Journal Home
Search for

Volume 11, Issue 1, Pages 3-4 (January 2004)


View previous. 6 of 19 View next.

Guest editorial: racial and ethnic disparities in kidney disease

John M Flack, MD, MPH (Guest Editor)

Article Outline

References

Copyright

This issue contains an informative group of articles regarding racial and ethnic disparities in chronic, inclusive of end-stage, kidney disease. However, simply describing this well-documented problem will neither substantially advance our understanding of the pathogenesis of chronic kidney disease (CKD) nor improve our ability to intervene to prevent, or at least forestall, the onset and ultimate progression of CKD. Within the well-documented excess of CKD in many racial and ethnic groups relative to the US white population1 are important clues to the likely genesis of kidney diseases not only in minorities, but in all populations.

The articles contained herein cover important issues related to reducing the burden of CKD in the population while also reducing racial and ethnic disparities. The articles identify likely important contributors to the rising burden of CKD. For example, application of knowledge already proven to slow the progression of CKD, such as blood pressure (BP) control, utilization of pharmacological agents acting on the renin-angiotensin system (RAS), glycemic control, and smoking cessation are not often adequately translated into routine clinical practice for patients who will likely benefit from these interventions. Without increased outreach and educational efforts to primary care physicians, many patients already in the medical system who would potentially benefit from these interventions will not receive them. This situation is due to the rising dialysis population, the projected stable number of nephrologists over the next decade, and the increased identification of persons with CKD through the use of equations that estimate glomerular filtration rate. The article by Stevens and Levin in this issue thoroughly covers these issues. They also appropriately argue for better systems support of our provision of medical care to persons at risk for CKD.

Even when covered by the same medical care provider (Medicare), blacks appear to have less access to preventive care than whites. This lack of access appears to be linked to their higher risk of end-stage renal disease (ESRD). The article by Li et al further highlights the fact that a substantial proportion of the excess risk for ESRD among black Medicare recipients relates to potentially modifiable medical care, health conditions, and socioeconomic variables. The reason(s) for the differential access to care when covered by the same provider are likely mediators of at least a portion of the known disparities in CKD between blacks and whites.

The article by Hall et al is an important one. It is unequivocally true that diabetes and hypertension are two major causes of ESRD, as they account for the numerical majority of cases.1 These two CKD risk factors are not mutually exclusive of one another, given that 70% of persons with diabetes have hypertension and that in persons with hypertension but no diabetes, the risk of incident diabetes is increased by approximately 2.5. However, this article elegantly describes the changes in renal hemodynamics, structure, and function caused by obesity, a major risk factor for both diabetes and hypertension. The renal changes induced by obesity largely appear to be deleterious to long-term kidney health. Given the strikingly disproportionate rates of obesity in minorities, especially in black women, relative to whites obesity prevention and mechanistic research into how obesity causes injury to the kidneys and validation of obesity-linked therapeutic targets are desperately needed.

The article by Hostetter points out potential research opportunities that will likely shed important light on more effective strategies for prevention of and/or slowing of the progression of CKD. As he points out, the African American Study of Kidney Disease (AASK)2 has validated the superiority of angiotensin-converting enzyme (ACE) inhibitors for preservation of kidney function in black hypertensives with nondiabetic kidney disease. The Chronic Renal Insufficiency Cohort (CRIC) study will also likely provide useful insight into the development of CKD and its longitudinal links to cardiovascular diseases in persons with CKD.

The article by Lopes nicely summarizes the racial and ethnic disparities in ESRD among minorities relative to U.S. whites. This article further describes some of the factors linked to poor renal outcomes, including late referral of minority patients to nephrologists. This article notes that lead, a deleterious environmental exposure, has been linked to both hypertension and CKD risk in blacks but not in whites. He also reports that blacks are less satisfied with their health care than whites and that, for common conditions such as hypertension and diabetes, indicators of quality medical care are low in blacks and Native Americans.

Finally, the article by Lakkis and Weir addresses the treatment issues for the control of CKD risk factors such as hypertension and diabetes. This article again highlights that better management of traditional risk factors has the potential to reduce the burden of CKD in all, while simultaneously closing the CKD risk-gap between minorities and whites. Clearly, non-pharmacological therapies, such as weight loss, dietary sodium restriction, and smoking cessation, play an important role in the management of CKD risk factors, such as hypertension and diabetes. These therapies may also have direct impact on the CKD process itself.

This collection of articles provides a fresh look at various areas, spanning from translation of known research findings to clinical practice all the way to mechanistic causes of renal injury. At present we know much, but we effectively put into practice much less than we know. Yet, it is also clear that we do not yet know enough about the triggers of renal injury nor do we fully understand the genesis of racial and ethnic disparities, as well as socioeconomic gradients within race. The future is likely dim unless we can stem the tide of the burgeoning obesity epidemic that is disproportionately affecting minority populations. Thus, a concentrated and sustained effort by public health and medical practitioners, as well as by behavioral scientists, will be required to stand a fighting chance of slowing the epidemic of CKD. We must also design “smarter” systems of health care delivery that facilitate the practice of higher quality medicine.

References 

return to Article Outline

1. 1 U.S. Renal Data System . USRDS 2002 Annual Data Report (Atlas of end-stage renal disease in the United States). Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2002;.

2. 2 Agodoa LY, Appel L, Bakris GL, et al.  Effect of ramipril vs amlodipine on renal outcomes in hypertensive nephrosclerosis (a randomized controlled trial). JAMA. 2001;285:2719–2728. MEDLINE | CrossRef

PII: S1073-4449(03)00143-2

doi:10.1053/j.arrt.2003.12.002


View previous. 6 of 19 View next.