regulator of PO4 levels in the body. FGF-23 has repeatedly demonstrated its use as an independent predictor of mortality in ESKD as well as an independent predictor of worsening renal function in non-diabetic patients with mild CKD. FGF-23 achieves PO4 level control by downregulating PO4 reabsorption via transporters in kidney's proximal tubules as well as the small intestines through an incompletely understood mechanism. This action allows the increased filtration of PO4 without proximal tubule reabsorption as well as indirectly decreased uptake of dietary PO4. In ESKD, the PO4-lowering effects of FGF-23 diminish despite rising FGF-23 levels; this indicates that pathologic hyperphosphatemia represents a decompensated state of PO4 regulation. There are studies that suggest FGF-23 is not only implicated in the worsening of CKD, but the pleiotropic effects of FGF-23 remain to be understood as a factor in cardiovascular disease. Increased FGF-23 levels have been associated with left ventricular dysfunction and atrial fibrillation as well as worsening CKD. In one study, not a single patient with Group 5 CKD had an FGF-23 level lower than 40.2ρg/dL, and more than 70% of those patients had and FGF-23 level greater than 66.1ρg/dL.14 Despite this information, it is not currently known how FGF-23 may be used as a predictor of mortality or progression of CKD in patients with cardiorenal syndrome prior to end-stage renal disease. Significant results from this study may provide a predictable classification scheme based on FGF-23 levels that may be employed in future studies to guide treatment evaluation. The prospect of treatment to reduce morbidity and mortality is supported by studies demonstrating that PO4 binders lower FGF-23 levels, even in healthy volunteers. The study proposed here is an early step in evaluating options to reduce the number of patients that progress to ESRD with a parallel step towards a reduction in significant healthcare costs. Participants in this study will only be observed after they have granted their informed consent. There are no significant potential risks posed by this study as blood collected would be from routine lab vials for the participant population. If the study has significant findings, there are immediate benefits to the population studied and the greater society.

Participants after this study will be equipped with more knowledge to help them understand their risk factors and help them make better decisions about their own healthcare. The investigators hope to achieve a better understanding of what levels of FGF-23 are significantly associated with morbidity and mortality in patients with CHF and CKD. This information can help us answer how current clinicians may better stratify the risks of CHF and CKD; translating theoretical disease predictions into a preventative medicine model. The answer to this question may lay the foundation for treatment and prevention option studies based on FGF-23 levels in patients that are not currently on hemodialysis.

We hypothesize (1) that in participants with congestive heart failure and chronic kidney disease who are not on hemodialysis, worsening heart disease or worsening kidney disease is associated with a significantly elevated FGF-23 serum level AND (2) participants with congestive heart failure and chronic kidney disease who are not on hemodialysis, decreased survival is associated with a significantly elevated FGF-23 serum level.

Inclusion Criteria:

• Patients must have a diagnosis of congestive heart failure

Exclusion Criteria:

• Patients cannot be on hemodialysis at the study onset.
• Patients cannot have hyperphosphatemia defined as persistent serum phosphorus level>4.5mg/dL at study onset.
• Patients cannot be part of another study for the investigational treatment of heart failure or chronic kidney disease.

Control Arm: People seen in the outpatient setting with congestive heart failure without renal impairment. Study Arm: People seen in the outpatient setting with congestive heart failure that have some form of renal impairment that did not start the study while on hemodialysis.