Rapid Fire Session

Session: Rapid Fire Session 4: Analysis, Machine Learning II (Monitor 6)

Redefining the cardiac phenotype of uraemic cardiomyopathy: Insights from contrast enhanced CMR

Friday, February 6, 2026

4:13 PM - 4:20 PM

Location: Galapagos / Aruba / Ilhabela (2nd Lower Level)

Presenting Author(s)

TA

Thomas Anderton, MD

Clinical Research Fellow
University of Leeds
Leeds, England, United Kingdom

Primary Author(s)

TA

Thomas Anderton, MD

Clinical Research Fellow
University of Leeds
Leeds, England, United Kingdom

Co-Author(s)

Bradley Chambers

Clinical Research Fellow
University of Leeds
Harewood, England, United Kingdom
Maryum Farooq, MB

Research Fellow
Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds
Leeds, England, United Kingdom
RT

Raluca Tomoaia, MD, PhD

Research Fellow
University of Leeds
Leeds, England, United Kingdom
CY

Chin Yit Soo, MD

Clinical Research Fellow
University of Leeds
Leeds, England, United Kingdom
ML

May Lwin, MD

Clinical Research Fellow
University of Leeds
Leeds, England, United Kingdom
MA

Mehak Asad, MD, MPH

Clinical research fellow
University of Leeds, Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, LS2 9JT, United Kingdom
Leeds, England, United Kingdom
MG

Michelle Gibbs

Medical Student
University of Leeds, England, United Kingdom
SS

Stan Schofield, MB

Doctor
University of Leeds, United Kingdom
ED

Erica Dall'Armellina, PhD

Associate Professor and Honorary Consultant Cardiologist
University of Leeds, England, United Kingdom
Sven Plein, MD, PhD

Professor of Cardiology
Leeds Institute of Cardiovascular and Metabolic Medicine
Leeds, England, United Kingdom
SC

Shanmugakumar Chinnappa, PhD

Consultant Nephrologist
University of Leeds, United Kingdom
Peter P. Swoboda, PhD

Consultant Cardiologist
Leeds Institute of Cardiovascular and Metabolic Medicine
Leeds, England, United Kingdom

Background: Patients with advanced chronic kidney disease (CKD) (eGFR < 30) have increased risk of heart failure (termed uraemic cardiomyopathy) with HR 3.24 compared to eGFR >90(1). There is particularly high risk of cardiovascular death in the weeks after haemodialysis initiation(2). Concentric left ventricular hypertrophy, diastolic dysfunction and fibrosis with a heart failure with preserved ejection fraction (HFpEF) pattern is commonly reported(3). The prevalence of coronary artery disease is reported to be high, though studies have primarily used SPECT(4).

Due to historic concerns regarding older, linear gadolinium agents, people with advanced CKD have been universally excluded from prospective contrast enhanced cardiovascular magnetic resonance (CMR) studies, other than in the setting of haemodialysis.

We aimed to describe the cardiac phenotype of patients with advanced, pre-dialysis CKD using multiparametric gadolinium enhanced CMR.

Methods: We screened and prospectively recruited patients under follow up from nephrology clinics. Exclusion criteria included ischaemic heart disease, heart failure diagnosis and current or previous renal replacement therapy. All attended for clinical assessment, bloods and CMR (Siemens Prisma 3T). CMR included cine, T1, T2 and extracellular volume (ECV) mapping, quantitative stress/rest perfusion(5) and late gadolinium enhancement (LGE). The CMR study was completed using a total of 0.1mmol/kg of Gadobutrol.

Participants were grouped according to their CKD level (3b/4/5). ANOVA was used to compare normally distributed variables, chi-squared was used to compare proportions.

Results: We recruited 106 patients with 98 consenting to gadolinium. The groups were matched for age, cardiac risk factors and medication use.

With declining eGFR, there was progressive LV cavity dilatation and eccentric remodelling, with mass/volume index unchanged. Stroke volume and cardiac output were significantly increased in keeping with a high-output state. Markers of HFpEF were not present; global longitudinal strain and left atrial area/function did not change with decreasing eGFR.

Parametric mapping revealed a prolonged native T1 and increased ECV, with QP values showing a significantly higher rMBF with corresponding fall in MPR (though not after rate pressure product correction), with sMBF unchanged.

Evidence of significant CAD (infarction or inducible ischaemia) was only 10% in the whole cohort, which was lower than anticipated, and was primarily seen in CKD 5 patients.

Conclusion: This pattern of cavity dilatation, eccentric LVH, high stroke volumes, and diffuse fibrosis is in keeping with high-output heart failure rather than the HFpEF phenotype which has been previously reported. Given the high cardiovascular risk in this patient group, we propose that CMR could have a role in risk stratification of patients commencing renal replacement therapy and transplantation.

Table 1

All

N= 106

CKD 3b

N= 20

CKD 4

N= 51

CKD 5

N= 35

p-value

3b vs 5

4 vs 5

Demographics

Age

(years)

(±15)

(±17)

(±13)

0.212

0.271

Male

(n)

(74%)

(50%)

(83%)

(74%)

0.071

0.369

BSA

1.97

(±0.25)

1.91

(±0.21)

1.98

(±0.24)

1.99

(±0.27)

0.246

0.9388

Laboratory results

eGFR

20.5

(±9.5)

36.5

(±3.7)

20.3

(±4.6)

11.7

(±2.7)

< 0.001

Creatinine

308

(±129)

149

(±28)

276

(±57)

442

(±106)

< 0.001

Urea

21.3

(±22.3)

12.0

(±2.4)

22.3

(±31.1)

25.4

(±8.7)

< 0.001

Hct

0.38

(±0.05)

0.41

(±0.04)

0.39

(±0.05)

0.36

(±0.06)

0.002

0.003

NTProBNP

840

(±1121)

278

(±414)

686

(±852)

1283

(±1464)

0.015

0.020

Urine Alb/Cr ratio

66.2

(±83.1)

20.8

(±35.4)

66.0

(±75.0)

93.2

(±103.4)

0.005

0.162

Medical History

HTN

(72%)

(65%)

(74%)

0.470

0.860

(22%)

(15%)

(28%)

(26%)

0.359

0.860

Type 2

(88%)

(100%)

(93%)

(78%)

0.540

0.691

Dyslipidemia

(44%)

(50%)

(46%)

(37%)

0.571

0.465

Current/past Smoker (n)

(45%)

(40%)

(54%)

(37%)

0.899

0.158

Hemodynamics

(bpm)

(±11)

(±10)

(±11)

0.042

0.008

Systolic BP

(mmHg)

137

(±22)

128

(±19)

136

(±20)

143

(±24)

0.038

0.143

Diastolic BP

(mmHg)

(±9)

(±6)

(±9)

(±11)

0.408

0.288

CMR

LVEDV/BSA

(ml/m²)

82.7

(±18.4)

(±13)

(±18)

(±19)

0.001

0.021

LV SV/BSA

(ml/m²)

48.5

(±11.2)

44.8

(±7.7)

46.9

(±11.4)

53.0

(±11.4)

0.006

0.017

LVEF

(%)

59.7

(±7.0)

61.1

(±4.3)

59.0

(±7.8)

60.1

(±7.0)

0.570

0.524

Cardiac Output

(L/min)

5.72

(±2.79)

3.79

(±2.80)

5.63

(±2.24)

6.73

(±3.15)

0.001

0.061

LV Mass/BSA (Dias.) (g/m²)

57.2

(±11.9)

50.3

(±9.2)

56.2

(±10.3)

62.6

(±13.2)

< 0.001

0.010

LV Mass Volume Index. (g/ml)

0.71

(±0.13)

0.68

(±0.11)

0.72

(±0.14)

0.70

(±0.13)

0.561

0.679

RVEDV/BSA

(ml/m²)

(±19)

(±15)

(±22)

(±16)

0.069

0.206

RV SV/BSA

(ml/m²)

44.1

(±12.0)

42.0

(±7.6)

41.3

(±13.6)

49.3

(±9.8)

0.006

0.004

RV EF

(%)

61.1

(±8.2)

61.0

(±6.5)

60.0

(±9.1)

62.8

(±7.6)

0.377

0.159

LA Vol/BSA

(ml/m²)

42.3

(±16.4)

40.2

(±15.8)

41.0

(±15.6)

45.5

(±17.8)

0.275

0.227

LA EF

(%)

55.8

(±15.1)

55.2

(±14.0)

53.9

(±15.3)

58.8

(±15.4)

0.405

0.154

PCWP

(mmHg)

14.6

(±2.7)

13.4

(±1.6)

14.4

(±2.4)

15.4

(±3.3)

0.026

0.124

Native T1

(ms)

1321

(±41)

1304

(±49)

1320

(±40)

1332

(±35)

0.020

0.183

(ms)

(±3)

(±2)

(±3)

0.254

0.433

GLS

(%)

-15.5

(±3.19)

-16.6

(±1.9)

-15.2

(±3.7)

-15.3

(±2.9)

0.112

0.911

Contrast CMR

N=98

N=18

N=48

N=32

ECV

(%)

26.3

(±3.2)

25.1

(±3.4)

26.3

(±3.3)

27.2

(±2.9)

0.029

0.213

rMBF

(ml/g/min)

0.83

(±0.23)

0.73

(±0.18)

0.79

(±0.19)

0.94

(±0.24)

0.003

rMBFcorr

(ml/g/min)

0.93

(±0.27)

1.06

(±0.17)

0.90

(±0.24)

0.95

(±0.33)

0.352

0.418

sMBF

(ml/g/min)

2.05

(±0.66)

2.22

(±0.86)

1.97

(±0.65)

2.05

(±0.59)

0.430

0.599

MPR

2.59

(±0.94)

3.10

(±1.22)

2.59

(±0.84)

2.35

(±0.87)

0.026

0.246

MPRcorr

2.22

(±0.95)

2.28

(±1.14)

2.22

(±0.88)

2.20

(±1.03)

0.853

0.929

Regional Ischaemia

(7%)

(0%)

(22%)

0.022

< 0.001

Ischaemic LGE

(7%)

(0%)

(4%)

(16%)

0.072

0.083

Non-ischaemic LGE

(34%)

(22%)

(40%)

(31%)

0.435

0.409

BSA: Body surface area, BP: Blood pressure, corr: Values corrected to rate pressure product, DM: Diabetes Mellitus, ECV: Extracellular volume, EDV: End diastolic volume, EF: Ejection fraction, eGFR: Estimated glomerular filtration rate, g: Grams, GLS: Global longitudinal strain, Hct: Haematocrit, HR: Heart rate, HTN: Hypertension, LA: Left atrium LGE: Late gadolinium enhancement, LV: Left ventricle, MBF: Myocardial blood flow, ml: Millilitres, MPR: Myocardial perfusion reserve, PCWP: Pulmonary capillary wedge pressure, RV: Right ventricle, SV: Stroke volumeFigure 1 – CMR Assessment of advanced CKD: ‘Uraemic cardiomyopathy'
Figure 2 – Scatter plots and regression lines with confidence intervals of (clockwise from top left) LVEDV/BSA, Native T1, rMBF and sMBF against eGFR.