Preface

The importance of the kidney in contributing to cardiovascular risk was largely underappreciated until the past decade. Data from several large epidemiologic studies make it clear that the presence of kidney disease, defined as an estimated glomerular filtration rate (eGFR) of less than 60 mL per minute, not only increases the risk of death from cardiovascular causes, but also makes management of heart failure much more difficult. The other unappreciated aspect of cardiovascular risk that frequently accompanies kidney disease is the presence of macroalbuminuria or proteinuria, defined as levels greater than 300 mg per day. Proteinuria at levels above 1 gram per day and especially above 3 grams per day result in hypoalbuminemia and consequent lower plasma oncotic pressure. These lower oncotic pressures translate into greater difficulty in management and maintenance of volume homeostasis.

I am honored that I was asked to serve as Guest Editor of this special issue of Heart Failure Clinics. This issue is dedicated to the discussion of how pre-existing reductions in kidney function due to various conditions contribute to difficulties in the management of pre-existing heart failure as well as development of new onset heart failure. The initial articles in this issue elucidate epidemiology and pathophysiology. These articles are then followed by a number of articles that focus on specific issues relating to the management of volume homeostasis, how to deal with acute changes in kidney function that result from overaggressive diuresis, and the use with blockers of the renin angiotensin aldosterone system. The final articles in the issue deal with various forms of dialysis and discuss which is appropriate for a specific clinical setting. Additionally, the approach of using functioning kidneys versus immediately starting ultrafiltration is reviewed.

Both a nephrologist and a cardiologist generally coauthored each article in this issue so that there is a balance between the data and their interpretation. I think I speak for the authors when I state that we hope the reader finds this issue stimulating and informative. Moreover, I hope that it gives both cardiologists and nephrologists the perspective that the heart and kidney are interdependent in clinical states of systolic dysfunction and that ignoring one organ over the other usually results in a worsening clinical state for the patient. Consequently, the disciplines should approach this clinical condition with a full understanding of the pathophysiology that portends its genesis.