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NDT Advance Access published online on June 20, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn334
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


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Correspondence and offprint requests to: E-mail: lstevens1{at}tuftsmedicalcenter.org

Sir,

We write in response to the reply by Glassock and Winearls to our editorial ‘Chronic Kidney Disease is Common: What Do We Do Next?’ and commentary by De Jong and Gansevoort published simultaneously [1–3]. We also respond to the debate on the definition and classification of chronic kidney disease (CKD) and the interpretation of estimates of the prevalence for CKD that is occurring in the editorial pages of other nephrology subspeciality journals [4–6]. Each of these editorials notes shortcomings in the currently accepted definition and classification of CKD [7, 8]. We acknowledge that the simplicity of the current stages has some shortcomings. While most suggestions would reduce the number of people classified as having CKD, this alone does not clearly improve on or justify a change in the definition.

CKD is a heterogeneous condition, with many different causes, manifestations, comorbid conditions and factors affecting prognosis. Estimated glomerular filtration rate (GFR) is one way to classify patients but not the only way. For example, we would all agree that a child with focal and segmental glomerulosclerosis requires the nephrologist's more urgent attention than an elderly patient with CKD Stage 3 due to hypertensive nephrosclerosis with well-controlled blood pressure. Within CKD Stages 1–3, nephrologists should focus on those at greatest risk for progressive GFR decline. At present, we lack sufficient data to quantify this risk. At the 2004 KDIGO Controversies Conference, modification of the classification system to incorporate risk for progression was thought to be too complex [8]. We think that adding a second dimension to CKD classification that summarizes the risk of kidney disease progression has merit. Going forward, our goal should be to articulate this differential risk while maintaining the appropriateness of the CKD classification system for use by all healthcare professionals.

Progressive GFR decline is not the only outcome of CKD and focusing only on this outcome may lead to missed opportunities to improve other health care outcomes, as suggested by a recent article showing reduced all-cause mortality among US veterans with CKD Stages 3 and 4 receiving care by nephrologists [9]. Similarly, focusing only on what nephrologists should do misses the point that CKD is common, especially in the elderly, and affects the management and outcome of other diseases, such as cardiovascular disease. In addition, CKD increases the risk for complications of diagnostic tests and procedures as well as for acute kidney disease [10]; thus, primary care physicians and non-nephrologist sub-specialists must also change their practices to account for the presence of CKD. This situation is analogous to the challenges in caring for type 2 diabetes. Diabetes is increasingly common, especially in the elderly, and affects the care and outcomes of virtually all other diseases. Endocrinologists do not care for all patients with type 2 diabetes but do have an important role to play in caring for the sickest patients, educating other physicians about appropriate care for diabetes and providing leadership in the public health approach to diabetes. Improving the outcomes of care for CKD, like diabetes, affects the public health and nephrologists need to take part [11].

We suggest that the tone of the debate should be changed to developing a research agenda to provide data to address the urgent questions posed in these editorials. These are a few of the important avenues for research that could provide evidence-based answers to the important questions posed by recent editorials:

  1. Representative values for measured GFR need to be established for the elderly and diverse racial and ethnic populations of all ages. Current age-associated values in whites are based on small, non-representative populations, which bear little resemblance to today's elderly population. There is very little data, even in younger people, from other races and ethnicities.
  2. More accurate GFR-estimating equations are required to overcome current limitations of systematic underestimation of measured GFR at higher values, imprecision throughout the GFR range and lack of applicability to many racial and ethnic populations.
  3. The causes of declining GFR with age are not well understood. Long considered ‘normal’, there is abundant evidence that kidney morphology is not normal, and the relationship of these age-associated morphologic changes to pathologic features in the rapidly growing elderly population with kidney failure is not known. There appears to be substantial heterogeneity within populations in GFR decline with age, and some factors may be modifiable.
  4. The cause of low levels of albuminuria and the mechanism of their relationship with cardiovascular disease risk is poorly understood. This may be one clue to the close association of kidney disease and cardiovascular disease.
  5. New urinary markers and imaging modalities for detection of kidney damage are needed for early detection of kidney disease and to better interpret reduced GFR in the elderly.
  6. The outcomes of CKD need to be understood better, especially in the elderly. Kidney failure, cardiovascular disease and traditional complications of decreased GFR (hypertension, anemia, malnutrition, metabolic and bone disorders, neuropathy) are well recognized; however, more information is necessary on risks for acute kidney injury, complications of medications and procedures, frailty, accidents and falls, medical errors, quality of care and successful rehabilitation from acute and chronic illness.
  7. More accurate prognosis for patients with CKD according to reduction in estimated GFR, albuminuria and other markers of kidney damage would clarify the overall importance of CKD to general health. Possibly, scoring systems for risks for various outcomes could provide opportunities for treatment and prevention by all physicians and be incorporated into clinical practice and public policy.
  8. Finally, there are too few clinical trials for chronic kidney disease. Ongoing laboratory work is necessary to discover new pathways and targets of treatment to ameliorate kidney damage and slow the progressive decline in GFR in CKD. In addition, trials to reduce risk for other CKD complications are also necessary. Design of these trials should be informed by the different risk profile of different patients. For example, reduction of albuminuria appears to provide an avenue for selecting treatment with the greatest promise for slowing progression of CKD. Alternatively, reduction of risk of AKI and drug complications may benefit from strategies to alert physicians and patients.

Answers to these questions could move the field forward. The current debate is healthy, but we should not lose sight of the common goal, which is to improve the outcomes of patients with CKD.

Conflict of interest statement. None declared.

Andrew S. Levey1, Lesley A. Stevens2 and Josef Coresh3

1 Department of Nephrology Tufts-New England Medical Center Boston, MA 2 Tufts Medical Center Tufts University School of Medicine 800 Washington St. Box 391 Boston, MA 02111 3 Department of Epidemiology The Johns Hopkins Medical Institutions, Welch Center for Prevention, 2024-E, Monument Street Suite 2600, Baltimore MD 21205, USA

References

  1. Glassock RJ, Winearls C. An epidemic of chronic kidney disease: fact or fiction? Nephrol Dial Transplant (2008) 23:1117–1121.[Free Full Text]
  2. Coresh J, Stevens LA, Levey AS. Chronic kidney disease is common: what do we do next? Nephrol Dial Transplant (2008) 23:1122–1125.[Free Full Text]
  3. de Jong PE, Gansevoort RT. Fact or fiction of the epidemic of chronic kidney disease—let us not squabble about estimated GFR only, but also focus on albuminuria. Nephrol Dial Transplant (2008) 23:1092–1095.[Free Full Text]
  4. Couser WG. Chronic kidney disease the promise and the perils. J Am Soc Nephrol (2007) 18:2803–2805.[Free Full Text]
  5. Poggio ED, Rule AD. Can we do better than a single estimated GFR threshold when screening for chronic kidney disease? Kidney Int (2007) 72:534–536.[CrossRef][Web of Science][Medline]
  6. Bauer C, Melamed ML, Hostetter TH. Staging of Chronic Kidney Disease: Time for a Course Correction. J Am Soc Nephrol (2008) 19:844–846.[Abstract/Free Full Text]
  7. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis (2002) 39:S1–S266.[CrossRef][Web of Science][Medline]
  8. Levey AS, et al. Definition and classification of chronic kidney disease: a position statement from kidney disease: improving global outcomes (KDIGO). Kidney Int (2005) 67:2089–2100.[CrossRef][Web of Science][Medline]
  9. Tseng CL, et al. Survival benefit of nephrologic care in patients with diabetes mellitus and chronic kidney disease. Arch Intern Med (2008) 168:55–62.[Abstract/Free Full Text]
  10. Hsu CY, et al. The risk of acute renal failure in patients with chronic kidney disease. Kidney Int (2008) [Epub ahead of print].
  11. Stevens L, Coresh J, Levey A. CKD in the elderly—a new challenge. World kidney day 2008 [editorial]. Am J Kidney Dis (2008) 51:353–357.[CrossRef][Web of Science][Medline]

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This Article
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