CLINICAL EPIDEMIOLOGY www.jasn.

org

Chronic Kidney Disease Increases Risk for Venous

Thromboembolism
Keattiyoat Wattanakit,* Mary Cushman,† Catherine Stehman-Breen,‡§ Susan R. Heckbert,§
and Aaron R. Folsom*
*Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis,
Minnesota; †Department of Medicine, University of Vermont, Burlington, Vermont; ‡Amgen, Thousand Oaks,
California; and §Department of Epidemiology, School of Public Health and Community Medicine, University of
Washington, Seattle, Washington

ABSTRACT
Chronic kidney disease (CKD) is associated with increased risk for cardiovascular disease morbidity and
mortality, but its association with incident venous thromboembolism (VTE) in non– dialysis-dependent
patients has not been evaluated in a community-based population. With the use of data from the
Longitudinal Investigation of Thromboembolism Etiology (LITE) study, 19,073 middle-aged and elderly
adults were categorized on the basis of estimated GFR, and cystatin C (available in 4734 participants) was
divided into quintiles. During a mean follow-up time of 11.8 yr, 413 participants developed VTE.
Compared with participants with normal kidney function, relative risk for VTE was 1.28 (95% confidence
interval [CI] 1.02 to 1.59) for those with mildly decreased kidney function and 2.09 (95% CI 1.47 to 2.96)
for those with stage 3/4 CKD, when adjusted for age, gender, race, and center. After additional

CLINICAL EPIDEMIOLOGY
adjustment for cardiovascular disease risk factors, an increased risk for VTE was still observed in
participants with stage 3/4 CKD, with a multivariable adjusted relative risk of 1.71 (95% CI 1.18 to 2.49).
There was no significant association between cystatin C and VTE. In conclusion, middle-aged and elderly
patients with CKD (stages 3 through 4) are at increased risk for incident VTE, suggesting that VTE
prophylaxis may be particularly important in this population.

J Am Soc Nephrol 19: 135–140, 2008. doi: 10.1681/ASN.2007030308

The epidemiology of deep vein thrombosis and pul-
monary embolism (PE), collectively referred as ve-
nous thromboembolism (VTE), has been well in-
vestigated in the general population.1–3 The overall
average VTE incidence rate in adults ranges from
0.7 to 1.9 events per 1000 persons-years.1,4 Risk fac-
tors for VTE include major surgery, trauma, cancer,
obesity, diabetes, and hereditary predisposition.5
Patients with chronic kidney disease (CKD)
share some of these predisposing risk factors and
might be at increased risk for VTE. Autopsy series
have suggested that VTE events are relatively com-
mon in patients with ESRD.6,7 Furthermore, epide-
miologic studies have reported an increased risk for
VTE in dialysis8 and in renal transplant patients.9
To our knowledge, CKD has not been evaluated as a
association were found, then this would increase
understanding of VTE etiology and identify a subset
of the population at high risk for possible prophy-
laxis. Using data from the Longitudinal Investiga-
tion of Thromboembolism Etiology (LITE), we
therefore conducted a prospective study to investi-
gate the association between CKD and VTE.
Received March 14, 2007. Accepted August 10, 2007.
Published online ahead of print. Publication date available at
www.jasn.org.
Correspondence: Dr. Aaron R. Folsom, Division of Epidemiology
& Community Health, School of Public Health, University of Min-
nesota, Suite 300, 1300 S. 2nd Street, Minneapolis, MN 55454-
1015. Phone: 612-626-8862; Fax: 612-624-0315; E-mail:
folsom@epi.umn.edu

risk factor for VTE in the general population. If an Copyright © 2008 by the American Society of Nephrology

J Am Soc Nephrol 19: 135–140, 2008 ISSN : 1046-6673/1901-135 135

 CLINICAL EPIDEMIOLOGY www.jasn.org
RESULTS
Among the 19,071 participants (mean age 59 yr), the mean
estimated GFR (eGFR) was 90.4 ml/min per 1.73 m2 (SD 22.4
ml/min per 1.73 m2). There were 8312 (43.6%) participants
with normal kidney function, 9472 (49.7%) with mildly de-
creased kidney function, and 1287 (6.8%) with stage 3/4 CKD.
The mean eGFR among the participants with stage 3/4 CKD
was 51.4 ml/min per 1.73 m2 (SD 8.5 ml/min per 1.73 m2).
Compared with participants with normal kidney function (Ta-
ble 1), those with CKD were more likely to be male, older, and
white; to have diabetes and hypertension; and to have greater
mean values of body mass index (BMI) and factor VIIIc. In
contrast, participants with mildly decreased kidney function
had a similar risk factor profile to those with normal kidney
function.
During a mean follow-up time of 11.8 yr (224,275 person-
years), 413 participants developed incident VTE (41% idio-
pathic and 59% secondary VTE). Participants with incident
VTE had a greater mean baseline age, BMI, and factor VIIIc
level and higher prevalence of diabetes and hypertension than
those without incident VTE. The incidence rates of VTE per
1000 person-years were 1.5, 1.9, and 4.5 for normal kidney
function, mildly decreased kidney function, and stage 3/4
CKD, respectively (Table 2). Compared with individuals with
normal kidney function, the age-, gender-, race-, and study-
adjusted relative risk (RR) for VTE was 1.28 (95% confidence
interval [CI] 1.02 to 1.59) for those with mildly decreased kid-
ney function and 2.09 (95% CI 1.47 to 2.96) for those with
stage 3/4 CKD. After additional adjustment for risk factors
associated with both CKD and VTE (model 2), patients with
mildly decreased kidney function and those with stage 3/4
CKD still had an increased incidence of VTE, with multivari-
able adjusted RR of 1.29 (95% CI 1.02 to 1.62) and 1.71 (95%
CI 1.18 to 2.49), respectively. Testing for effect modification
showed no statistically significant interaction on the multipli-
cative scale between level of kidney function and gender, race,
diabetes, hypertension, smoking, lipids, BMI, or factor VIIIc.
As shown in Table 3, the incidence rates and RR for VTE with
lower eGFR were similar for idiopathic and secondary VTE.
For further examination of the dose-response relation be-
tween renal function and VTE, a smoothed curve of predicted
Table 1. Baseline characteristics of participants (means or prevalences) according to eGFR: LITE
eGFR (ml/min per 1.73 m2)
Characteristic >90
(n ⴝ 8312)
Age (yr) 56
Male (%) 42
White (%) 62
Diabetes (%)a 14.1
Hypertension (%)a 36.4
BMI (kg/m2)a 27.2
Factor VIIIc (%)a 126
a
Adjusted for age, gender, and race.
136 Journal of the American Society of Nephrology
RR with adjustment for the full set of covariates was graphed
against eGFR (Figure 1). The predicted RR for VTE increased
below eGFR of 75 ml/min per 1.73 m2. Compared with indi-
viduals with eGFR of 90 ml/min per 1.73 m2, the predicted RR
for VTE for those with eGFR of 75, 60, 45, 30, and 15 ml/min
per 1.73 m2 were 1.14, 1.38, 1.68, 2.08, and 2.53, respectively.
These results were largely supportive of the categorical analy-
sis.
We also examined the incidence rate and RR for VTE with
increasing level of serum creatinine. The incidence rates of
VTE per 1000 person-years were 1.6, 1.9, 2.2, and 4.6 for serum
creatinine levels ⬍1.10, 1.10 to 1.29, 1.30 to 1.49, and ⱖ1.5
mg/dl, respectively. In the multivariable adjusted model, com-
pared with the first category of serum creatinine, the second
and third categories of serum creatinine had a similar VTE risk
(RR 1.17 [95% CI 0.89 to 1.53] and RR 1.15 [95% CI 0.75 to
1.78], respectively), but the fourth category had almost double
the VTE risk (RR 1.86; 95% CI 1.21 to 2.81).
Supplemental Analyses
During VTE case review, we recorded whether the patients
with VTE developed renal failure or required dialysis within
90 d before the VTE. Of the 413 participants with incident
VTE, 31 (7.5%) had medical chart documentation of renal
failure or dialysis; 13 came from the 146 participants with nor-
mal kidney function at baseline (8.9%); nine came from the
215 participants with mildly decreased kidney function at
baseline (4.2%); and nine came from the 52 participants with
stage 3/4 CKD at baseline (17.3%). Thus, proportionately
more participants with baseline stage 3/4 CKD had incident
VTE events in the presence of renal failure.
Cystatin C was available for 4013 patients from the Cardio-
vascular Health Study (CHS). During 9.7 yr (39,079 person-
years) of follow-up, 129 patients developed incident VTE (40%
idiopathic). There was no association between cystatin C and
VTE. The multivariable adjusted RR for VTE were 0.53 (95%
CI 0.25 to 1.10), 0.85 (95% CI 0.44 to 1.63), 1.02 (95% CI 0.54
to 1.92), and 1.12 (95% CI 0.58 to 2.16) comparing the second
(0.89 to 0.99 mg/L), third (1.00 to 1.10 mg/L), fourth (1.11 to
1.26 mg/L), and fifth (⬎1.27 mg/L) quintiles of cystatin C with
the first (⬍0.89 mg/L) quintile, respectively (P ⫽ 0.18 for
trend).
P, eGFR 15 to 59
60 to 89 15 to 59 versus >90
(n ⴝ 9472) (n ⴝ 1287)
59 69 ⬍0.0001
47 45 ⬍0.0001
85 87 ⬍0.0001
10.4 20.1 ⬍0.0001
33.6 64.6 ⬍0.0001
27.6 27.9 ⬍0.0001
129 141 ⬍0.0001
J Am Soc Nephrol 19: 135–140, 2008
 www.jasn.org CLINICAL EPIDEMIOLOGY

Table 2. Rates of and RR for incident VTE by level of eGFR: LITE

eGFR (ml/min per 1.73 m2)
Parameter P for trend
>90 60 to 89 15 to 59
LITE
no. of participants 8312 9472 1287
no. of VTE cases (n ⫽ 413) 146 215 52
incidence rate per 1000 person-years 1.5 1.9 4.5
model 1 (95% CI)a 1.0 1.28 (1.02 to 1.59) 2.09 (1.47 to 2.96) ⬍0.0001
model 2 (95% CI)b 1.0 1.29 (1.02 to 1.62) 1.71 (1.18 to 2.49) 0.005
ARIC
no. of participants (n ⫽ 14435) 6983 7065 387
no. of VTE cases (n ⫽ 265) 109 137 19
incidence rate per 1000 person-years 1.2 1.5 4.5
model 1 (95% CI)a 1.0 1.28 (0.98 to 1.66) 3.57 (2.17 to 5.85) ⬍0.0001
model 2 (95% CI)b 1.0 1.21 (0.93 to 1.57) 2.65 (1.60 to 4.39) 0.0001
CHS
no. of participants (n ⫽ 4636) 1329 2407 900
no. of VTE cases (n ⫽ 148) 37 78 33
incidence rate per 1000 person-years 3.0 3.4 4.4
model 1 (95% CI)a 1.0 1.26 (0.83 to 1.91) 1.72 (1.04 to 2.85) 0.04
model 2 (95% CI)b 1.0 1.46 (0.90 to 2.37) 1.65 (0.92 to 2.97) 0.10
a
Adjusted for age, gender, race, and study (except in study-specific models).
b
Additionally adjusted for diabetes, hypertension, BMI, and factor VIIIc.

Table 3. Rates of and RR for idiopathic and secondary VTE by level of eGFR: LITE
eGFR (ml/min per 1.73 m2)
Parameter >90 60 to 89 15 to 59 P for trend
(n ⴝ 8312) (n ⴝ 9472) (n ⴝ 1287)
Idiopathic VTE
no. of VTE cases (n ⫽ 168) 65 80 23
incidence rate per 1000 person-years 0.6 0.7 2.0
model 1 (95% CI)a 1.0 1.11 (0.78 to 1.56) 2.21 (1.30 to 3.75) 0.003
model 2 (95% CI)b 1.0 1.19 (0.83 to 1.71) 1.98 (1.14 to 3.45) 0.02
Secondary VTE
no. of VTE cases (n ⫽ 245) 81 135 29
incidence rate per 1000 person-years 0.8 1.2 2.5
model 1 (95% CI)a 1.0 1.40 (1.05 to 1.88) 2.00 (1.25 to 3.18) 0.004
model 2 (95% CI)b 1.0 1.34 (0.99 to 1.82) 1.51 (0.91 to 2.53) 0.11
a
Adjusted for age, gender, race, and study.
b
Additionally adjusted for diabetes, hypertension, BMI, and factor VIIIc.

DISCUSSION
In this large community-based sample, mildly decreased kid-
ney function and CKD, measured by eGFR, was a moderate,
independent risk factor for VTE. Patients with CKD (eGFR
between 15 and 59 m/min per 1.73 m2) had an almost two-fold
increased risk for VTE compared with those with normal renal
function (eGFR ⬎90 ml/min per 1.73 m2). This risk is similar
in magnitude to several other established VTE risk factors,
such as bed rest, prolonged immobilization, and obesity.5 This
study was not able to demonstrate an independent association
between cystatin C and VTE in CHS, perhaps because insuffi-
cient statistical power.
This study is largely consistent with data from the dialysis
and transplant population demonstrating a higher risk for
VTE in dialysis patients compared with the general population.
Using data from the US Renal Data System record in 1996 and
the National Center for Health Statistics, Tveit et al.8 reported
that the incidence of PE occurring within 1 yr after initiation of
dialysis therapy was approximately 149.9 events per 100,000
dialysis-dependent patients compared with an expected rate of
24.6 per 100,000 people in the US population, with an age-
adjusted incidence ratio of 2.34. Similarly, Abbott et al.9 re-
ported that the incidence rate of VTE in a cohort of 28,924
Medicare renal transplant patients was 9.8 events per 1000 per-
son-years; those with renal insufficiency (eGFR ⬍30 ml/min
per 1.73 m2) at 1 yr after renal transplantation had a two-fold
higher risk for VTE compared with those with eGFR ⬎30 ml/
min per 1.73 m2. Our study seems to be the first to report an
association between mildly decreased kidney function and
stage 3/4 CKD and VTE in the general population. The inci-
dence rates for the mildly decreased kidney function (1.9

J Am Soc Nephrol 19: 135–140, 2008 CKD and Venous Thrombosis 137
 CLINICAL EPIDEMIOLOGY www.jasn.org

plain an increased risk for VTE in the CKD

population. Patients with CKD, particu-
larly those with the nephrotic syndrome,
have elevated blood levels of fibrinogen and
inflammatory markers; however, these fac-
tors were not VTE risk factors in LITE. Pa-
tients with CKD and nephrotic syndrome
may also have endothelial cell dysfunc-
tion,14 enhanced platelet activation and ag-
gregation,15 activation of the coagulation
system,16,17 and decreased endogenous an-
ticoagulants.17,18 Larger studies, with data
on proteinuria, are needed to evaluate the
hemostatic mechanisms mediating the as-
sociation between CKD and VTE.
Figure 1. Spline regression of predicted RR of incident VTE in relation to eGFR: LITE.
The strengths of our study were that it
was a large, prospective, population-
events per 1000 person-years) and stage 3/4 CKD groups (4.5 based study and that VTE was classified by standardized
events per 1000 person-years) were lower than that reported by criteria. Our study was performed in a population generally
Abbott et al., perhaps because our population had less severe without previous diagnosis of CKD, which should reduce
CKD and fewer coexisting medical conditions than in renal diagnostic suspicion bias that might arise if VTE were
transplant patients. Unique to this study is that our spline re- sought more thoroughly in patients with diagnosed CKD
gression analysis demonstrated that the risk for VTE began to than in patients without CKD; therefore, the findings seem
increase with eGFR as high as 75 ml/min per 1.73 m2 and to be valid and should be generalizable to the CKD popula-
gradually increased for lower levels of eGFR. Overall, our find- tion in the United States. We also acknowledge a series of
ings are consistent with the previous large studies in more se- limitations. First, there are potential sources of misclassifi-
vere CKD and provide supporting evidence of increased risk cation. Renal function estimated by the Modification of
for VTE in relation to impaired kidney function in the general Diet in Renal Disease (MDRD) formula and serum creati-
population. nine is not as accurate as a direct measurement from
This finding has potentially important clinical implications. iothalamate or creatinine clearance using a 24-h urine col-
The American College of Chest Physicians has recommended lection; however, direct measurement of GFR is not feasible
routine VTE prophylaxis for several groups of hospitalized pa- in a large epidemiologic study. Estimation of renal function
tients. These include patients with congestive heart failure, se- was based on only one measure of serum creatinine and may
vere lung disease, and cancer; patients who are on bed rest; and be subject to intraindividual variation. Furthermore, creat-
patients who undergo major general, urologic, and gyneco- inine was measured on average 11.8 yr before incident VTE
logic surgery, hip surgery, and lower extremity arthroplas- events. Change in kidney function during the interval would
ty.10,11 Conversely, patients with CKD—inpatients or outpa- have resulted in misclassification of CKD status. In fact, our
tients— generally do not receive routine prophylaxis unless supplemental analysis showed that small numbers of pa-
there are other known concomitant risk factors placing them tients who had VTE and whose baseline kidney function was
in the high-risk group.10 The findings of our study call for an normal (n ⫽ 13) or mildly decreased (n ⫽ 10) had renal
awareness of increased VTE risk in patients with CKD. Recog- failure or were on dialysis around the time of incident VTE.
nition of the increased risk in this population is important Nevertheless, these numbers were small and still propor-
because clinical trials have demonstrated that VTE is prevent- tionately fewer than for those who had CKD at baseline.
able with prophylactic anticoagulation treatment12,13; how- Second, we pooled two large population-based studies be-
ever, further studies are needed to show at what level of eGFR cause of similar protocols. Differences in exposure mea-
prophylaxis might be cost-effective or safe, given the increased surement could have affected results, but RR for CKD were
bleeding risk associated with anticoagulation. There are other elevated in the same direction in each study. Third, we un-
considerations for safety of VTE diagnosis and treatment in fortunately did not have information on proteinuria before
CKD, such as the risk for contrast-induced nephropathy for VTE onset. It would be useful to explore whether protein-
contrast-based imaging and that low molecular weight heparin uria identifies a subset of patients who have CKD and are at
is not recommended in advanced kidney disease. risk for VTE and therefore deserve VTE prophylaxis.
Mechanisms linking CKD and VTE are unknown. In our Fourth, VTE cases could have been missed if VTE events had
study, the strength of association was attenuated only modestly not occurred in the hospital or been recognized by clini-
after adjustment for demographic factors, diabetes, BMI, and cians, but this is true of any epidemiologic study. We believe
factor VIIIc, suggesting that these factors may only partly ex- that such events were uncommon. In fact, LITE data suggest

138 Journal of the American Society of Nephrology J Am Soc Nephrol 19: 135–140, 2008

through 2001 that most VTE were treated in the hospital.
We believe that many of these limitations would lead to bias
toward the null hypothesis.
In conclusion, non-dialysis and non-renal transplant CKD
patients are at increased risk for incident VTE events. An
awareness of the increased risk in the CKD population is im-
portant to prevent morbidity and mortality related to VTE.
CONCISE METHODS
Study Population
The LITE combined the established cohorts from the Atherosclerosis
Risk in Communities (ARIC) Study and the CHS, involving six US
communities. The ARIC Study enrolled 15,792 adults aged 45 to 64 yr
at baseline, and the CHS enrolled 5888 adults aged ⱖ65 yr (5201
recruited between 1989 and 1990 and an additional 687 black patients
between 1992 and 1993). Cardiovascular risk factors were collected at
the baseline examination conducted from 1987 to 1989 in ARIC and
from 1989 to 1990 or 1992 to 1993 (black cohort) in CHS. Informed
consent was obtained from participants, with approval of methods by
the institutional review boards at each study center.
Measurement of Baseline Risk Factors
Factor VIIIc was measured.19,20 BMI was calculated. Diabetes was
defined as a fasting serum glucose level ⱖ7.0 mmol/L (126 mg/dl),
nonfasting glucose level ⱖ11.1 mmol/L (200 mg/L), or current use of
any diabetes medication. Hypertension was defined as seated diastolic
BP ⱖ90 mmHg, systolic BP ⱖ140 mmHg, or use of antihypertensive
medications within the past 2 wk.
Estimation of the Level of Kidney Function
Serum creatinine was measured by each study using the modified
kinetic Jaffe method. Level of kidney function was defined by eGFR
using the MDRD formula21: eGFR ⫽ 186.3 ⫻ (serum creati-
nine⫺1.154) ⫻ (age⫺0.203) ⫻ 1.212 (if black) ⫻ 0.742 (if female). Be-
cause serum creatinine values measured in different laboratories may
vary, we indirectly calibrated ARIC and CHS serum creatinine values
to results obtained at the Cleveland Clinic Laboratory (where serum
creatinine was measured in the MDRD study) by using the Third
National Health and Nutrition Examination Survey (NHANES III)
data. Because both NHANES III and the studies were designed as
population samples, it was assumed that the mean serum creatinine in
the studies for a given age, race, and gender should be comparable to
NHANES III. A linear regression of data showed that serum creatinine
values were 0.24 higher in ARIC22 and 0.11 higher in CHS23 than
among NHANES III participants. We therefore subtracted these val-
ues from measured serum creatinine levels before using the MDRD
formula in this study. We assigned participants with an implausibly
high eGFR to a value of 200 ml/min per 1.73 m2 (n ⫽ 21). Baseline
eGFR was divided into the following categories on the basis of the
National Kidney Foundation guidelines: eGFR ⬎90 ml/min per 1.73
m2 for normal kidney function, eGFR between 60 and 89 ml/min per
1.73 m2 for mildly decreased kidney function, and eGFR between 15
and 59 ml/min per 1.73 m2 for stage 3/4 CKD.
J Am Soc Nephrol 19: 135–140, 2008
www.jasn.org CLINICAL EPIDEMIOLOGY
Cystatin C (available only in CHS), a sensitive marker of renal
function,24 was measured by means of a particle-enhanced immu-
nonephelometric assay with a nephelometer (BNII; Dade Behring,
Deerfield, IL).25 The assay has an intraindividual coefficient of varia-
tion of 7.7%.
VTE Identification and Classification
ARIC participants were contacted annually by telephone or through
clinic visits, and CHS participants were contacted twice a year, alter-
nating clinic visits and telephone calls. Hospitalizations were identi-
fied by participants or proxy reports in both ARIC and CHS, by sur-
veillance of local hospital discharge lists in ARIC, and by a search of
Health Care Financing Administration records in CHS. All records
with possible VTE were identified and copied.
Deep vein thrombosis was classified independently by two physi-
cians (A.R.F. and M.C.) and was defined on the basis of duplex ultra-
sound or venogram or, in rare cases, by impedance plethysmography,
computed tomography, or autopsy. Definite PE required ventilation/
perfusion scanning showing multiple segmental or subsegmental
mismatched perfusion defects, or a positive pulmonary angiogram,
computed tomography, or autopsy.26 Thrombosis events were fur-
ther classified as idiopathic or secondary (occurring within 90 d of
major trauma, surgery, hospitalization, or marked immobility or as-
sociated with active cancer or chemotherapy).
Statistical Analyses
Of 21,680 participants, we excluded those who at baseline reported a
history of VTE (n ⫽ 630) or cancer (n ⫽ 1629) or were taking warfarin
(n ⫽ 128). In addition, we excluded 195 participants with missing
data on creatinine and 27 participants with eGFR ⬍15 ml/min per
1.73 m2, leaving a total of 19,071 participants for the final analyses.
Length of follow-up was calculated as a time elapsed between the
baseline examination and the VTE event; date of last known contact;
death; or December 31, 2001.
We compared baseline risk factors of the participants according to
the three categories of renal function using a ␹2 test for categorical
variables and ANOVA for continuous variables. Incidence rates per
1000 person-years were estimated for the three categories of kidney
function by dividing the number of cases by the follow-up time. With
normal kidney function as a reference group, proportional hazards
regression was used to calculate RR and 95% CI for incident VTE,
adjusting for age, gender, race (white, black), and study (ARIC, CHS).
A subsequent model additionally adjusted for risk factors related to
both CKD and VTE: Diabetes (yes, no), BMI (continuous variable),
and factor VIIIc (continuous variable). To examine the dose-response
relation between the risk for VTE and eGFR, we fitted a restricted
cubic spline regression model to the data with three knots placed at
eGFR values (ml/min per 1.73 m2) of 62 (fifth percentile), 90 (50th
percentile), and 141 (95th percentile). We also repeated the same
analyses using serum creatinine levels categorized as ⬍1.10, 1.10 to
1.29, 1.30 to 1.49, and ⱖ1.5 mg/dl. Because eGFR during the fol-
low-up period was not available, change in kidney function during the
interval would have resulted in misclassification of CKD status. In a
supplemental analysis, we therefore evaluated the number of patients
who had baseline kidney function that was misclassified around the
CKD and Venous Thrombosis 139
 CLINICAL EPIDEMIOLOGY www.jasn.org
time of VTE incidence. We also calculated the associations of cystatin
C (CHS only) in quintiles with VTE events. All statistical analyses
were conducted using SAS 8.2 software (SAS Institute, Cary, NC).
ACKNOWLEDGMENTS
Support was provided by the National Heart, Lung, and Blood Insti-
tute under grant R01 HL59367 (LITE) and contracts N01-HC-55015,
N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020,
N01-HC-55021, and N01-HC-55022 (ARIC) and N01-HC-85079 to
N01-HC-85086, N01-HC-75150, and N01-HC-45133 (CHS).
DISCLOSURES
None.
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