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. 2023 Mar 24;65(11):624–630. doi: 10.4103/singaporemedj.SMJ-2021-427

Clinical profile and outcomes in patients with moderate to severe aortic stenosis with or without concomitant chronic kidney disease

Jinghao Nicholas Ngiam 1,*, Ching-Hui Sia 2,*, Nicholas Wen Sheng Chew 2, Tze Sian Liong 1, Zi Yun Chang 3, Chi Hang Lee 2,4, Wen Ruan 5, Edgar Lik-Wui Tay 2,4, William Kok-Fai Kong 2,4, Huay Cheem Tan 2,4, Tiong-Cheng Yeo 2,4, Kian Keong Poh 2,4,✉
PMCID: PMC11630491  PMID: 37026360

Abstract

Introduction:

Management of aortic stenosis (AS) in patients with chronic kidney disease (CKD) may often be overlooked, and this could confer poorer outcomes.

Methods:

Consecutive patients (n = 727) with index echocardiographic diagnosis of moderate to severe AS (aortic valve area <1.5 cm2) were examined. They were divided into those with CKD (estimated glomerular filtration rate < 60 mL/min) and those without. Baseline clinical and echocardiographic parameters were compared, and a multivariate Cox regression model was constructed. Clinical outcomes were compared using Kaplan–Meier curves.

Results:

There were 270 (37.1%) patients with concomitant CKD. The CKD group was older (78.0 ± 10.3 vs. 72.1 ± 12.9 years, P < 0.001), with a higher prevalence of hypertension, diabetes mellitus, hyperlipidaemia and ischaemic heart disease. AS severity did not differ significantly, but left ventricular (LV) mass index (119.4 ± 43.7 vs. 112.3 ± 40.6 g/m2, P = 0.027) and Doppler mitral inflow E to annular tissue Doppler e’ ratio (E: e’ 21.5 ± 14.6 vs. 17.8 ± 12.2, P = 0.001) were higher in the CKD group. There was higher mortality (log-rank 51.5, P < 0.001) and more frequent admissions for cardiac failure (log-rank 25.9, P < 0.001) in the CKD group, with a lower incidence of aortic valve replacement (log-rank 7.12, P = 0.008). On multivariate analyses, after adjusting for aortic valve area, age, left ventricular ejection fraction and clinical comorbidities, CKD remained independently associated with mortality (hazard ratio 1.96, 95% confidence interval 1.50–2.57, P < 0.001).

Conclusion:

Concomitant CKD in patients with moderate to severe AS was associated with increased mortality, more frequent admissions for cardiac failure and a lower incidence of aortic valve replacement.

Keywords: Aortic stenosis, chronic kidney disease, clinical outcomes

INTRODUCTION

Chronic kidney disease (CKD) is highly prevalent in aortic stenosis (AS). CKD shares many common risk factors with AS and may be an important under-recognised comorbidity.[1,2,3] It is known to affect up to 50% of patients with AS.[4] Poorly controlled cardiovascular risk factors like hypertension, hyperlipidaemia and diabetes mellitus can accelerate the progression of AS and lead to the development of CKD.[5] Aortic stenosis, being the most common valvular disease, is further increasing in disease burden as a result of an ageing population worldwide.[6] At the same time, CKD has also become increasingly prevalent.[7]

Coexistent CKD may interact with AS, where CKD can worsen AS.[8] CKD is known to accelerate atherosclerosis, which would contribute to more extensive calcification, sclerosis and, subsequently, stenosis of the aortic valve.[9,10,11] It has been reliably demonstrated that progression of aortic valve calcification is associated with adverse clinical outcomes.[12] Furthermore, patients with end-stage renal disease (ESRD) are more likely to have AS and experience more rapid progression of the underlying disease.[13,14]

Furthermore, CKD in AS has been associated with poorer outcomes after valve replacement, with higher postoperative or postprocedural mortality in both the short and long term.[15,16,17] In patients with ESRD on dialysis, although valve replacement confers mortality benefit, the magnitude of this benefit is significantly lower than in patients who are not on haemodialysis.[18] Many studies on transcatheter aortic valve replacement (TAVR), however, have excluded (or included relatively few) patients with ESRD or advanced CKD from analyses.[19,20] This may not have been intentional but may be because many patients with advanced CKD were deemed to be unfit to go through the valve replacement procedure.[21] To our knowledge, though advanced CKD and ESRD have been studied in the clinical outcomes of patients with severe AS undergoing valve replacement, few studies have examined this association earlier in the course of disease in patients with moderate to severe AS. We sought to characterise the clinical profile and outcomes of patients with moderate to severe AS and concomitant CKD compared to those with normal kidney function.

METHODS

We examined a total of 727 consecutive Asian patients who presented to our centre with an index echocardiographic diagnosis of moderate or severe AS (aortic valve area [AVA] <1.5 cm2) between the years 2011 and 2015. We studied only patients with isolated AS and excluded patients with concomitant valvular pathology of at least moderate severity. Echocardiographic parameters and measurements, including the diagnosis and classification of AS, were made in accordance with the guidelines of the American Society of Echocardiography/European Association of Cardiovascular Imaging.[22,23,24]

Patients were divided into those with and those without concomitant CKD. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 mL/m2, which was measured in a baseline renal function test within 1 year of the index echocardiographic diagnosis of AS. We further stratified those with CKD into their respective stages: CKD 3 (eGFR 31–60 mL/min/1.73 m2), CKD 4 (eGFR 15–29 mL/min/1.73 m2), CKD 5 (eGFR <15 mL/min/1.73 m2) or ESRD requiring dialysis. Other demographics as well as baseline clinical characteristics were tabulated. Patients were subsequently followed up prospectively for at least 3 years after the index echocardiography. Clinical outcomes were measured in terms of: (a) all-cause mortality; (b) admissions for congestive cardiac failure; and (c) surgical aortic valve placement or TAVR.

Statistical analyses were performed using appropriate univariate analyses of baseline characteristics and echocardiographic parameters. These tests included the Student’s t-test to examine the association between continuous variables and Pearson’s chi-square test (or Fisher’s exact test where appropriate) to evaluate categorical variables. Kaplan–Meier survival curves (time-to-event analysis) were also constructed to compare survival between the groups, and the log-rank test statistic was calculated. The other clinical outcomes (admissions for congestive cardiac failure and aortic valve replacement) were analysed similarly. A P value of less than 0.05 was considered significant. All data analysis was done on IBM SPSS Statistics version 20.0 (IBM Corp, Armonk, NY, USA). This study was conducted ethically in accordance with the World Medical Association Declaration of Helsinki. It was approved by the National Healthcare Group Domain Specific Review Board (Singapore) (2016/00358) before the conduct of the study. Informed consent was waived, as this was an anonymised retrospective study and all patient identifiers had been removed.

RESULTS

Of the 727 patients with moderate to severe AS (AVA <1.5 cm2), 270 (37.1%) patients had CKD. Of these, 40 (14.8%) patients had ESRD and were on dialysis. The majority of our patients had moderate AS (AVA 1–1.5 cm2, n = 504, 69.3%), while the remaining had severe AS (AVA <1 cm2, n = 223, 30.7%). Of the patients with CKD, 28.0% (n = 75) had severe AS, while 30.7% of the patients without CKD had severe AS (n = 138). The patients with CKD were approximately 6 years older (78.0 ± 10.3 vs. 72.1 ± 12.9 years, P < 0.001), but their body mass index and systolic blood pressure did not differ significantly from those of patients without CKD. Cardiovascular risk factors such as hypertension (84.1% vs. 71.8%), hypercholesterolaemia (69.9% vs. 58.3%) and diabetes mellitus (52.4% vs. 31.9%) were uniformly higher in the CKD group. In terms of cardiovascular complications, the prevalence of ischaemic heart disease (48.1% vs. 32.4%), stroke (18.5% vs. 13.1%) and atrial fibrillation (22.6% vs. 13.3%) was consistently higher in the CKD group. Anaemia was more prominent in the group with CKD, as the haemoglobin concentration was significantly lower (11.0 ± 2.1 vs. 12.4 ± 2.1 g/dL, P < 0.001) [Table 1].

Table 1.

Comparison of the characteristics of patients with moderate to severe aortic stenosis with and without coexisting chronic kidney disease (AVA <1.5 cm2).

Parameter Mean±SD/n (%) OR/mean difference (95% CI) P
CKD (n=270) No CKD (n=457)
Age (yr) 78.0±10.3 72.1±12.9 5.8 (4.1 to 7.7) <0.001
Female gender 165 (61.1) 245 (53.6) 1.19 (0.99 to 1.43) 0.058
Body mass index (kg/m2) 24.5±4.8 25.0±5.8 −0.5 (−1.3 to 0.4) 0.268
Systolic blood pressure (mmHg) 135.9±26.1 135.9±23.3 0.1 (−3.7 to 3.7) 0.996
Diastolic blood pressure (mmHg) 67.7±10.9 69.6±11.0 −1.9 (−3.6 to −0.3) 0.023
Diabetes mellitus 141 (52.4) 144 (31.9) 2.35 (1.72 to 3.20) <0.001
Hypertension 227 (84.1) 324 (71.8) 2.07 (1.41 to 3.04) <0.001
Hypercholesterolaemia 188 (69.9) 263 (58.3) 1.66 (1.20 to 2.29) 0.002
Ischaemic heart disease 130 (48.1) 32.4 (32.4) 1.94 (1.42 to 2.64) <0.001
Stroke 50 (18.5) 60 (13.1) 1.50 (0.99 to 2.27) 0.051
Atrial fibrillation 61 (22.6) 60 (13.3) 1.90 (1.28 to 2.82) 0.001
Renal replacement therapy 40 (14.8) 0 - -
Haemoglobin (g/dL) 11.0±2.1 12.4±2.1 −1.4 (−1.7 to−1.1) <0.001
Platelet count 229.8±88.8 243.7±90.3 −13.9 (−27.8 to−0.1) 0.049
Creatinine (µmol/L) 222.0±203.1 69.6±15.6 152.5 (132.8 to 172.1) <0.001
Estimated glomerular filtration rate (mL/min/1.73 m2) 34.7±18.1 83.3±14.2 −48.6 (−51.0 to−46.2) <0.001
LV ejection fraction (%) 58.9±17.2 62.0±15.5 −3.1 (−5.6 to−0.7) 0.012
LV internal diameter in diastole (mm) 46.9±9.6 47.0±9.3 −0.1 (−1.5 to 1.4) 0.925
LV mass index (g/m2) 119.4±43.7 112.3±40.6 7.1 (0.9 to 13.4) 0.027
End-systolic wall stress (dyn/cm2) 71.8±30.9 70.1±28.1 1.7 (−2.7 to 6.1) 0.461
Left atrial diameter (mm) 43.0±9.1 41.5±9.8 1.6 (0.1 to 3.0) 0.034
E: e’ 21.5±14.6 17.8±12.2 3.7 (1.6 to 5.8) 0.001
Transaortic mean pressure gradient (mmHg) 23.2±27.5 24.6±18.4 −1.4 (−4.8 to 1.9) 0.400
Transaortic peak velocity (cm/s) 281.4±99.6 301.2±99.4 −19.8 (−35.0 to−4.6) 0.011
AVA (cm2) 1.13±0.28 1.11±0.30 0.01 (−0.03 to 0.06) 0.554
Severe aortic stenosis (AVA <1 cm2) 75 (28.0) 138 (30.7) 0.89 (0.63 to 1.22) 0.436
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AVA: aortic valve area, CI: confidence interval, CKD: chronic kidney disease, E: e’: Doppler mitral inflow E to annular tissue Doppler e’ ratio, LV: left ventricular, OR: odds ratio, SD: standard deviation

In terms of echocardiographic profile, patients with CKD had a lower left ventricular ejection fraction (LVEF; 58.9% ± 17.2% vs. 62.0% ± 15.5%), but with a higher left ventricular (LV) mass index (119.4 ± 43.7 vs. 112.3 ± 40.6 g/m2) and left atrial diameter (43.0 ± 9.1 vs. 41.5 ± 9.8 mm). Doppler mitral inflow E to annular tissue Doppler e’ ratio (E: e’) was higher in those with CKD (21.5 ± 14.6 vs. 17.8 ± 12.2, P = 0.001). AS was similarly severe with no significant differences in the AVA or mean transaortic pressure gradient. However, the transaortic peak velocity was slightly lower in the group with CKD (281.4 ± 99.6 vs. 301.2 ± 99.4 cm/s, P = 0.011) [Table 1].

We examined the subgroup of patients with CKD (n = 270). They were stratified based on CKD severity (stage 3, 4, 5 as well as ESRD on dialysis). The majority of patients had CKD 3 (n = 170, 63.0%), while the remaining had CKD 4 (n = 36), CKD 5 (n = 24) and ESRD (n = 40). Across the groups, we did not demonstrate any significant differences in the proportion of patients with severe AS or in the transaortic mean pressure gradient, peak velocity and valve area. There was slightly increased LV mass index with increasing severity of CKD [Table 2].

Table 2.

Comparison of the characteristics of patients with moderate to severe aortic stenosis (AVA <1.5 cm2) by stage of CKD.

Mean±SD/n (%)
Parameter CKD 3 (n=170) CKD 4 (n=36) CKD 5 (n=24) ESRD on dialysis (n=40) P
Age (yr) 80.2±8.8 80.7±9.2 75.8±11.5 67.3±9.6 <0.001
Female gender 102 (60.0) 22 (61.1) 20 (83.3) 21 (52.5) 0.097
Body mass index (kg/m2) 24.8±4.9 22.3±3.5 25.3±5.3 24.8±4.6 0.026
Systolic blood pressure (mmHg) 136.3±24.5 147.2±25.1 125.2±21.2 133.1±26.7 0.006
Diastolic blood pressure (mmHg) 67.9±10.8 69.7±10.8 62.8±12.2 67.3±10.3 0.102
Diabetes mellitus 81 (47.9) 22 (61.1) 14 (58.3) 24 (60.0) 0.294
Hypertension 143 (84.1) 31 (86.1) 23 (95.8) 30 (75.0) 0.168
Hypercholesterolaemia 122 (71.8) 29 (80.6) 14 (60.9) 23 (57.5) 0.110
Ischaemic heart disease 82 (48.2) 17 (47.2) 11 (45.8) 20 (50.0) <0.001
Estimated glomerular filtration rate (mL/min/1.73 m2) 46.8±9.6 22.4±4.6 9.5±3.2 9.8±6.2 <0.001
LV ejection fraction (%) 59.4±17.3 59.8±18.1 62.8±11.4 53.5±18.2 0.138
LV mass index (g/m2) 114.9±43.9 114.3±40.5 132.0±31.6 135.7±47.8 0.019
End-systolic wall stress (dyn/cm2) 70.9±29.9 74.3±31.8 65.5±28.5 77.0±35.9 0.475
Left atrial diameter (mm) 42.7±9.3 42.4±10.1 43.6±5.7 44.6±9.0 0.648
E: e’ 20.8±14.8 23.9±15.6 19.4±8.9 24.1±15.5 0.410
Transaortic mean pressure gradient (mmHg) 24.7±32.5 18.9±13.2 20.6±16.1 22.2±17.1 0.645
Transaortic peak velocity (cm/s) 286.8±95.1 258.3±103.9 278.7±80.9 281.2±121.9 0.500
AVA (cm2) 1.12±0.27 1.12±0.29 1.22±0.23 1.13±0.28 0.391
Severe aortic stenosis (AVA <1 cm2) 49 (29.0) 9 (25.7) 3 (12.5) 14 (35.0) 0.261
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AVA: aortic valve area, CKD: chronic kidney disease, E: e’: Doppler mitral inflow E to annular tissue Doppler e’ ratio, ESRD: end-stage renal disease, LV: left ventricular, SD: standard deviation

On subsequent follow-up, mortality was higher in the group with CKD (n = 135, 50.4%) compared to the group without (n = 112, 24.9%; log-rank 51.5, P < 0.001) [Figure 1]. Similarly, the admissions for congestive cardiac failure were also more frequent in the group with CKD (n = 65, 26.6%) compared to the group without (n = 54, 13.1%; log-rank 25.9, P < 0.001) [Figure 2]. However, aortic valve replacement (either transcatheter or surgical) was far less common in those with CKD (n = 16, 5.9% vs. n = 57, 12.5%; log-rank 7.18, P = 0.008) during the follow-up period [Figure 3]. When the subgroup of patients with ESRD on dialysis was further identified (n = 40), they had even poorer survival compared to those with non-dialysis CKD and those without CKD, as demonstrated by the Kaplan–Meier curves (log-rank 57.1, P < 0.001) [Figure 4]. On multivariable Cox regression analysis, CKD was found to be independently associated with an increased risk of mortality (hazard ratio [HR] 1.96, 95% confidence interval [CI] 1.50–2.57, P < 0.001) even after adjusting for confounders such as age, medical comorbidities, LVEF and AVA [Table 3].

Figure 1.

Figure 1

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Kaplan–Meier curve shows improved survival in the group without chronic kidney disease (CKD) compared to patients with cancer in moderate to severe aortic stenosis.

Figure 2.

Figure 2

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Kaplan–Meier curve compares admissions for congestive cardiac failure between the groups with and without chronic kidney disease (CKD) in moderate to severe aortic stenosis.

Figure 3.

Figure 3

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Kaplan–Meier curve compares aortic valve replacement (transcatheter or surgical) between patients with and without chronic kidney disease (CKD) in moderate to severe aortic stenosis.

Figure 4.

Figure 4

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Kaplan–Meier curve shows increased mortality in patients with end-stage renal disease and chronic kidney disease (CKD) over those with no CKD in moderate to severe aortic stenosis.

Table 3.

Multivariate Cox regression analysis showing chronic kidney disease to be independently associated with increased mortality.

Parameter Adjusted HR (95% CI) P
Age 1.03 (1.02–1.05) <0.001
Hypertension 1.47 (0.76–1.51) 0.680
Diabetes mellitus 1.52 (1.15–2.02) 0.003
Hyperlipidaemia 1.49 (1.12–1.99) 0.006
Ischaemic heart disease 1.11 (0.84–1.47) 0.450
Left ventricular ejection fraction 0.98 (0.97–0.99) <0.001
Aortic valve area 0.93 (0.58–1.49) 0.756
Chronic kidney disease 1.96 (1.50–2.57) <0.001
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CI: confidence ratio, HR: hazard ratio

DISCUSSION

Similar to previous studies on severe AS, we demonstrated a significant prevalence of CKD (37.1%) in patients with moderate to severe AS, of which 5.5% (n = 40) of the study population had ESRD on dialysis.[4,25,26] These patients with CKD had more prominent cardiovascular risk factors and a worse echocardiographic profile, with increased LV mass and larger left atrial diameter and E: e’, despite showing a similar degree of AS severity. Furthermore, patients with concomitant CKD also had poorer clinical outcomes in the form of mortality and admissions for congestive cardiac failure. Despite this, they were less likely to have undergone aortic valve replacement.

Importantly, we demonstrated that the trends present in patients with severe AS also applied to patients with moderate to severe AS who are in the earlier course of disease. The reasons for the increased adverse outcomes would likely have been multifactorial. Firstly, the coexistence of CKD could accelerate the progression of AS and lead to more rapid clinical deterioration as a result of accelerated atherosclerosis and valve calcification.[11,12,13] In fact, CKD has been consistently described as an independent risk factor for mortality in patients with severe AS.[27,28]

Furthermore, CKD also may have direct effects on myocardial function. In our patients with concomitant CKD in AS, we found a distinct echocardiographic profile that is different from those without CKD. Although the severity of AS as measured by the aortic valve area and transaortic pressure gradients was similar, these patients demonstrated evidence of increased LV mass and slightly lower LVEF. The septal E: e’ was also higher and may represent a component of diastolic dysfunction and increased LV filling pressure. In fact, CKD has been described to be associated with pathological LV remodelling and may lead to increased LV stiffness and, subsequently, diastolic dysfunction.[29,30] In patients with CKD and AS, several factors may have driven the pathological LV remodelling, including increased AS severity, CKD itself, or the underlying cause for the CKD, such as uncontrolled hypertension or diabetes mellitus. Indeed, all of these factors may have contributed to the development of diastolic dysfunction in this context and may also have precipitated the development of symptoms, which contributed to the adverse clinical outcomes.[31,32]

In addition to the above, both AS and CKD have been described as independent risk factors for severe life-threatening events such as stroke, myocardial infarction and congestive cardiac failure.[33] The pathophysiology for this may be related to more rapid atherosclerosis, but intensive therapy with statins to lower the lipid levels and retard the progression of atherosclerotic disease has only shown attenuated results.[34] While earlier retrospective and observation studies may have demonstrated lower valve calcification in patients treated with statins, large and well-controlled prospective randomised controlled trials have consistently failed to show a benefit of statin therapy in those with severe AS.[35]

Optimal therapy for AS may also be limited by advanced CKD and ESRD. For example, symptom status such as shortness of breath or reduced effort tolerance may be difficult to interpret in patients with both AS and CKD, as both diseases may contribute to the symptoms described. Determination of a patient’s symptom status has important implications on the timing of valve replacement.[36]

Moreover, patients with advanced CKD are at higher risk of complications when they undergo valve replacement. These include perioperative complications and long-term complications such as difficulty with anticoagulation and increased bleeding risk after valve replacement due to anaemia and platelet dysfunction, which may be attributed to the CKD.[37] For patients who are unable to tolerate valve replacement surgery, TAVR has been described to be a viable alternative with comparable outcomes.[38] Shorter length of hospital stay and faster recovery make TAVR more affordable than surgical valve replacement.[39] However, even with the less-invasive TAVR, patients with CKD still experience more adverse clinical outcomes and both short- and long-term mortality.[40,41]

It would appear that CKD constitutes an important comorbidity in patients with AS, affecting the natural history, complicating the management and limiting the therapeutic options for patients with AS. Our study remained exploratory and demonstrated a strong association between CKD and adverse clinical outcomes in moderate to severe AS. Further prospective studies examining the role and timing of valve intervention in patients with concomitant CKD and AS would be warranted to guide prognostication and optimal therapeutic options in this group of patients. The cohort examined was from a single centre, but it was a moderately sized cohort of patients with moderate to severe AS. Although prospective in terms of clinical outcomes, the study examined one echocardiographic study cross-sectionally, which means that the data was subject to lead-time bias, where patients may have been at different time points along the course of their disease. Furthermore, although we compared clinical outcomes such as mortality and admissions for congestive cardiac failure and aortic valve replacement, we did not look at serial echocardiographic studies for progression of aortic valve disease or serial measurements of serum creatinine for deterioration of renal function over time. AVA was not shown to be a predictor of adverse outcome, but this may have been limited by the study’s small proportion of patients with severe AS (30.7%) and exclusion of the full spectrum of patients with AS (e.g. mild AS).

As this study was cross-sectional, there was no prospective patient follow-up on the progression of CKD or AS. Future prospective studies are vital to systemically assess and correlate the echocardiographic progression of AS with the progression of CKD. Indeed, in advanced CKD, we may have expected accelerated progression of AS. These patients may have been more likely to undergo aortic valve replacement. However, we were not able to demonstrate this trend. Patients with advanced CKD could have been deemed unfit for surgical valve replacement or intervention, as they may be frail or have multiple comorbidities. In some cases, the patients themselves may have declined intervention for the underlying AS.

Furthermore, patients in the group with no CKD may have developed CKD during the course of follow-up, but this had not been accounted for. Nevertheless, we demonstrated striking trends of adverse clinical outcomes in CKD patients with moderate to severe AS compared to those with normal kidney function at the time of AS diagnosis.

In conclusion, CKD is common in patients with moderate to severe AS and is associated with increased mortality, more frequent admissions for cardiac failure and a lower incidence of aortic valve replacement. Further studies are warranted to better prognosticate and guide therapy in this subgroup of patients.

Financial support and sponsorship

Sia CH was supported by the National University of Singapore Yong Loo Lin School of Medicine’s Junior Academic Faculty Scheme.

Conflicts of interest

Poh KK and Sia CH are members of the SMJ Editorial Board.

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