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Alternate Marker (Cystatin C) Picks Out High-Risk CKD Patients - published text below, pdf attached
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"Detection of CKD is likely an important step for preventing complications associated with this disease.....We found that only subjects with confirmed de- creased GFR by cystatin C had elevated risk of death, cardiovascular disease, and heart failure, and they had an extremely elevated risk of kidney failure. ......Among those with an eGFRcreat >/=60 ml/min per 1.73 m2, only 4% of CHS participants had eGFRcys <60 ml/min per 1.73 m2 (n = 227), and 2% in MESA (n = 107). The prevalence varied by age, with increasing proportions in the elderly (see Figure 2A below).....Participants classified as decreased GFR by cystatin C but not by creatinine were also at increased risk for adverse events, although the number needed to screen to detect these individuals was an order of magnitude higher than the number needed to confirm decreased GFR....Now that cystatin C is Food and Drug Administration approved and more readily available across United States laboratories, this strategy could greatly improve the specificity of CKD screening programs and limit the resulting burden of nephrology referrals, disease-labeling, and additional diagnostic tests and treatments."
We were surprised to find that the prevalence of decreased GFR on the basis of cystatin C only was relatively low in this diverse cohort of ambulatory subjects, particularly in the nonelderly. However, this group was at very high risk for adverse events. The number needed to screen to detect such individuals was high overall but decreased to about 10 among persons over the age of 75. Even although the screening yield for detecting decreased GFR <60 ml/min per 1.73 m2 may be relatively low, cystatin C has also been shown to detect preclinical kidney disease, which is associated with higher risk of mortality, cardiovascular disease, heart failure, and kidney disease progression.16 As demonstrated by our risk stratification tree, the likelihood of high risk CKD in adults can be stratified from 1 to 67% on the basis of the creatinine-based GFR, age, sex, and race. These proportions can be used to estimate the yield for cystatin C testing as either a confirmatory test or as a screening test in high risk groups. Since the presence of albuminuria can also detect persons at high risk for adverse events who have an eGFRcreat >60 ml/min per 1.73 m2,22 future studies should focus on evaluating the cost effectiveness of a triple screen of renal markers strategy to include creati- nine, albuminuria, and cystatin C measurements."
MedPage Today
Published: December 17, 2010
Action Points
* Explain that a blood test for the kidney function marker cystatin C may identify patients at highest risk for complications from chronic kidney disease.
* Note that further studies are needed to better define the role of cystatin C, but in addition to identifying patients at high risk for complications, it also may be useful as a confirmatory test for diagnosing chronic kidney disease.
A blood test for the kidney function marker cystatin C may identify patients at highest risk for complications from chronic kidney disease, researchers found.
CKD diagnosed only on the basis of cystatin C predicted higher mortality than CKD diagnosed on the basis of creatinine only or on the basis of both markers, Carmen A. Peralta, MD, of the San Francisco VA Medical Center and University of California San Francisco, and colleagues found.
The same was true for risk of cardiovascular disease, heart failure, and kidney failure, they reported online in the Journal of the American Society of Nephrology.
These results "suggest a possible targeted approach whereby cystatin C confirmation can be used in a step-wise manner to identify individuals at higher risk for CKD complications among those with eGFR [estimated glomerular filtration rate] creatinine under 60 ml/min per 1.73 m2 with or without albuminuria," they wrote.
Such an approach "could greatly improve the specificity of CKD screening programs and limit the resulting burden of nephrology referrals, disease-labeling, and additional diagnostic tests and treatments," they added.
Cystatin C is FDA-approved as a test but its clinical role has been unclear, Peralta's group noted.
The researchers thus analyzed its comparative performance in two cohort studies
-- the Multi-Ethnic Study of Atherosclerosis (MESA) and the Cardiovascular Health Study (CHS). CHS consisted of an older group of patients, with an average age of 72 to MESA's 62.
The 11,909 participants across the two trials were categorized into mutually exclusive groups on the basis of the biomarkers that supported a diagnosis of CKD defined by an eGFR of less than 60 ml/min per 1.73 m2 -- by creatinine only (9% in MESA, 21% in CHS), by cystatin C only (2% and 4%), by both (4% and 13%), or by neither.
The relatively low prevalence of decreased GFR by cystatin C came as a surprise, Peralta's group said in the paper.
"However, this group was at very high risk for adverse events," they pointed out. "The number needed to screen to detect such individuals was high overall but decreased to about 10 among persons over the age of 75."
CKD was only associated with significantly elevated risk of death, cardiovascular events, and heart failure if it was confirmed by cystatin C alone or with creatinine, whereas decreased GFR detected by creatinine alone was associated with risks of these events equivalent to those without decreased GFR.
CHS also looked at kidney failure risk, which was highest for those with reduced GFR detected by both biomarkers, at 24-fold that of patients without decreased GFR. Cystatin C-only detected cases showed six-fold elevated kidney failure risk followed by creatinine-only detected cases at two-fold elevated risk.
Cystatin C also held the advantage for risk reclassification, particularly for reclassifying individuals to lower risk.
Among CHS patients initially defined as having CKD by creatinine measures, reclassification into higher risk by cystatin C was associated with an annualized death rate of 4% compared with the 1.8% rate for those reclassified into a low risk category. In MESA, the rates were 2.5% and 1%, respectively.
Cystatin C picked up CKD missed by creatinine in 12% of white and 6% of non-white patients over age 75.
"The creatinine-based eGFR equations may be sensitive for detecting persons with risk for adverse outcomes related to kidney disease; however, in these cohorts of multi-ethnic and older adults, specificity was greatly improved with cystatin C," the researchers concluded in the paper. "This suggests a potential role for cystatin C as a confirmation test for diagnosing CKD."
They cautioned that their study was limited by lack of information on cause of kidney failure in MESA, lack of albuminuria measures at baseline, and more importantly by lack of measured GFR.
Also, cystatin C has been shown to be associated with factors other than kidney function, they noted.
The study was supported by the National Institute of Diabetes and Digestive and Kidney Diseases, and contracts from the National Heart, Lung, and Blood Institute for MESA. For CHS, the research reported was supported by contracts and a grant from the National Heart, Lung, and Blood Institute, with additional contributions from the National Institute of Neurologic Disorders and Stroke.
The researchers reported having no conflicts of interest to disclose.
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Cystatin C Identifies Chronic Kidney Disease Patients at Higher Risk for Complications
J Am Soc Nephrol 22: 147-155, 2011 (Dec 2010 ahead of print)
Carmen A. Peralta,* Ronit Katz, Mark J. Sarnak, Joachim Ix, Linda F. Fried, Ian De Boer,** Walter Palmas, David Siscovick, Andrew S. Levey, and Michael G. Shlipak*
*San Francisco Veterans Affairs Medical Center, San Francisco, California; Department of Medicine, University of California San Francisco, San Francisco, California; Departments of Epidemiology and Laboratory Medicine, University of Washington, Seattle, Washington; Department of Medicine, Tufts-New England Medical Center, Boston, Massachusetts; Department of Medicine, University of California San Diego, San Diego, California; Pittsburgh Veterans Affairs Medical Center, Pittsburgh, Pennsylvania; **Department of Medicine, University of Washington, Seattle, Washington; Department of Medicine, Columbia University, New York, New York; Departments of Medicine and Epidemiology, University of Washington, Seattle, Seattle, Washington; and Department of Epidemiology and Biostatistics, University of California, San Francisco, California
ABSTRACT
Although cystatin C is a stronger predictor of clinical outcomes associated with CKD than creatinine, the clinical role for cystatin C is unclear. We included 11,909 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) and the Cardiovascular Health Study (CHS) and assessed risks for death, cardiovascular events, heart failure, and ESRD among persons categorized into mutually exclusive groups on the basis of the biomarkers that supported a diagnosis of CKD (eGFR 60 ml/min per 1.73 m2): creatinine only, cystatin C only, both, or neither. We used CKD-EPI equations to estimate GFR from these biomarkers. In MESA, 9% had CKD by the creatinine-based equation only, 2% had CKD by the cystatin C-based equation only, and 4% had CKD by both equations; in CHS, these percentages were 12, 4, and 13%, respectively. Compared with those without CKD, the adjusted hazard ratios (HR) for mortality in MESA were: 0.80 (95% CI 0.50 to 1.26) for CKD by creatinine only; 3.23 (95% CI 1.84 to 5.67) for CKD by cystatin C only; and 1.93 (95% CI 1.27 to 2.92) for CKD by both; in CHS, the adjusted HR were 1.09 (95% CI 0.98 to 1.21), 1.78 (95% CI 1.53 to 2.08), and 1.74 (95% CI 1.58 to 1.93), respectively. The pattern was similar for cardiovascular disease (CVD), heart failure, and kidney failure outcomes. In conclusion, among adults diagnosed with CKD using the creatinine-based CKD-EPI equation, the adverse prognosis is limited to the subset who also have CKD according to the cystatin C-based equation. Cystatin C may have a role in identifying persons with CKD who have the highest risk for complications.
Chronic kidney disease (CKD) affects millions of adults in the United States, and its prevalence is rising, particularly in the elderly.1 Decreased GFR (GFR < 60 ml/min per 1.73 m2) has been associated with increased mortality, cardiovascular adverse events, hospitalizations, fractures, and unsuccessful aging.2-5 International guidelines recommend using creatinine-based equations to estimate GFR, particularly the Modification of Diet in Renal Disease equation.6,7 Recently, a new creatinine-based equation was developed by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) that reported better accuracy than the Modifi- cation of Diet in Renal7 Disease study equation, especially at estimated GFR levels above 60 ml/min per 1.73 m2.8 How- ever, all creatinine-based estimating equations have limita- tions due to non-GFR determinants of serum creatinine, largely muscle mass, which cannot be accounted for entirely by age, sex, and race. This is a particular problem among the elderly, among non-white populations, and in the range of mildly reduced GFR, where equations have bias. Therefore, the clini- cian's reliance on creatinine-based equations for estimating GFR and the risk associated with low GFR could cause misclassification of patients who may be at high risk of CKD and its complications.
Recently, cystatin C has emerged as an alternative marker of kidney function that is less influenced by muscle mass.9 -12 However, the clinical role for cystatin C measure- ment has not been elucidated. Cystatin C can be used to estimate GFR, and it has been associated with subsequent adverse clinical events. In prior studies in the general pop- ulation and in the elderly, cystatin C has been shown to be a better predictor of mortality and adverse cardiovascular events than serum creatinine.13-15 In epidemiologic studies, an elevated cystatin C level (>1 mg/L) in persons with eGFRcreat >60 ml/min per 1.73 m2 has been used to classify persons as having preclinical kidney disease, which por- tends an increased risk of cardiovascular disease, incident CKD, and death.16 Several equations to estimate GFR on the basis of cystatin C have now been developed, including a CKD-EPI cystatin C equation.17 The utility of estimating reduced GFR by cystatin C versus creatinine-based estimates for predicting clinical outcomes has not been well studied.
We designed this study to compare CKD classification by the estimated GFR values of creatinine (eGFRcreat) and cysta- tin C (eGFRcys) in ambulatory adults. Specifically, we: (1) determined the proportions with eGFR <60 ml/min per 1.73 m2 on the basis of creatinine, cystatin C, both, and neither; (2) compared the risks for mortality, cardiovascular events, heart failure, and kidney failure among the four groups; (3) evaluated the ability of eGFRcys to detect additional cases of decreased GFR among persons with eGFRcreat >/=60; and (4) evaluated the capacity of eGFRcys to distinguish a group at higher risk for CKD compli- cations among those with GFRcreat <60 ml/min per 1.73 m2.
DISCUSSION
CKD is increasingly recognized as a risk factor for adverse events, including death, cardiovascular disease, and kidney failure.2,18,19 Thus, efforts to increase detection and recognition of decreased GFR have been the focus of national and international campaigns. In these analyses, we found that the presence of eGFR <60 ml/ min per 1.73 m2 was only associated with elevated risk of death, cardiovascular events, and heart failure if it was confirmed by cystatin C. Persons with decreased GFR by creatinine alone had equivalent risks to persons without decreased GFR. Thus, cystatin C may have an important clinical role in distinguishing between "higher risk" and "lower risk" individuals for CKD complications with creatinine-based eGFR <60 ml/min per 1.73 m2 on the basis of this differential risk for cardiovascular and mortality outcomes.
National and international efforts have advocated improved detection of CKD by using creatinine-based equations to estimate GFR.7 Early detection requires screening tests that balance sensitivity and specificity. The creatinine-based eGFR equations may be sensitive for detecting persons with risk for adverse outcomes related to kidney disease; however, in these cohorts of multi-ethnic and older adults, specificity was greatly improved with cystatin C. This suggests a potential role for cystatin C as a confirmation test for diagnosing CKD.
Automatic reporting of eGFR by creatinine-based equations has now been widely adopted by many medical centers in the United States and abroad, which may lead to improved CKD detection. However, some have suggested that automatic reporting of eGFR labels certain persons as having kidney disease who may be at low risk for complications. Recently, auto- matic reporting of eGFR was shown to be as- sociated with an increase in referrals to nephrologists,20,21 which in some studies has been associated with improved survival but may also result in unnecessary testing, treatments, and cost. If confirmed by future studies, cystatin C may be a useful test to determine which patients warrant prioritization for ne- phrology referral or additional testing.
We were surprised to find that the prevalence of decreased GFR on the basis of cystatin C only was relatively low in this diverse cohort of ambulatory subjects, particularly in the nonelderly. However, this group was at very high risk for adverse events. The number needed to screen to detect such individuals was high overall but decreased to about 10 among persons over the age of 75. Even although the screening yield for detecting decreased GFR <60 ml/min per 1.73 m2 may be relatively low, cystatin C has also been shown to detect preclinical kidney disease, which is associated with higher risk of mortality, cardiovascular disease, heart failure, and kidney disease progression.16 As demonstrated by our risk stratification tree, the likelihood of high risk CKD in adults can be stratified from 1 to 67% on the basis of the creatinine-based GFR, age, sex, and race. These proportions can be used to estimate the yield for cystatin C testing as either a confirmatory test or as a screening test in high risk groups. Since the presence of albuminuria can also detect persons at high risk for adverse events who have an eGFRcreat >60 ml/min per 1.73 m2,22 future studies should focus on evaluating the cost effectiveness of a triple screen of renal markers strategy to include creati- nine, albuminuria, and cystatin C measurements.
The strength of our study is that it is the first to demonstrate a potentially important role for cystatin C in the clinical setting of CKD detection and confirmation. Our sample size is large, ethni- cally diverse, and fairly representative of the U.S. population. Moreover, CHS and MESA are very well characterized cohorts with standardized measures of kidney function and rigorously adjudicated outcomes. However, our study lacks information on kidney failure in MESA, thus limiting some of our findings to the elderly. Moreover, cystatin C has been shown to be associated with factors other than kidney function.23 However, our results are robust after adjustment for most of these factors, suggesting that cystatin C's associations with adverse events are predomi- nantly due to its approximation of kidney filtration. Most importantly, like all population-based epidemiologic studies, our study is limited by the lack of measured GFR. Thus, we cannot deter- mine which participants actually have a decreased GFR, as mea- sured by the clearance of an exogenous filtration marker. Al- though we are limited by the lack of albuminuria measures at baseline, our secondary analyses in CHS suggest that cystatin C has utility for risk stratification, even when combined with albu- minuria among elderly participants with decreased eGFR by creatinine.
Detection of CKD is likely an important step for preventing complications associated with this disease. We believe that our findings suggest a possible targeted approach whereby cystatin C confirmation can be used in a step-wise manner to identify individuals at higher risk for CKD complications among those with eGFR creatinine <60 ml/min per 1.73 m2 with or without albuminuria. We found that only subjects with confirmed decreased GFR by cystatin C had elevated risk of death, cardiovascular disease, and heart failure, and they had an extremely elevated risk of kidney failure. In addition, only a limited number of cystatin C tests would need to be used, with high-yield results, to confirm the diagnosis in ambulatory adults. Participants classified as decreased GFR by cystatin C but not by creatinine were also at increased risk for adverse events, although the number needed to screen to detect these individuals was an order of magnitude higher than the number needed to confirm decreased GFR. Now that cystatin C is Food and Drug Administration approved and more readily available across United States laboratories, this strategy could greatly improve the specificity of CKD screening programs and limit the resulting burden of nephrology referrals, disease-labeling, and additional diagnostic tests and treatments.
RESULTS
Study Cohort Characteristics
Overall, there were 6749 Multi-Ethnic Study of Atherosclerosis (MESA) participants, with a mean age 62 +/- 10 years. MESA had four major racial/ethnic groups: 39% white, 28% black, 12% Chinese, and 22% Hispanic. There was no prevalent car- diovascular disease at baseline in MESA. There were 5160 Car- diovascular Health Study (CHS) participants, with a mean age of 72 +/- 5 years. CHS participants were predominantly white (84%) and 16% black. Prevalent cardiovascular disease was present in 24% of the CHS participants. We classified the co- horts into four mutually exclusive groups using cystatin C and creatinine as described above. (Table 1). In MESA and CHS, those with decreased GFR both were older and had higher prev- alence of diabetes and hypertension. In MESA and CHS, the group with decreased GFR both had the lowest eGFRcreat (Table 1).
Death, Cardiovascular Events, and Kidney Failure by eGFR Group
Overall, there were 223 deaths and 212 CVD events in MESA after an average follow-up of 4.7 years; 3345 deaths, 2249 CVD events, 1407 incident heart failure events, and 84 confirmed ESRD cases occurred during an average of 12.2 years of CHS follow-up.
Participants with decreased GFRcys only or decreased GFR both had the highest rates of death and kidney failure, whereas those with decreased GFRcreat only had rates of death and kidney failure comparable to those with GFR not decreased. (Figure 1). In MESA, participants with decreased GFRcys only and decreased GFR both also had the highest mortality rates (3.2 and 2.7% per year, respectively), whereas participants with decreased GFRcreat only had rates of death similar to those with GFR not decreased (0.8 and 0.6%, respectively) (Figure 1).
In multivariable models for MESA, the risk of death was elevated for those participants with decreased GFRcys only and decreased GFR both compared with participants with GFR not decreased. MESA participants with decreased GFRcreat only had risks of death similar to those with GFR not decreased. The risk of CVD was highest for those with decreased GFRcys only and decreased GFR both compared with those with GFR not decreased in demographic adjusted models in MESA. This effect was attenuated after full adjust- ment for those with decreased GFRcys only but remained significant for those with decreased GFR both (Table 2).
In CHS, participants identified as having decreased GFRcys only or decreased GFR both had similarly elevated risk of death, cardiovascular events, and heart failure compared with those with GFR not decreased (Table 2). In contrast, those with de- creased GFRcreat only had risks similar to those with GFR not decreased for death, CVD, and heart failure. The risk of kidney failure was the highest for those with decreased GFR both (24- fold higher), followed by decreased GFRcys only (six-fold higher) and decreased GFRcr only (two-fold) compared with those with GFR not decreased (referent) (Table 2).
Prevalence of eGFRcys <60 ml/min per 1.73 m2 among Those with eGFR Creatinine > and <60 ml/min per 1.73 m2
Due to the striking differences in prognosis observed among these groups, we estimated the proportion of participants classified differently by eGFRcys and eGFRcreat. Among those with an eGFRcreat >/=60 ml/min per 1.73 m2, only 4% of CHS participants had eGFRcys <60 ml/min per 1.73 m2 (n = 227), and 2% in MESA (n = 107). The prevalence varied by age, with increasing proportions in the elderly (Figure 2A).
Among those with eGFRcreat <60 ml/min per 1.73 m2, the proportion confirmed by eGFRcys <60 ml/min per 1.73 m2 also increased by age (Figure 2B). Among persons under age 75, less than 40% were confirmed, whereas over half of cases of eGFRcreat <60 ml/min per 1.73 m2 were confirmed by eGFRcys in the oldest age group.
Figure 2. (A) The prevalence of eGFRc>/=60 ml/min per 1.73 m2 and the proportion missed by creatinine but detected by cystatin C varies by age. (B) The overall prevalence of eGF<60 ml/min per 1.73 m2 by creatinine and proportion confirmed by cystatin C varies by age.
Number Needed to Screen and Number Needed to Confirm
Among those with eGFRcreat >/=60 ml/min per 1.73 m2, we found that the number needed to screen to detect a single case of eGFRcys <60 ml/min per 1.73 m2 varied over 10-fold by age. Among those aged 45 to 54 years, 135 tests (95% CI 89, 283) would be needed, 60 tests (95% CI 44, 94) among those 55 to 64, 25 tests (95% CI 22,29) among those 65 to 74, and 10 tests (95% CI 9, 11) among those >/=75 years.
Among those with eGFRcreat <60 ml/min per 1.73 m2, the number needed to confirm by cystatin C was very low and decreased by age: 2.6 tests (1.8, 4.6) for those aged 45 to 54 years, 4.6 tests (95% CI 3.5, 6.8) for ages 55 to 64, 2.5 tests (95% CI 2.4, 2.8) for ages 65 to 74, and 1.5 tests (95% CI 1.4, 1.6) tests for those aged >/=75 years.
Net Reclassification Improvement
Overall, we found that the addition of eGFRcys was useful in reclassifying mortality risk among persons initially defined by eGFRcreat alone. In CHS, the annualized risk of death for persons classified by eGFRcreat as having 10 to 20% risk in 10 years was 2.7%/year. Persons who were reclassified into the lower risk category had an annual risk of 1.8%, whereas persons classified into the higher risk had an annualized rate of death of 4%. In MESA, the annual rate of death for those classified as having a 5 to 10% risk of death in 5 years was 1.3% in the CKD-EPI model. When using cystatin C, per- sons reclassified to the higher risk category had an annual- ized death rate of 2.5%, and those reclassified to the lower risk category had an annualized death rate of 1%.
In general, cystatin C was most useful in reclassifying persons to lower risk categories, particularly among CHS participants (elderly). In CHS, among persons whose risk of death was determined to be <10% by eGFRcreat, only 22 persons were reclassified as higher risk (net reclassification improvement [NRI] 1%, P value 0.46). Among persons at 10 to 20% risk of death, 213 persons were reclassified as being at higher risk for death, and 160 were reclassified as being at lower risk (NRI 15%, P value <0.001), whereas among persons classi- fied as having a >20% risk of death by eGFRcreat, 329 persons were reclassified as having a lower risk (NRI 14%, P value <0.001). In MESA, among persons whose risk of death was determined to be <5% by eGFRcreat, 220 persons were reclassified as having higher risk (NRI 6%, P value 0.04). Among persons at 5 to 10% risk of death, 132 persons were reclassified as being at higher risk for death, and 262 were reclassified as being at lower risk (NRI 17%, P value 0.01), whereas among persons classified as having a >10% risk of death by eGFRcreat, 105 persons were reclassified as having a lower risk (NRI 8%, P value 0.07).
Predictors of High Risk CKD (eGFRcys <60 ml/min per 1.73 m2)
Due to the findings that the decreased GFRcreat only group had similar rates of death, CVD and heart failure to those with GFR not decreased, we defined "high risk CKD" as eGFRcys <60 ml/min per 1.73 m2. Of the variables evaluated by classification and regression tree analysis (CART), we found that an eGFRcreat <60 ml/min per 1.73 m2 and age were the best discriminators of likelihood of high risk CKD (Figure 3). Im- portantly, among younger participants with eGFRcreat <60 ml/min per 1.73 m2, only 21 to 46% had high risk CKD. Among persons aged >75 years with eGFRcreat >60 ml/min per 1.73 m2, 12% of white patients and 6% of non-white patients had high risk CKD that was missed by creatinine (Figure 3).
Albuminuria and Cystatin C among CHS Participants with eGFRcreat <60 ml/min per 1.73 m2
At year 7 of follow-up, the mean age for CHS participants was 78 +/- 5 years, and 789 participants had eGFRcreat <60 ml/min per 1.73 m2. Of those, 239 (30%) had an albumin to creatinine ratio >30 mg/g, whereas 580 (73%) had decreased eGFRcys, and 170 (22%) had neither albuminuria nor decreased eGFRcys. Only 5% (n = 39) of these participants with eGFRcreat <60 ml/min per 1.73 m2 had microalbuminuria without eGFRcys <60 ml/ min per 1.73 m2. Both albuminuria and eGFRcys <60 ml/min per 1.73 m2 were associated with higher mortality rates, and participants with both had the highest risk. After multivariable adjust- ment, both albuminuria and GFRcys <60 ml/min per 1.73 m2 were independently associated with mortality risk, and the presence of both retained the highest risk of death compared with those with eGFRcys >/=60 ml/min per 1.73 m2 and no albuminuria (Table 3).
Sensitivity Analyses
We repeated all of the analyses using the cystatin C-based equation with demographic coefficients to estimate GFR, and we found very similar results. The primary difference was that the prevalence of eGFRcysc <60 ml/min per 1.73 m2 increased from 11 to 17% (n = 1965) in the combined MESA and CHS participants. Although the prevalence of the decreased GFRcys only group increased, the risk es- timates remained similar to the results provided.
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