American Journal of Kidney Diseases
Volume 41, Supplement 5 , Pages 1-2, June 2003

Introduction

  • Steven Fishbane, MD

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Steven Fishbane, MD, Director of Dialysis Services, Winthrop-University Hospital, 200 Old Country Rd, #135, Mineola, NY 11501, USA
    • Winthrop-University Hospital, Mineola, NY, USA

Article Outline

 

WE HAVE MADE significant gains in the treatment of patients with chronic kidney disease (CKD) during the past several decades. Beginning with technological advances in equipment, such as the artificial kidney and Teflon (DuPont, Wilmington, DE) shunt, we have successfully moved CKD from an imminently fatal disease to one that can be managed successfully as a chronic illness. Along the way, we have made significant gains in our understanding of CKD, especially with regard to the pathophysiological process underlying anemia and the relationship between CKD and cardiovascular disease.

However, despite these gains, the benefits of intervention have been leveling off, leaving us short of our goal of optimized survival and quality of life. Much of our failure to achieve these goals has been related to a lack of standardization of CKD treatments and dialysis protocols, leading to important variations in morbidity and mortality among centers. Reports from the US Renal Data System have shown that some hemodialysis centers have an annual mortality rate of 30%, substantially higher than the national average.1 Our inability to make continued gains also has been related to our failure to treat CKD as a lifelong process that requires intervention long before the patient presents for hemodialysis therapy. Focusing on the early stages of CKD, when glomerular filtration rate (GFR) first begins to decrease, may potentially prevent thousands of patients each year from advancing to the point at which hemodialysis is required.

Recognizing these needs, the National Kidney Foundation-Kidney Disease Outcomes Quality Initiative (K/DOQI) recently released guidelines for the management of patients with CKD.2 These guidelines, developed in an evidence-based manner, are discussed by Dr Eknoyan in the first part of this supplement to the American Journal of Kidney Diseases. An important highlight of the guidelines is their focus on GFR or the presence of kidney damage to define CKD; using these two factors, a diagnosis of CKD can be made early in the course of the disease, well before the need for hemodialysis, and the patient’s level of disease can be staged according to the level of damage or reduced GFR.

In the second portion of this supplement, Dr Sarnak discusses some of the latest data on the association between CKD and cardiovascular disease. Although patients with CKD have many of the same risk factors for cardiovascular disease as the general population, including dyslipidemia and diabetes, they also have several risk factors specific to CKD, including abnormal calcium and/or phosphate metabolism and anemia. It appears that the positive calcium balance experienced by most patients with CKD is especially important to the pathophysiological process of cardiovascular disease because it leads to vessel remodeling, loss of elasticity and metastatic calcification, and, ultimately, increased pulse pressure and strain on the renal system.

In the third section of this supplement, I discuss recent findings regarding the safety of iron to manage anemia in patients with CKD undergoing hemodialysis. Intravenous (IV) iron has an integral role in achieving adequate hemoglobin levels in patients with anemia, and its importance has been recognized by the K/DOQI anemia guidelines, which state that most hemodialysis patients will require IV iron on a regular basis to achieve target hemoglobin/hematocrit levels.3 Nevertheless, continued questions about the short- and long-term safety of IV iron use have made some providers hesitant to use this therapy in hemodialysis patients. These concerns include anaphylactoid reactions (largely associated with IV iron dextran), release of free iron into serum, and risks related to infection and cardiovascular disease. In this article, I explore the body of evidence surrounding each of these risks and potential differences in risk between iron dextran and the two newer agents introduced in the United States, sodium ferric gluconate and iron sucrose. It is our hope that you find the discussions contained in this supplement informative and that you can incorporate some of the research contained in these articles into your nephrology practice.

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References 

  1. US Renal Data System . Excerpts from the US Renal Data System 2000 Annual Data Report (Atlas of End-Stage Renal Disease in the United States). Am J Kidney Dis. 2000;36(suppl 2):S1–S239
  2. National Kidney Foundation . K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease (Executive Summary). New York, NY: National Kidney Foundation; 2002;
  3. National Kidney Foundation . K/DOQI Clinical Practice Guidelines for Anemia of Chronic Kidney Disease, 2000. Am J Kidney Dis. 2001;37(suppl 1):S182–S238

PII: S0272-6386(03)00370-6

doi:10.1016/S0272-6386(03)00370-6

American Journal of Kidney Diseases
Volume 41, Supplement 5 , Pages 1-2, June 2003

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