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Douglas S. Keith, MD; Gregory A. Nichols, MBA, PhD; Christina M. Gullion, PhD; Jonathan Betz Brown, MPP, PhD; David H. Smith, RPh, PhD

Arch Intern Med. 2004;164:659-663.

ABSTRACT
Background  Chronic kidney disease is the primary cause of end-stage renal disease in the United States. The purpose of this study was to understand the natural history of chronic kidney disease with regard to progression to renal replacement therapy (transplant or dialysis) and death in a representative patient population.

Methods  In 1996 we identified 27 998 patients in our health plan who had estimated glomerular filtration rates of less than 90 mL/min per 1.73 m² on 2 separate measurements at least 90 days apart. We followed up patients from the index date of the first glomerular filtration rates of less than 90 mL/min per 1.73 m² until renal replacement therapy, death, disenrollment from the health plan, or June 30, 2001. We extracted from the computerized medical records the prevalence of the following comorbidities at the index date and end point: hypertension, diabetes mellitus, coronary artery disease, congestive heart failure, hyperlipidemia, and renal anemia.

Results  Our data showed that the rate of renal replacement therapy over the 5-year observation period was 1.1%, 1.3%, and 19.9%, respectively, for the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) stages 2, 3, and 4, but that the mortality rate was 19.5%, 24.3%, and 45.7%. Thus, death was far more common than dialysis at all stages. In addition, congestive heart failure, coronary artery disease, diabetes, and anemia were more prevalent in the patients who died but hypertension prevalence was similar across all stages.

Conclusion  Our data suggest that efforts to reduce mortality in this population should be focused on treatment and prevention of coronary artery disease, congestive heart failure, diabetes mellitus, and anemia.

INTRODUCTION

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Based on calculations from the Third National Health and Nutrition Examination Survey (NHANES III),¹ it is estimated that 20 million adults in the United States have chronic kidney disease (CKD). In contrast, the estimated prevalence of end-stage renal disease (ESRD) in the US population is 344 000.² This suggests that less than 2% of the CKD population progresses to renal replacement therapy (RRT).

Relatively little is known about the 98% of patients with CKD who do not advance to ESRD. Recently, the National Kidney Foundation (NKF) published its Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines that provide an evidence-based definition of CKD and a framework for staging the severity of CKD.¹ The objectives of the present work were to study the natural history of CKD in a large health maintenance organization (HMO) population in the context of that framework, examining the prevalence of comorbid conditions associated with CKD and describing clinical outcomes (death, transplantation, and renal dialysis) over a 5-year observation period.

METHODS

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RESEARCH SETTING AND STUDY POPULATION

Participants were adult (>17 years old) members of Kaiser Permanente Northwest Division (KPNW), a large not-for-profit, group-model HMO that provides comprehensive, prepaid medical coverage to approximately 20% of the metropolitan population of Portland, Ore. Subscriber demographics are representative of the area population in ethnic makeup, with non-Hispanic whites representing about 78% of the population. The remainder of the population includes African Americans, Asians/Pacific Islanders, Native Americans, and persons of Hispanic descent. More than 18% of members are Medicare-eligible (>64 years old), and 8% are Medicaid members.

Kaiser Permanente Northwest Division maintains electronic administrative and clinical databases containing information on inpatient admissions, ambulatory contacts, pharmacy dispensations, laboratory tests, and outside claims and referrals. These databases are linked through unique health record numbers that are given to each member at the time of first enrollment in the health plan.

Laboratory tests are performed by a single regional laboratory using standardized methods that are periodically recalibrated against reference samples. We estimated glomerular filtration rates (GFRs) from serum creatinine values captured in KPNW's laboratory information system using the abbreviated Modification of Diet in Renal Disease Study (MDRD) formula³ as follows: estimated GFR (in milliliters per minute per 1.73 m²) = 186.3 x [serum creatinine]^-1.154 x age^-0.203 x [0.742 if a woman] x [1.21 if black].

Because data on race were not available, they were not included in the estimation of GFR. This missing variable had the effect of underestimating GFR by 21% for African Americans. However, less than 5% of our population is African American, so the overall population-level effect of this missing variable was minimal.

We identified all 42 293 HMO members who, in 1996, had an estimated GFR greater than 15 mL/min per 1.73 m² and less than 90 mL/min per 1.73 m² (index GFR), followed by a second GFR below 90 mL/min per 1.73 m² at the first creatinine measurement taken at least 90 days after the index GFR. We then staged the severity of their CKD based on the NKF K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification.¹ The index GFR of patients with stage 4 disease (n = 777) was estimated to be 15 to 29 mL/min per 1.73 m² and the index GFR of patients with stage 3 disease (n = 11 278) was estimated to be 30 to 59 mL/min per 1.73 m². The NKF K/DOQI guidelines require that patients with stage 2 disease (GFR of 60-89 mL/min per 1.73 m²) also be checked for proteinuria. Although the current staging guidelines consider other renal markers, such as renal cysts, on radiologic examination in patients with polycystic kidney disease, we did not include them because these data were not readily obtainable and make up a small minority of renal markers. We defined proteinuria as urine protein of 1 + or greater by dipstick analysis, with leukocyte esterase less than 10/µL, measured within 6 months of the index GFR. About half (14 295) of the patients with a GFR of 60 to 89 mL/min per 1.73 m² did not have a qualifying urinalysis and were excluded from further analysis. Of the remaining 15 943 subjects, it was determined that 1741 had stage 2 disease. For comparison, we also included the 14 202 individuals with an index GFR of 60 to 89 mL/min per 1.73 m² in whom proteinuria was found to be absent. Our final case population totaled 27 998. A comparison group was selected by using a 1:1 age (year of birth) and sex match from enrollees who did not meet the criteria for inclusion as a study patient and were eligible for at least 90 days from the index GFR of their matched case.

FOLLOW-UP AND END POINTS

Subjects were observed for up to 66 months from the date of their index GFR through June 30, 2001, or until death, disenrollment from the health plan, or advancement to RRT defined as initiation of dialysis or renal transplantation. Death and disenrollment were identified from HMO membership records. Transplant and dialysis were captured in the medical record.

DEMOGRAPHICS AND COMORBIDITIES

Sex and age at index date were extracted from HMO membership electronic records using the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) diagnosis and procedure codes. We identified diagnoses for coronary artery disease, congestive heart failure, diabetes mellitus, hypertension, and hyperlipidemia. We defined anemia as hemoglobin levels less than 12 g/dL with normal mean corpuscular volume. Comorbidities were considered present at baseline if they were charted at any time before or up to 3 months following the index date. Anemia was considered present at baseline if it was identified within 30 days of the index date. We further identified the comorbidities that were charted at any time prior to end of observation, and anemia that was measured at any time prior to end of observation.

RESULTS

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The relevant baseline characteristics of the study subjects by GFR and disease stage are shown in Table 1. Age at index increased with stage while the percentage of male subjects declined with stage. Months of observation, in total and by year, were approximately similar for all stages except stage 4, for which observation time was substantially shorter.

View this table: [in this window] [in a new window] Table 1. Relevant Patient Characteristics, Disease Stages, and Glomerular Filtration Rates (GFRs) at Baseline*

Nearly half of subjects in stage 4 (mean ± 95% confidence bound, 45.7% ± 3.5%) died during observation (Table 2), a substantially higher proportion than in any other group. The mean ± 95% confidence bound proportion of subjects who died in stages 2 and 3 was 19.5% ± 1.9% and 24.3% ± 0.8%, respectively, while only 10.2% ± 0.5% of those in the comparison group (GFR, 60-89 mL/min per 1.73 m² without proteinuria) died, regardless of hypertension status (not shown). The likelihood of renal replacement therapy, either transplant or dialysis, was near zero (1.3%) for patients in all stages except stage 4, where 2.3% ± 1.1% of patients received a transplant and 17.6% ± 2.7% had dialysis initiated. Disenrollment from the health plan decreased with increasing stage, but was low in all stages over the 5 years.

View this table: [in this window] [in a new window] Table 2. Study End points*

Table 3 shows the prevalence of comorbidities at index date and the change in prevalence that occurred during follow-up for patients who survived, died, and disenrolled from the health plan. For all comorbidities, the prevalence was higher at the end point of the study than at baseline for all stages of disease. Among patients who died in each stage, the prevalence of coronary artery disease, congestive heart failure, diabetes mellitus, and anemia was higher both at baseline and end point than among patients who survived or disenrolled. The increase in prevalence for these 4 comorbidities was also highest in those who died.

View this table: [in this window] [in a new window] Table 3. Baseline Comorbidities and Change in Prevalence From Baseline to Follow-up in Patients With Chronic Kidney Disease

The prevalence of hyperlipidemia was lower at baseline in those who died than in survivors for all stages except stage 4, where the prevalence was similar to that of patients who survived or disenrolled from the health plan. Across all stages, hyperlipidemia increased 2- to 3-fold in survivors compared with those who died. We further found that 26.6% of survivors, 13.7% of those who died, 15.5% of those who disenrolled, 39.3% of dialysis patients, and 50.0% of patients with a transplant had received at least 1 prescription for a statin (data not shown). The prevalence of hypertension at baseline was similar for all 3 end points across all stages. However, the prevalence of hypertension at end point increased considerably more in survivors than in patients who died or disenrolled.

Table 4 shows the comorbidities and change in prevalence from baseline to follow-up for patients with CKD and their controls. At baseline, 44.4% of patients with CKD and 73.7% of controls had no comorbidities. Patients with CKD were more likely to have disease in every category. They were also more likely to have accrued additional disease burden in every category, especially anemia (24.5% for patients with CKD vs 0.1% for controls) and congestive heart failure (10.4% for patients with CKD vs 5.2% for controls).

View this table: [in this window] [in a new window] Table 4. Baseline Comorbidities and Change in Prevalence From Baseline to Follow-up in Patients With Chronic Kidney Disease (CKD) and Controls Matched for Age and Sex*

COMMENT

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Most of the approximately 350 000 persons who have ESRD in the United States emerge from the estimated 20 million patients with CKD.¹ The results reported in this study indicate that the population with ESRD is actually a highly specific group of patients who have progressive renal failure and survive to require dialysis; and that, even among those with advanced stage 4 disease, death prior to RRT is more than twice as likely as progression to ESRD.

Although we cannot isolate cause of death in our data, it is likely that cardiac disease is predominantly responsible. Cardiovascular disease is the most common cause of death among dialysis and transplant patients.⁴ We found higher baseline prevalence of coronary artery disease, congestive heart failure, diabetes mellitus, and anemia in patients who died than in patients who survived or disenrolled. Furthermore, the increase in prevalence of these 4 comorbidities over the 5-year observation period was greatest in patients who died despite a shorter period of observation. There was also a higher prevalence of these cardiac conditions among study patients at both baseline and end of observation than among controls.

The high rates of heart disease and anemia in the patients who died are consistent with the hypothesis that anemia accelerates the progression of heart disease and increases the risk of death. However, anemia may be a marker for severity of CKD rather than a causative factor. Inflammation, as evidenced by a high level of C-reactive protein, is also a risk factor for cardiovascular mortality, and inflammation is an important factor of reduced erythropoiesis in this population.⁴ Additionally, if anemia is more prevalent in patients with congestive heart failure, coronary artery disease, and diabetes mellitus, the apparent association between death and anemia may be confounded by these diseases with a high mortality. Finally, some evidence suggests that treatments for these comorbidities, such as angiotensin-converting enzyme inhibition, also decrease red cell production.⁵ While these data do not suggest that changes should be made to current treatment recommendations in CKD, further research designed to help disentangle the associations between anemia, heart disease, and inflammatory processes might yield important clues for better patient care.

Contrary to common expectation, hypertension and hyperlipidemia were less common in patients who died before advancing to ESRD or RRT than in survivors. This finding is similar to findings in patients with ESRD for whom high blood pressure was not associated with greater mortality. What is unclear from our data, however, is the extent to which low blood pressure may be a risk factor for mortality, as has been found in the dialysis population.⁶ Although each of these risk factors was identified through diagnoses extracted from medical records, we have no reason to believe that recording was less regular for one of these outcome groups. Thus, any bias resulting from our definition would likely be equally distributed between those who died and those who survived. It is possible that the greater prevalence of cardiovascular risk factors in survivors represents a higher rate of documentation of treatment. Clinicians might be more likely to record hypertension or hyperlipidemia when initiating pharmacological treatment. If this is the case, the greater prevalence of cardiovascular risk factors in survivors represents successful treatment and a subsequent decrease in mortality. In our analysis, survivors were more likely to have initiated statin therapy than those who died, which perhaps reflects the added cardioprotective effects of statin therapy that were recently reported.⁷ The finding that patients receiving RRT had the highest rates of statin use may be a consequence of closer management following ESRD diagnosis. Finally, the age of our population may be an important factor in the apparent lack of effect of the traditional cardiac risk factors of hypertension and hyperlipidemia. The mean age of our study population was 65 years. Previous studies have shown that in patients older than 65 years, the relative risk of mortality imparted by hypertension diminishes significantly and may cease to add measurable risk.^8-13 Similarly, hyperlipidemia in epidemiologic studies in the elderly had no effect on cardiovascular mortality, and overall mortality was higher in patients with lower cholesterol levels.¹³

Although the population with stage 2 disease was nearly 11 years younger than the stage 3 population, the outcomes for stage 3 disease were remarkably similar to those of stage 2. The requirement of proteinuria in stage 2 disease appears to identify a population that is at greater risk for death and RRT. The risk of death was double and the risk of RRT was 10 times higher in the stage 2 population with proteinuria, compared with the population of patients who also had a GFR of 60 to 89 mL/min per 1.73 m² but no proteinuria. Proteinuria has been shown in previous studies to be a risk factor for progressive renal dysfunction and increased cardiovascular mortality,^14-15 which is consistent with our findings. The proteinuria requirement also identifies a population with a greater prevalence of diabetes mellitus, which may explain some portion of the excessive morbidity and mortality that we found in stage 2.

Although we did not determine the etiology of the renal disease in our study, the data provide indirect evidence that the prevalence of the different etiologies of kidney disease in the overall CKD population may be different from those of patients who progress to ESRD. Based on United States Renal Data System data from Oregon in 1999, the primary diagnosis for patients with renal disease initiating RRT was diabetes mellitus (43%).² In the present study, in all stages of CKD at baseline, the prevalence of diabetes mellitus was well below 43%, although a significant number of CKD patients with diabetes mellitus likely have alternative diagnoses for their primary renal disease.

An important limitation of our study was that only patients who sought medical care and had a creatinine measurement in 1996 were included. Thus, we cannot claim that the patients we identified represent the entire population with prevalent CKD. Our study population may represent a biased population in whom adverse outcomes would be more likely than in patients who did not seek medical care but had renal dysfunction. However, CKD is associated with advancing age, and elderly patients are more likely to access the health care system and have laboratory testing. The average age of our population was 65 years and the proportion of the entire health plan membership that received a creatinine measurement increased steadily with age (data not shown). These factors will have minimized whatever bias was introduced in our population selection process. Another limitation is that the criterion of 2 measurements at least 90 days apart added an "early survival" bias to the population, as some patients with CKD were excluded from the study because they died prior to having a second creatinine measurement after 90 days. Though minimal, this would result in an underestimation of mortality. One of our main findings, that death is far more likely than advancement to RRT, would only be strengthened by the elimination of the early survival bias.

In conclusion, the application of the NKF K/DOQI guidelines to our data indicate that previous reports describing patients having ESRD are not representative of patients with CKD. During our 5-year observation period, only 3.1% of patients with stage 2 through stage 4 disease progressed to RRT while 24.9% died. Furthermore, the prevalence of comorbidities differed between patients who died and patients who survived. For example, our data suggest that the contribution of anemia and diabetes mellitus to mortality may be larger in CKD than other traditional cardiac risk factors. It remains unclear whether the high mortality rate in patients with CKD can be improved. Our data suggest that treatment and prevention of coronary artery disease, congestive heart failure, diabetes mellitus, and anemia may be important elements of a strategy to improve outcomes in this population.

AUTHOR INFORMATION

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Corresponding author: David H. Smith, RPh, PhD, 3800 N Interstate Ave, Portland, OR 97211 (e-mail: david.h.smith{at}kpchr.org).

Accepted for publication May 9, 2003.

This study was funded by Amgen, Thousand Oaks, Calif. The funders reviewed the study but participated neither in its conceptual design, nor in its data analysis or interpretational aspects.

We thank Wing Chan and Seonyoung Ryu for their helpful comments and Martha Swain and Debra Burch for their assistance in preparing the manuscript.

From the Division of Nephrology and Hypertension, Oregon Health and Science University (Dr Keith), the Kaiser Permanente Center for Health Research (Drs Nichols, Gullion, Brown, and Smith), and the University of Washington School of Pharmacy (Dr Smith). Dr Keith is now with McGill University. The authors have no relevant financial interest in this article.

REFERENCES

Jump to Section  • Top  • Introduction  • Methods  • Results  • Comment  • Author information  • References

1. National Kidney Foundation (NKF) Kidney Disease Outcome Quality Initiative (K/DOQI) Advisory Board. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification: Kidney Disease Outcome Quality Initiative. Am J Kidney Dis. 2002;39(2, suppl 2):S17-31. FULL TEXT | ISI | PUBMED 2. United States Renal Data System (USRDS). USRDS 2001 Annual Data Report: Atlas of End-Stage Renal Diseases in the United States. Bethesda, Md: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2001. 3. Manjunath G, Sarnak MJ, Levey AS. Prediction equations to estimate glomerular filtration rate: an update. Curr Opin Nephrol Hypertens. 2001;10:785-792. FULL TEXT | ISI | PUBMED 4. Owen WF, Lowrie EG. C-reactive protein as an outcome predictor for maintenance hemodialysis patients. Kidney Int. 1998;54:627-636. FULL TEXT | ISI | PUBMED 5. Le Meur Y, Lorgeot V, Comte L, et al. Plasma levels and metabolism of AcSDKP in patients with chronic renal failure: relationship with erythropoietin requirements. Am J Kidney Dis. 2001;38:510-517. ISI | PUBMED 6. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33:507-517. ISI | PUBMED 7. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360:7-22. FULL TEXT | ISI | PUBMED 8. Kannel WB, D'Agostino RB, Silbershatz H. Blood pressure and cardiovascular morbidity and mortality rates in the elderly. Am Heart J. 1997;134:758-763. FULL TEXT | ISI | PUBMED 9. Trenkwalder P, Hendricks P, Schoniger R, Rossberg J, Lydtin H, Hense HW. Hypertension as a risk factor for cardiovascular morbidity and mortality in an elderly German population: the prospective STEPHY II study: Starnberg Study on Epidemiology of Parkinsonism and Hypertension in the Elderly. Eur Heart J. 1999;20:1752-1756. FREE FULL TEXT 10. Boshuizen HC, Izaks GJ, van Buuren S, Ligthart GJ. Blood pressure and mortality in elderly people aged 85 and older: community based study. BMJ. 1998;316:1780-1784. FREE FULL TEXT 11. Menotti A, Mulder I, Nissinen A, et al. Cardiovascular risk factors and 10-year all-cause mortality in elderly European male populations: the FINE study: Finland, Italy, Netherlands, Elderly. Eur Heart J. 2001;22:573-579. FREE FULL TEXT 12. Hakala SM, Tilvis RS, Strandberg TE. Blood pressure and mortality in an older population: a 5-year follow-up of the Helsinki Ageing Study. Eur Heart J. 1997;18:1019-1023. FREE FULL TEXT 13. Casiglia E, Mazza A, Tikhonoff V, et al. Weak effect of hypertension and other classic risk factors in the elderly who have already paid their toll. J Hum Hypertens. 2002;16:21-31. FULL TEXT | ISI | PUBMED 14. Peterson JC, Adler S, Burkart JM, et al. Blood pressure control, proteinuria, and the progression of renal disease: the Modification of Diet in Renal Disease Study. Ann Intern Med. 1995;123:754-762. FREE FULL TEXT 15. Gerstein HC, Mann JF, Yi Q, et al. Albuminuria and risk of cardiovascular events, death, and heart failure in diabetic and nondiabetic individuals. JAMA. 2001;286:421-426. FREE FULL TEXT

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ABSTRACT | FULL TEXT  

Chronic Kidney Disease The Promise and the Perils
Couser
J. Am. Soc. Nephrol. 2007;18:2803-2805.
FULL TEXT  

Age Affects Outcomes in Chronic Kidney Disease
O'Hare et al.
J. Am. Soc. Nephrol. 2007;18:2758-2765.
ABSTRACT | FULL TEXT  

The cost of implementing UK guidelines for the management of chronic kidney disease
Klebe et al.
Nephrol Dial Transplant 2007;22:2504-2512.
ABSTRACT | FULL TEXT  

Why we should sub-divide CKD stage 3 into early (3a) and late (3b) components
Abutaleb
Nephrol Dial Transplant 2007;22:2728-2729.
FULL TEXT  

Is early chronic kidney disease an important risk factor for cardiovascular disease?: A Background Paper prepared for the UK Consensus Conference on Early Chronic Kidney Disease
Daly
Nephrol Dial Transplant 2007;22:ix19-ix25.
FULL TEXT  

Speaker Abstracts: Tuesday, 6 February 2007
Lamb et al.
Nephrol Dial Transplant 2007;22:ix45-ix53.
FULL TEXT  

Prevalence and clinical correlates of white coat hypertension in chronic kidney disease
Minutolo et al.
Nephrol Dial Transplant 2007;22:2217-2223.
ABSTRACT | FULL TEXT  

Kidney dysfunction as a risk factor for first symptomatic stroke events in a general Japanese population--the Ohasama study
Nakayama et al.
Nephrol Dial Transplant 2007;22:1910-1915.
ABSTRACT | FULL TEXT  

Mineral metabolism parameters throughout chronic kidney disease stages 1-5--achievement of K/DOQI target ranges
Craver et al.
Nephrol Dial Transplant 2007;22:1171-1176.
ABSTRACT | FULL TEXT  

A call to action on World Kidney Day, 8 March 2007
Couser et al.
Nephrol Dial Transplant 2007;22:676-677.
FULL TEXT  

Chronic Kidney Disease: Common, Harmful, and Treatable--World Kidney Day 2007
Levey et al.
CJASN 2007;2:401-405.
FULL TEXT  

Association between Multidisciplinary Care and Survival for Elderly Patients with Chronic Kidney Disease
Hemmelgarn et al.
J. Am. Soc. Nephrol. 2007;18:993-999.
ABSTRACT | FULL TEXT  

Chronic Kidney Disease: Common, Harmful, and Treatable--World Kidney Day 2007
Levey et al.
J. Am. Soc. Nephrol. 2007;18:374-378.
FULL TEXT  

Association between Serum Lipids and Survival in Hemodialysis Patients and Impact of Race
Kilpatrick et al.
J. Am. Soc. Nephrol. 2007;18:293-303.
ABSTRACT | FULL TEXT  

Lipid Changes and Statins in Chronic Renal Insufficiency
Ritz and Wanner
J. Am. Soc. Nephrol. 2006;17:S226-S230.
ABSTRACT | FULL TEXT  

Role of Pulse Pressure on Cardiovascular Risk in Chronic Kidney Disease Patients
Fernandez-Fresnedo et al.
J. Am. Soc. Nephrol. 2006;17:S246-S249.
ABSTRACT | FULL TEXT  

Anemia and Cardiovascular Risk: The Lesson of the CREATE Trial
Locatelli et al.
J. Am. Soc. Nephrol. 2006;17:S262-S266.
ABSTRACT | FULL TEXT  

Screening strategies for chronic kidney disease in the general population: follow-up of cross sectional health survey
Hallan et al.
BMJ 2006;333:1047-1047.
ABSTRACT | FULL TEXT  

Early Referral for Chronic Kidney Disease: Good for Those Who Need It, but Who Are They?
Schwartz and Textor
Mayo Clin Proc. 2006;81:1420-1422.
FULL TEXT  

Baseline Predictors of Renal Disease Progression in the African American Study of Hypertension and Kidney Disease
Norris et al.
J. Am. Soc. Nephrol. 2006;17:2928-2936.
ABSTRACT | FULL TEXT  

The impact of traditional and non-traditional risk factors on coronary calcification in pre-dialysis patients
Tomiyama et al.
Nephrol Dial Transplant 2006;21:2464-2471.
ABSTRACT | FULL TEXT  

Darbepoetin Alfa Administration to Achieve and Maintain Target Hemoglobin Levels for 1 Year in Patients With Chronic Kidney Disease
Hertel et al.
Mayo Clin Proc. 2006;81:1188-1194.
ABSTRACT | FULL TEXT  

Decline in kidney function before and after nephrology referral and the effect on survival in moderate to advanced chronic kidney disease
Jones et al.
Nephrol Dial Transplant 2006;21:2133-2143.
ABSTRACT | FULL TEXT  

Surrogate End Points for Clinical Trials of Kidney Disease Progression
Stevens et al.
CJASN 2006;1:874-884.
FULL TEXT  

Assessing kidney function--measured and estimated glomerular filtration rate.
Stevens et al.
NEJM 2006;354:2473-2483.
FULL TEXT  

Chronic kidney disease: evolving strategies for detection and management of impaired renal function
MacGregor et al.
QJM 2006;99:365-375.
ABSTRACT | FULL TEXT  

Body Mass Index and Risk for End-Stage Renal Disease
Kalantar-Zadeh and Kopple
ANN INTERN MED 2006;144:701-701.
FULL TEXT  

Current chronic kidney disease practice patterns in the UK: a national survey
Ahmad et al.
QJM 2006;99:245-251.
ABSTRACT | FULL TEXT  

Renal Manifestations in the Metabolic Syndrome.
Locatelli et al.
J. Am. Soc. Nephrol. 2006;17:S81-S85.
ABSTRACT | FULL TEXT  

Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences
Vaziri
Am. J. Physiol. Renal Physiol. 2006;290:F262-F272.
ABSTRACT | FULL TEXT  

Antiatherogenic Effects of Angiotensin Receptor Antagonism in Mild Renal Dysfunction
Suganuma et al.
J. Am. Soc. Nephrol. 2006;17:433-441.
ABSTRACT | FULL TEXT  

Pressure, Waves, and Kidney Outcomes in Kidney Transplant Donors and Recipients
Toto
Hypertension 2006;47:141-142.
FULL TEXT  

Kidney-Heart Interactions: Epidemiology, Pathogenesis, and Treatment
Berl and Henrich
CJASN 2006;1:8-18.
FULL TEXT  

Coronary Heart Disease in Patients with Chronic Kidney Disease
Dennis
J. Am. Soc. Nephrol. 2005;16:S103-S106.
FULL TEXT  

A Prospective Study of Anemia Status, Hemoglobin Concentration, and Mortality in an Elderly Cohort: The Cardiovascular Health Study
Zakai et al.
Arch Intern Med 2005;165:2214-2220.
ABSTRACT | FULL TEXT  

Low Rates of Testing and Diagnostic Codes Usage in a Commercial Clinical Laboratory: Evidence for Lack of Physician Awareness of Chronic Kidney Disease
Stevens et al.
J. Am. Soc. Nephrol. 2005;16:2439-2448.
ABSTRACT | FULL TEXT  

Myeloperoxidase serves as a marker of oxidative stress during single haemodialysis session using two different biocompatible dialysis membranes
Wu et al.
Nephrol Dial Transplant 2005;20:1134-1139.
ABSTRACT | FULL TEXT  

Effects of Anemia and Left Ventricular Hypertrophy on Cardiovascular Disease in Patients with Chronic Kidney Disease
Weiner et al.
J. Am. Soc. Nephrol. 2005;16:1803-1810.
ABSTRACT | FULL TEXT