Farshid et al.

BMC Nephrology 2013, 14:280

http://www.biomedcentral.com/1471-2369/14/280

RESEARCH ARTICLE Open Access

Diastolic function is a strong predictor of

mortality in patients with chronic kidney disease
Ahmad Farshid1*, Rajeev Pathak1, Bruce Shadbolt2,4, Leonard Arnolda1,4 and Girish Talaulikar3,4

Abstract
Background: Cardiovascular disease is a major cause of death in patients with stage 45 Chronic Kidney disease
(CKD, eGFR < 30). There are only limited data on the risk factors predicting these complications in CKD patients. Our
aim was to determine the role of clinical and echocardiographic parameters in predicting mortality and
cardiovascular complications in CKD patients.
Methods: We conducted a prospective observational cohort study of 153 CKD patients between 2007 and 2009. All
patients underwent echocardiography at baseline and were followed for a mean of 2.6 years using regular clinic
visits and review of files and hospital presentations to record the incidence of cardiovascular events and death.
Results: Of 153 patients enrolled, 57 (37%) were on dialysis and 45 (78%) of these patients were on haemodialysis. An
enlarged LV was present in 32% of patients and in 22% the LVEF was below 55%. LV mass index was increased in 75%
of patients. Some degree of diastolic dysfunction was present in 85% of patients and 35% had grade 2 or higher
diastolic dysfunction. During follow up 41 patients (27%) died, 15 (39%) from cardiovascular causes. Mortality was 24.0%
in the non-dialysis patients versus 31.6% in patients on dialysis (p=ns). On multivariate analysis age >75 years, previous
history of MI, diastolic dysfunction and detectable serum troponin T were significant independent predictor of mortality
(P < 0.01).
Conclusion: Patients with stage 45 CKD had a mortality rate of 27% over a mean follow up of 2.6 years.
Age >75 years, history of MI, diastolic dysfunction and troponin T were independent predictors of mortality.
Keywords: Chronic kidney disease, Echocardiography, Diastolic function, Cardiovascular disease, Troponin T

Background associated with increased arterial stiffness and adverse out-

Cardiovascular disease is the major cause of death in pa- comes [5,6].
tients with advanced chronic kidney disease (CKD stages Echocardiography provides a non-invasive assessment of
45, eGFR <30 mL/min/1.73 m2), accounting for about cardiac structures and function. There is limited data on
40% of deaths in international registries [1]. The risk of car- echocardiographic parameters predicting cardiovascular
diovascular mortality is more than 10 times higher in this complications in patients with advanced CKD, including
population compared with an age, sex, and race matched those who have not commenced dialysis [7-9]. Our aim
population [2]. Data on cardiovascular risk factors from was to assess the role of echocardiographic and clinical pa-
the general population cannot simply be extrapolated to rameters and cardiac biomarkers in predicting death and
CKD patients as they are subject not only to traditional risk cardiovascular complications in patients with advanced
factors, but also to CKD-related risk factors such as inflam- CKD and to compare non-dialysis patients with those on
mation, increased calcium and phosphorus products, dialysis.
uremic toxins, anemia, and fluid overload [3,4]. Addition-
ally, CKD patients show a very high prevalence of vascular
and valvular calcification which have been shown to be Methods
Study subjects
* Correspondence: afarshid@tpg.com.au We conducted a 4 year prospective observational study,
1
Cardiology Unit, The Canberra Hospital, PO Box 11, Woden, ACT 2605,
Australia
enrolling 153 consecutive patients between May 2007
Full list of author information is available at the end of the article and May 2009. The setting of the study was the Renal
2013 Farshid et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
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Outpatient Clinic of a Public tertiary referral hospital with Endpoints and Follow up
approximately 400 outpatients with GFR <30 ml/min and The primary endpoint was death from any cause. The sec-
200 dialysis patients. Consecutive adult patients with stage ondary endpoint was the incidence of Major Adverse Car-
45 CKD (eGRF < 30 mL/min/1.73 m2 using the modified diovascular Events (MACE) including death, myocardial
MDRD equation) attending the Clinic were screened and infarction (MI), unstable angina, stroke and heart failure.
invited to take part, including patients who were already MI was defined according to ESC guidelines 2007 as a rise
on dialysis. Patients were excluded if they were unable or and fall of troponin-I with at least one value above the 99th
unwilling to return for regular follow up or were at high percentile of the upper reference limit together with evi-
risk of death due to any cause within 6 months of enrol- dence of myocardial ischaemia [12]. Unstable angina was
ment. The investigation conforms with the principles out- defined as cardiac ischaemic pain associated with 1 mm
lined in the Declaration of Helsinki and was approved by ST segment depression on ECG resulting in hospitalisation.
the Australian Capital Territory Human Research Ethics Cardiac failure was defined according to the ESC definition
Committee. All subjects gave informed written consent to of heart failure (2005) as presentation to a health care facil-
take part in the study. Demographic and clinical character- ity with symptoms of heart failure (typically breathlessness
istics were recorded and patients underwent echocardiog- or fatigue), or ankle swelling and objective evidence of car-
raphy and blood tests (full blood count, electrolytes, urea diac dysfunction at rest [13]. Cerebrovascular accident was
and creatinine, calcium, phosphate and serum troponin T) defined as in the TREAT Study as a focal neurological def-
at the time of entry into the study. icit resulting from a vascular cause involving the central
nervous system with a sudden onset and lasting longer
than 24 hours [14]. Follow up of the patients was by clinic
Troponin T analysis visits, phone calls and review of the clinical notes every six
Analysis was carried out on the Roche Elecsys1010 months.
(Roche Diagnostics Australia, Sydney, Australia). The
limit of detection for this assay is 0.01 mcg/L with assay Statistical analysis
coefficients of variation (CV) being 6.0% at 0.11 mg/L In addition to descriptive analyses, Cox proportional haz-
and 2.5% at 2.5 mg/L. ards models were used to test the univariate and multivari-
ate associations between survival and the subjects risk
factors. In the multivariate analysis, after adjusting for age
Echocardiography and gender as well as diabetes and other risk factors
2D and Doppler echocardiography was carried out on all (hypertension, smoking, hyperlipidaemia), a likelihood ratio
patients lying in the left decubitus position at baseline. All method for factor inclusion was employed. Hazard ratios
studies were performed by a single experienced sonogra- and the associated 95% confidence intervals and p values
pher blinded to the clinical details of patients using a are shown in the results. SPSS version 19.0 was used to
Philips iE33 echocardiographic system with a S5-1 probe. conduct the analyses and a two sided p value of <0.05 was
For patients on dialysis all studies were performed within considered significant.
24 hour after dialysis. All echocardiographic data were
measured according to the guidelines of the American So- Results
ciety of Echocardiography (ASE) [10]. LV mass was calcu- Baseline characteristics for 153 enrolled patients are shown
lated using the ASE-recommended formula for estimation in Table 1. Patients on dialysis made up 38% of the study
of LV mass from linear dimensions and was indexed to population, 78% of whom were on haemodialysis. A history
body mass. The left ventricular ejection fraction (LVEF) of MI was present in 20% of patients and 46% were dia-
was measured in the apical views using Simpsons betic. An enlarged left ventricle was present in 32% and in
method. Diastolic function was assessed using several 22% the LVEF was below 55%. LV mass index was in-
parameters including the pattern of mitral inflow and creased in 75% of patients. Some degree of diastolic dys-
the ratio of peak early (E) filling velocity to late dia- function was present in 85% of patients and 35% had grade
stolic filing (A) velocity (E/A ratio), deceleration time 2 or higher diastolic dysfunction. Diastolic function could
of early filling velocity (DT), and the isovolumic relax- not be assessed in 16 patients (10%), mostly due to pres-
ation time (IVRT). PW Tissue Doppler Imaging was ence of atrial fibrillation. Follow up was for a mean of
performed in the apical views to acquire mitral annular 2.6 years (median 2.89 years) and was available in all but 1
velocities. The ratio of early mitral inflow velocity to patient who moved to another state.
Tissue Doppler velocity e (E/e) was used for the Clinical, biochemical and echocardiographic results as
estimation of LV filling pressures. Diastolic function well as incidence of adverse events for dialysis and non-
was classified into grades I-IV according to the ASE dialysis patients are shown in Table 2. There was a higher
guidelines [11]. incidence of LV dysfunction and troponin T elevation in
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Table 1 Baseline characteristics of patients Table 2 Clinical and echocardiographic characteristics in

Number (%) dialysis and non-dialysis patients
Mean age (year) 65.6 14.0 Non- Dialysis P
dialysis value
Male gender 88 (57.5%)
Number 96 57 NA
Medical history
Mean age 69.7 11.7 58.7 15.0 <0.0001
Hypertension 127 (85%)
Female sex 40 (42%) 25 (44%) NS
Diabetes 69 (46%)
Diabetes 45 (47%) 24 (42%) NS
Oral hypoglycaemics 25 (17%)
History of MI 18 (19%) 12 (21%) NS
Insulin 34 (23%)
Blood indices:
Heart failure 20 (13%)
Haemoglobin (g/L) 123.8 15.4 117.0 12.3 0.0058
Stroke 23 (15%)
White cell count 7.38 2.0 7.57 2.13 NS
Hyperlipidaemia 90 (60%)
Platelet count 238 63 232 88 NS
Current smoker 15 (10%)
Sodium 139.9 2.6 137.4 <0.0001
Atrial fibrillation 10 (6.5%)
Potassium 4.46 0.59 4.41 NS
AMI 30 (20%)
Urea (mmol/L) 18.9 6.9 19.2 6.7 NS
PCI 25 (16%)
Creatinine (umol/L) 255 88 646 229 <0.0001
CABG 17 (11%)
eGFR (mL/min/1.73 m2) 22.3 7.4 8.3 4.9 <0.0001
Patients on dialysis 56 (37%)
Calcium (mmol/L) 2.40 0.12 2.38 0.17 NS
Haemodialysis 45 (29%)
Phosphate (mmol/L) 1.31 0.29 1.84 0.55 <0.0001
Peritoneal dialysis 13 (8%)
Parathyroid hormane 23.6 29.1 51.4 48.6 <0.0001
Aetiology of kidney disease:
Troponin T detected 36 (38%) 44 (79%) <0.001
Diabetes 48 (31%)
Echocardiographic results
Glomerulonephritis 39 (25%)
LV diameter (mm) 49.5 5.9 49.8 6.2 NS
Vascular 13 (8%)
LV ejection fraction 62.1 10.0 61.0 14.0 NS
Hypertension 10 (7%)
LV mass index 121.7 35.4 126.8 33.6 NS
Vesicoureteric reflux 9 (6%)
Left atrial area (cm2) 22.1 6.0 21.6 4.9 NS
Congenital 6 (4%)
Aortic peak velocity (m/s) 1.50 0.42 1.57 0.47 NS
Other 28 (18%)
Mitral regurgitation 8 (8.3%) 6 (10.5%) NS
Medications (moderate or severe)
ACEI/ARB 86 (56%) Tricuspid regurgitation 2.53 0.44 2.59 0.45 NS
peak velocity (m/s)
Diuretic 58 (38%)
Beta blocker 64 (42%) Diastolic grade:

Statin 92 (60%) Grade 0 14 (16.3%) 7 (13.7%) NS

Calcium antagonist 60 (39%) Grade 1 48 (55.8%) 24 (47.1%) NS

Aspirin 42 (27%) Grade 2 16 (18.6%) 15 (29.4%) NS

EPO 65 (42%) Grade 3-4 8 (9.3%) 5 (9.8%) NS

Indeterminate grade 9 (9.5%) 7 (12.1%) NS

dialysis patients but there were no other significant differ- Clinical outcomes
ences between the two groups. Mortality was 24% in the Death 23 (24.0%) 18 (31.6%) NS
non-dialysis patients versus 31.6% in patients on dialysis MACE 27 (28.1%) 24 (42.1%) 0.06
(p=ns). LVEF, Left ventricular ejection fraction; LVMI, Left ventricular mass index; MACE,
Adverse events during follow up for the entire cohort are Major adverse cardiovascular events, diastolic function was classified into
grades 14 according to the ASE guidelines.
shown in Table 3. During this time 41 patients (27%) died,
15 (39%) of whom died from cardiovascular causes. Sur-
vival analysis was performed to determine univariate clin- Univariate echocardiographic predictors of mortality in-
ical and echocardiographic factors predictive of death and cluded enlargement of left ventricle and the left atrium,
adverse cardiovascular events (Table 4). Clinical predictors low LVEF, increased LV mass index and grade 2 or higher
of death included age >75 years and a history of MI. diastolic dysfunction. On multivariate analysis (Cox
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Table 3 Incidence of adverse events during 2.6 years 5447 patients starting dialysis (mean age 64) docu-
follow up mented a mortality rate of 29.7% after 3 years [16]. The
Adverse events Number (%) mortality rate in our non-dialysis group, a cohort which
Acute MI 14 (9.1%) has not been studied extensively in other studies, was
Unstable angina 13 (8.5%) surprisingly high at 24%. TREAT which studied diabetic
patients with a GFR of 2060 mL/min/1.73 m2 reported
Cardiac failure 10 (6.5%)
a mortality of 20% after a median 2.4 years follow up
Cerebrovascular accident 6 (3.9%)
[17]. The CRIC study which enrolled 3939 patients with
Percutaneous coronary intervention 7 (4.6%) stage 24 CKD recently reported an overall mortality
Death from any cause 41 (27%) rate of 9.5% and a combined incidence of MI, CVA and
Cause of death: peripheral vascular disease of 8.4% [18]. Mean eGFR in
Sepsis 9 (22%) the CRIC study patients was 44.8 ml/min/1.73 m2 com-
pared with 22.3 ml/min/1.73 m2 in our non-dialysis
Renal failure 8 (20%)
(stage 4) patients.
Cancer 7 (17%)
The pathophysiology of cardiac disease in CKD is related
Acute MI 4 (10%) to the interaction of multiple factors including hyperten-
Sudden death 5 (12%) sion, chronic volume overload, anaemia, presence of an AV
Cardiac failure 3 (7%) fistula in patients on dialysis, as well as metabolic factors
Cerebrovascular accident 4 (10%) such as acidosis, hypoxia, hypocalcaemia and high levels of
parathyroid hormone [3,4]. Morphological changes in the
All cardiovascular death 16 (39%)
heart include LVH, advanced coronary atherosclerosis,
Accident 1 (2%)
microvascular disease and diffuse interstitial myocardial
fibrosis [19,20]. These abnormalities are common in
Regression) age >75 and previous history of MI remained CKD patients and have been shown in to be predictive
significant. With regard to echo parameters, diastolic dys- of mortality [21,22].
function remained as a significant predictor of mortality, Assessment of diastolic function by echocardiography
whereas LV mass index and LVEF were no longer signifi- has shown a high incidence of abnormalities in dialysis and
cant. Detection of Troponin T in the serum was also an non-dialysis CKD patients [23,24]. Some investigators have
independent predictor of mortality during follow up. found abnormalities in tissue Doppler velocity in virtually
all patients with CKD, suggesting a degree of subclinical
Discussion myocardial disease in all such patients [25]. In the CRIC
Cardiovascular disease is the leading cause of death in study (stage 24 CKD) diastolic function was abnormal in
patients with advanced CKD [2]. Our study has shown 71% of patients [26]. In our cohort some degree of dia-
that patients with advanced CKD had a mortality rate of stolic dysfunction was present in 85% of patients and 35%
27% (39% from cardiovascular causes) over a mean fol- had grade 2 or higher diastolic dysfunction, which was a
low up of 2.6 years. The overall mortality rate was powerful independent predictor of mortality. Patients with
higher than in the placebo group in the SHARP Trial abnormal diastolic function have been found to have in-
which enrolled patients with moderate to severe CKD creased integrated backscatter which is a measure of colla-
with one third on dialysis (24.1% after 4.9 years) [15]. gen content of myocardial tissue [27]. We used E/ as part
This is possibly explained by the higher age of our co- of our grading of diastolic function and this has been
hort (66 years v 62 years in SHARP) and the inclusion shown to reflect LV filling pressure and has been associ-
of more patients on dialysis. The UK Renal Registry of ated with mortality in CKD patients [24].

Table 4 Univariate and multivariate predictors of mortality in advanced CKD patients

Factor Univariate P value Multivariate P Value Hazard ratio Lower 95% CI Upper 95% CI
Age >75 0.0005 0.002 3.21 1.53 6.74
History of MI <0.0001 0.007 2.72 1.32 5.64
LVEF < 55% 0.02 NS NA NA NA
High LVMI 0.03 NS NA NA NA
Diastolic grade > 1 0.0005 0.001 3.42 1.66 7.08
Elevated troponin T <0.0001 0.005 3.70 1.50 9.18
Independent variables entered in the Cox Regression model: age, sex, diabetes, history of MI, LVEF, LVMI, Diastolic grade >1, Troponin T. CI, confidence interval;
LVEF, left ventricular ejection fraction; LVMI, left ventricular mass index.
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We detected troponin T in 38% of non-dialysis and 79% Conclusion

of dialysis patients. Troponin T was detected in 45% of Patients with advanced CKD have a high incidence of
diabetic CKD patients in TREAT and was an independent structural cardiac abnormalities including increased LV
predictor of adverse outcomes in this and other studies mass, diastolic dysfunction and raised troponin T. These
[17,28]. The precise mechanism for increased Troponin T factors are associated with increased mortality and ad-
concentrations in advanced CKD patients is not clear. verse cardiac events compared to CKD patients without
Acute myocardial ischaemia may be a factor in a minority these factors, even in the non-dialysis population. We
of patients as suggested by an MRI study in ESRD patients therefore suggest routine evaluation of diastolic function
with raised troponins [29]. None of our patients had clin- by echocardiography, measurement of serum troponin T
ical evidence of myocardial infarction at the time of their and screening for vascular risk factors in all CKD pa-
blood test. A post-mortem study of patients with raised tients. Whether early identification of these risk markers
troponin T which included 6 haemodialysis patients found and intervention in CKD patients will lead to improved
histologic evidence of myocardial infarction in some pa- outcomes should be the subject of further investigation.
tients but also other cellular pathologies in virtually all
subjects including degenerative changes associated with Competing interests
heart failure, inflammation, fibrosis, endocarditis, sepsis, The authors declare that they have no competing interests.
amyloid deposition, and infiltration by tumour [30]. The
concept of myocyte damage in these patients is supported Authors contributions
AF conceived and designed the study, analysed the results and drafted the
by findings of a higher incidence of LV dilatation, in- manuscript. RP participated in drafting the manuscript and analysing the
creased LV mass, impaired systolic function and raised LV results. GT participated in designing the study and writing the manuscript.
filling pressures [24]. The situation is made more complex BS participated in designing the study and performed the statistical analysis.
LA participated in data analysis and drafting the manuscript. All authors read
by availability of high sensitivity assays which detect tropo- and approved the final manuscript.
nin T in virtually all advanced CKD patients [31]. In the
CRIC study high sensitivity Troponin T was detected in Acknowledgements
84% of stage 24 CKD patients and was associated with The authors would like to thank Pearle Taverner and Patricia Johnson for their
LVH and systolic dysfunction [32]. assistance with patient enrolment, data collection and follow up. The study was
funded by the Private Practice Fund of the Canberra Hospital which did not
Detection of significant diastolic dysfunction and ele- have any involvement in carrying out the study or writing the manuscript.
vated troponin T can be early markers of myocardial
disease and increased risk in advanced CKD. However, Author details
1
Cardiology Unit, The Canberra Hospital, PO Box 11, Woden, ACT 2605,
the optimal management of these patients is not well Australia. 2Centre for Advances in Epidemiology and Information Technology,
defined. Therapeutic modalities that have been success- The Canberra Hospital, Canberra, Australia. 3Renal Unit, The Canberra
fully used include aggressive lipid lowering [15], treat- Hospital, Canberra, Australia. 4Australian National University, Canberra,
Australia.
ment for hypertension and anaemia [33], increased
frequency of dialysis [34], implantable defibrillator in- Received: 13 July 2013 Accepted: 17 December 2013
sertion [35], coronary revascularisation [36], multiple Published: 23 December 2013

risk factor intervention [37] and renal transplantation.

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