VASCULAR CALCIFICATION IN PATIENTS WITH KIDNEY DISEASE
Techniques and Technologies to Assess Vascular
Calcification
Antonio Bellasi*  and Paolo Raggi 
*Department of Nephrology, Ospedale San Paolo, University of Milan, Milan, Italy and  Division of
Cardiology, Department of Radiology, Emory University School of Medicine, Atlanta, Georgia
ABSTRACT
Cardiovascular calcification (CV) is highly prevalent in chronic
kidney disease stage V and has been associated with an
increased risk for all-cause as well as cardiovascular mortality.
A number of noninvasive imaging techniques are available to
screen for the presence of CV—plain x-rays of the abdomen
and extremities to identify macroscopic calcifications of aorta
and peripheral arteries; echocardiography for assessment of
valvular calcification; two-dimensional ultrasound for calcifi-
cation of carotid arteries, femoral arteries and aorta, and com-
Increasing awareness of the detrimental effect of vas-
cular calcification on cardiovascular morbidity and mor-
tality in dialysis patients (1,2), has led to a renewed
interest in the natural history and pathogenesis of car-
diac and arterial calcification in chronic kidney disease
(CKD). Indeed, CV is highly prevalent in CKD stage V
(CKD-V) and has been associated with a significantly
increased risk for all-cause as well as cardiovascular
mortality both in the general population (3) and in dialy-
sis patients (1,4,5). Diffuse calcification of the large con-
duit arteries promotes arterial stiffness, as measured by
an increase in pulse wave velocity (PWV) and early pulse
wave reflection with deleterious hemodynamic conse-
quences (5). The resulting increase in systolic blood pres-
sure, in conjunction with a decrease in diastolic blood
pressure, lead to altered coronary perfusion and left ven-
tricular hypertrophy, all predisposing to myocardial isc-
hemia and arrhythmias (6).
Over the past several years, a number of noninvasive
imaging techniques have become available to screen for
the presence of CV. Plain x-rays of the abdomen and
extremities can reveal the presence of macroscopic calci-
fications of those arterial territories. Echocardiography
is the primary noninvasive tool used for assessment of
morphological and functional changes of myocardium
Address correspondence to: Paolo Raggi, MD, FACP,
FACC, Prof. of Cardiology and Radiology, Emory University
School of Medicine, 1365 Clifton Road NE, AT-504, Atlanta,
GA 30322, or e-mail: praggi@emory.edu
Seminars in Dialysis—Vol 20, No 2 (March–April) 2007
pp. 129–133
129
puted tomography technologies that constitute the gold
standard for quantification of coronary artery and aorta calci-
fication. Some of these modalities are also useful to monitor
calcification progression and to assess the effect of different
therapeutic strategies directed at modifying calcification pro-
gression. In this article we review the strengths and limitations
of the most common noninvasive techniques employed for the
imaging of vascular calcification.
and cardiac valves. Similarly, two-dimensional ultra-
sound can be used to identify the presence of vascular
calcification in various arterial territories such as carotid
arteries, femoral arteries, and the aorta. However, none
of these radiological and ultrasound techniques permit
quantification of the extent of calcification. New ima-
ging techniques such as electron beam computed tomog-
raphy (EBCT) and multi-slice computed tomography
(MSCT) have emerged as tools to evaluate and accu-
rately quantify CV. These modalities allow the monitor-
ing of CV progression and the assessment of the effect of
different therapeutic strategies on calcification progres-
sion.
The high prevalence, progressive nature, and prognos-
tic significance of vascular calcification suggest that an
approach based on a combination of these techniques
may provide substantial aid in daily clinical practice. In
this article we review the strengths and limitations of the
most commonly employed noninvasive techniques for
the imaging of vascular calcification.
Computed Tomography Techniques
Electron beam computed tomography and MSCT
represent the gold standard for assessing the extent of
VC and its progression. Although the two technologies
operate on the basis of very different imaging platforms
(EBCT was the first type of CT scanner with sufficient
time resolution to image the moving heart), they can
be considered equivalent, especially when comparing
EBCT with the most recent MSCT scanners (16 simul-
taneous sections or greater) (7–9). EBCT employs a
130 Bellasi and Raggi
rotating fan of X-rays produced by the impact of a beam
of electrons against a tungsten ring and 3 mm contigu-
ous slices are obtained at very high speed (high temporal
resolution) from the top to the base of the heart. At the
same time the image quality (spatial resolution) is
slightly lower compared with MSCT scanners. The latter
employ a paired X-ray source-detector revolving around
the patient laying on the radiologic cradle and obtaining
(according to model and brand) 2–64 simultaneous sec-
tions. The nominal thickness of the slices varies from
1.5–0.6 mm and this ensures a higher spatial resolution
than EBCT. With CT imaging it is possible to accurately
detect VC and to precisely quantify its extent by means
of scores such as the Agatston (10) and volume score
(11).
Both EBCT and MSCT have been adopted in the
recent past to investigate the natural history and patho-
genesis as well as the impact of different therapeutic
strategies of VC in CKD. Evidence indicates that as the
estimated glomerular filtration rate (eGFR) declines, the
prevalence of VC increases. The prevalence of coronary
artery calcification was reported to be 40% in 85 CKD-
IV patients as opposed to 13% in controls with normal
renal function (12). In a prospective study of 313 high-
risk hypertensive patients a reduced eGFR was shown
to be the major determinant of the rate of progression of
coronary artery calcification (odds ratios for calcium
progression in the group with eGFR £ 60ml ⁄ min: 2.1;
95% CI 1.2–3.7) (13). Consistent with these findings,
Sigrist et al. (14) reported a prevalence of coronary calci-
fication of 46% in 46 CKD-IV patients compared to
70% and 73%, respectively, in 60 hemodialysis and 28
peritoneal dialysis patients (p = 0.02).
The prevalence of coronary artery calcium increases
dramatically after initiation of dialysis. Indeed, coronary
calcification has been reported in 60% of patients new
to hemodialysis (15) and in as many as 80–83% of adult-
prevalent hemodialysis patients (16). In a small longitud-
inal study, the baseline coronary artery calcium score
calculated on EBCT in 49 prevalent hemodialysis
patients was on average two- to fivefold higher than in
age and sex-matched individuals with established coron-
ary artery disease. A repeated examination after an inter-
val of 12 months showed a significant progression of
coronary calcification (p < 0.05) (17).
Extensive coronary artery calcium was also noted in
young hemodialysis patients (aged 19–39 years) by Oh
et al. (18) and Goodman et al. (19) . The latter also con-
firmed the strong trend for progression of VC shown
earlier by Braun et al. (17). Of note, none of the 23
patients younger than 20 years of age had evidence of
coronary artery calcium (19). This may suggest that VC
does not occur until calcium and phosphorus are utilized
by the growing bone plates or that our current CT ima-
ging modalities are not sensitive enough to detect early
deposition of VC in the form of micro-crystals of
hydroxyapatite.
Despite a poor correlation with angiographic findings
(20), CT-generated calcium scores appear to be predic-
tive of an unfavorable outcome in dialysis patients (4).
Matsuoka et al. (4), followed 104 chronic hemodialysis
patients for an average of 43 months after a screening
EBCT. Patients were divided in two groups according to
a baseline coronary calcium score falling below or above
the median (score  200). The 5-year cumulative survi-
val was significantly lower for patients with a score
>200 than for those with a score <200 (67.9% versus
84.2%, p = 0.0003).
A number of factors have been associated with pro-
gression of VC in dialysis patients. Associations with age
and duration of dialysis (16,19), diabetes mellitus (16),
abnormalities of mineral metabolism (18,21,22), as well
as use and dose of calcium-based phosphate binders
(23,24) have all been reported. To investigate the impact
of therapy for hyperphosphatemia on the progression of
VC, a randomized clinical trial compared the effect of
sevelamer and calcium-based phosphate binders in 200
hemodialysis patients (23). The subjects were random-
ized to 1 year of open label treatment with either seve-
lamer or calcium salts. Throughout the study both drugs
provided a comparable phosphate control (p = 0.33).
However, a significantly higher serum calcium concen-
tration (p = 0.002), a higher incidence of episodes of
hypercalcemia (16% versus 5%; p = 0.04), and a larger
number of subjects with PTH levels below the target of
150 to 300 pg ⁄ ml (57% versus 30%, p = 0.001) were
noted in the calcium-treated arm. At study completion,
sevelamer-treated subjects were less likely to experience
VC progression (median absolute progression of coron-
ary artery calcium score 0 versus 36.6, p = 0.03 and
aorta 0 versus 75.1, p = 0.01, respectively) (23).
Similar conclusions were reached in another series of
129 patients new to hemodialysis (25). Subjects treated
with calcium-containing phosphate binders showed a
more rapid and more severe increase in coronary artery
calcium score compared with those receiving sevelamer
(p = 0.056 at 12 months, p = 0.01 at 18 months) (25).
In a smaller series of 35 hemodialysis patients, MSCT
was used to assess the effect of cyclic intermittent
etidronate therapy in attenuating progression of VC.
Twenty-six of thirty-five hemodialysis patients showed a
significant decrease in coronary artery calcium score
progression with etidronate treatment (median absolute
increase in calcified volume without and with treatment
195 mm3 versus )490 mm3; p < 0.01) (26).
In conclusion, the strength of modern cardiac CT
techniques resides in their high sensitivity for detection
and quantification of VC with useful applications in
studies of calcification pathogenesis and progression.
However, there are also substantial limitations to these
technologies. Intimal (atherosclerotic) calcification and
medial calcification (extensive in patients with advanced
renal failure) cannot be differentiated with the current
methodologies. All CT technologies are expensive and
provide substantial exposure to ionized radiation and, at
least for EBCT, the paucity of scanners appears to be a
major obstacle to its routine application. Thus, a num-
ber of other noninvasive imaging techniques have been
used to screen for the presence of VC.
Plain X-ray Studies
Despite a number of new noninvasive techniques now
available, plain radiographs still represent a valuable
 ASSESSING VASCULAR CALCIFICATION
and inexpensive tool for identification of VC both in the
general populations (27) and in CKD patients (28). The
pattern of VC seen on plain radiographs may yield some
information about the localization of calcification in the
context of the arterial wall (intima versus media layer).
Medial calcification is usually considered present when
linear tram-track radio-opaque lesions are visible along
the course of an artery while intimal calcification is more
characteristically identified by patchy and irregular
radio-opaque lesion. Despite the absence of occlusive
luminal lesions, medial calcification is associated with a
significant clinical risk. Indeed, the loss of elastic recoil
of the arterial wall ultimately reduces end-organ perfu-
sion and increases myocardial after-load with an attend-
ant high cardiovascular morbidity and mortality. In a
cross-sectional study of 202 hemodialysis patients,
both medial calcification and intimal calcification were
shown to be independently and significantly associated
with all-cause mortality [RR 15.7 (95% CI 4.8–51.4;
p < 0.00001) and 4.85 (1.68–14.1; p = 0.0036), respect-
ively]. Of note, medial and intimal calcifications were
detected in as many as 27% and 37% of the X-ray films
of the pelvis and thigh.
Radiographic films of the pelvis and hands were used
in another cross-sectional study of 123 hemodialysis
patients to generate a simple VC score (29). The presence
of linear calcification in the iliac, femoral, digital, and
radial arteries was scored from 0 (no visible calcification)
to 8 (if all four vessels were calcified bilaterally). Some
degree of VC was detected in 75% of the study patients
and almost half of the patients had a score ‡3. During 37
months of follow-up, the mortality rate was  5-fold
higher in patients with a baseline score ‡3 compared to
patients with a score <3 (23% versus 5%; p = 0.01).
Even after adjustment for confounding variables, this
simple score of VC was predictive of mortality (hazard
ratio for score ‡3: 3.9 [95%CI 1.1–12.4; p = 0.03]).
Plain radiographs allow a semi-quantitative (although
mostly qualitative) assessment of VC and may not reli-
ably detect subtle temporal changes of VC. In an early
study, X-ray films of the peripheral arteries were used to
assess ectopic and VC progression in a retrospective ana-
lyses of 38 hemodialysis patients. At the start of dialysis
VC was found in 15 of 38 patients (39%), most com-
monly in the aorto-iliac region. After a median follow-
up of almost 10 years, only 3 of the original 23 patients
without VC at baseline remained free of VC on X-ray
(30). A semi-quantitative score of calcification of the
abdominal aorta seen on lateral lumbar X-rays (31) was
shown to be predictive of outcome in the Framingham
heart study (27). Whether this methodology may be of
help in risk stratification and follow-up of CKD-V
patients remains to be elucidated.
In summary, plain radiographs provide a solid and
inexpensive approach for the detection of VC and there
is fair evidence of the clinical significance of VC detected
with this approach. Of interest, this is the only radiologi-
cal technique for the detection of VC recommended by a
group of experts convened by the National Kidney
Foundation to provide guidance on the assessment
—and subsequent treatment—of VC according to the
131
most recent K ⁄ DOQI guidelines for cardiovascular
disease in CKD-V patients (32).
Echocardiography
Echocardiography is a readily available, noninvasive
and moderately expensive tool that can be easily
employed to detect calcification of the valves and other
cardiac structures. Calcification of the cardiac valves is
found in dialysis patients with a prevalence four to five
times higher than in the general population (33).
Although a less frequent finding than VC, valvular calci-
fication shares common risk factors and pathogenic fea-
tures with VC (34). Indeed, the demonstration of the
presence of inflammatory cells, lipoproteins, and bone
matrix proteins in the calcified regions of the cardiac
valves (35) suggests that these are likely associated syn-
dromes (34).
Not unlike VC, calcification of the mitral and the aor-
tic valve is associated with poor prognosis both in CKD-
V patients (21) and in the general population (36). Wang
et al. (21) showed a stepwise increase in all-cause as well
as cardiovascular mortality associated with no (15%),
one (40%), or two (57%) calcified valves in a cohort of
192 patients on continuous ambulatory peritoneal dialy-
sis. Of note, all-cause and cardiovascular mortality did
not differ significantly between patients having either
valvular calcification or atherosclerotic vascular disease,
reinforcing the hypothesis that valvular calcification rep-
resents a marker of systemic cardiovascular disease.
Consistent with this observation, the same group
subsequently showed that for each 1-mm increase in the
carotid intima-media thickness there was a 6.5-fold
(95% CI 1.58–26.73; p = 0.009) increased risk of valvu-
lar calcification in a cohort of 92 continuous ambulatory
peritoneal dialysis patients (37). Furthermore, the pres-
ence of carotid calcification and carotid plaques was
associated with a 7.2-fold (95% CI, 2.39–21.51; p =
0.001) and 5.0-fold (95% CI, 1.77–14.13; p = 0.002)
increased risk of valvular calcification.
Prior to Wang, Ribeiro et al. (33) found that valvular
calcifications were a more prominent feature in hemodi-
alysis patients than in risk-matched cohorts without evi-
dence of renal dysfunction (mitral calcification 44.5%
versus 10%, p = 0.02; aortic calcification 52% versus
4.3%, p = 0.01). In that study mitral and aortic calcifi-
cation were significantly associated with peripheral
arterial calcification (p = 0.009) and alterations in min-
eral metabolism (33).
Several other clinical (17) and autopsy studies (38)
have also identified an association between mitral and
aortic calcification and coronary artery calcification
both in CKD (17) and non-CKD patients (39,40).
Finally, attenuation of valvular calcification progression
has been demonstrated in the general population
with statins (40) and in CKD-V patients treated with
sevelamer (41).
Taken together, these findings suggest that valvular
calcification is a marker of systemic cardiovascular
disease and risk in CKD patients. Indeed, it is conceiv-
able that in the near future identification of valvular
132 Bellasi and Raggi
calcification in dialysis patients may lead to changes
in treatment to attenuate progression of cardiovascular
disease.
Ultrasonography
Ultrasound-based imaging methodologies have been
wildly adopted to study VC in dialysis patients. Ultra-
sound studies rely on the universal availability of the
tool, the relative inexpensive nature of the test, and
the ease of identification of superficial vessels such as the
carotid and femoral arteries. Furthermore, new genera-
tion ultrasound equipments allow measurement of func-
tional parameters such as aortic PWV and common
carotid artery incremental elastic modulus (Einc). Ultra-
sound-based methods, however, provide only qualitative
and semi-quantitative assessment of VC and have been
mostly adopted in combination with plain X-rays to
improve on the variability of the technique. Nonetheless,
there is good evidence for the prognostic validity of the
information obtained with ultrasound techniques.
Blacher et al. prospectively followed (average follow-
up 53  21 months) 110 patients on maintenance
hemodialysis stratified according to a score generated by
the combination of ultrasound-detected VC of the com-
mon carotid arteries and plain radiographs of the
abdominal aorta and femoro-tibial axes (1). At baseline
the patients were divided into four groups according to
the number of arterial sites showing evidence of VC. The
investigators showed that the presence and extent of VC
was strongly associated with all-cause as well as cardio-
vascular mortality. The adjusted hazard ratios for
all-cause and cardiovascular mortality for each
point increase in calcification severity were 1.9 (95% CI
1.4–2.6) and 2.6 (95% CI 1.2–2.4), respectively (p <
0.01 for both) (1).
Although ultrasound imaging cannot distinguish inti-
mal from medial calcification, scores generated with this
methodology appear to be a reliable means for VC
screening and outcome prediction in the face of substan-
tial cost and radiation exposure saving.
Arterial Compliance
Aging and multiple cardiovascular risk factors, as well
as uremic factors, contribute to the development of vas-
cular calcification and all of these, in turn, are associated
with increased vascular stiffness. As eGFR declines a
marked increase in arterial stiffness is observed (42). A
well-validated method for assessment of arterial stiffness
is PWV. With this noninvasive method the investigator
measures the velocity of propagation of a wave-front
caused by the sequential distension and recoil that
occurs along the course of a vessel due to the ejection of
a bolus of blood. The traveling velocity increases as the
stiffness of the vessel increases. Hence, an increased
PWV is an indirect marker of the presence of VC,
though it is not uniquely due to VC.
In a series of 120 hemodialysis patients, increased
PWV was associated with a simple calcification score
obtained with a combination of carotid ultrasound and
plain radiographs of the abdominal aorta and the
femoro-tibial axes (24). A significant stepwise increase in
mean PWV was noted across different VC groups (from
9.14 m ⁄ second in the group with no evidence of VC to
13.02 m ⁄ second in the group with all four of the arterial
regions calcified; p = 0.001) (24). Furthermore, an
increased aortic PWV was shown to be an independent
predictor of all-cause and CV mortality (43).
Another demonstration of the association between
arterial stiffness and VC was provided by Haydar et al.
(44). In a cohort of 82 CKD patients aortic PWV
was significantly and strongly correlated with EBCT-
generated coronary artery calcium scores (r = 0.65;
p = 0.0001) even after adjustment for confounding
variables.
Hence, it appears that reduced arterial compliance
and VC are closely related and both are independently
associated with mortality. Prospective studies will be
required to investigate whether changes in VC will also
result in changes in arterial stiffness.
Conclusion
Increasing awareness of the detrimental effects of
VC on the cardiovascular system, together with the
very high mortality rates noted in patients undergoing
dialysis, has generated a large amount of interest in
the natural history and pathogenesis of this condition
in CKD. A great effort has been made to identify fac-
tors associated with the deposition of VC as well as
the monitoring of its progression. Though quantita-
tively accurate, both EBCT and the more modern
MSCT technologies are expensive, deliver a substantial
dose of radiation and cannot be easily performed in
an ambulatory setting. However, considering the
importance of detecting VC, the Global Bone and
Mineral Initiative on behalf of the National Kidney
Foundation (32) recently proposed a simplified ap-
proach to identify and semi-quantitatively assess the
extent of VC in patients suffering from end-stage renal
disease. The use of simple in-office measurements such
as echocardiography for detection of valvular calcifica-
tion, lateral lumbar spine X-rays for abdominal aorta
calcification, and measurement of pulse pressure—as
an index of arterial stiffness—could provide a readily
available and inexpensive approach to VC assessment.
Nonetheless, the diagnostic utility and prognostic sig-
nificance of this approach need to be evaluated in
future prospective trials.
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