Characterizing Cardiac Involvement in Chronic Kidney Disease Using CMR—a Systematic Review

Mangion, Kenneth; McDowell, Kirsty; Mark, Patrick B.; Rutherford, Elaine

doi:10.1007/s12410-018-9441-9

Cited by 15 publications

(17 citation statements)

References 63 publications

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“…To the best of our knowledge, our study is the largest observational prospective study using in-depth and comprehensive characterization of CVD in CKD, providing novel pathophysiological insights that might shed light to the excess of CVD in CKD [2]. Several previous studies reported on T1 mapping in the CKD patients, generally revealing significantly higher values compared to controls, which were reproducible and unaffected by the fluid status [27,28].…”

Section: Discussionmentioning

confidence: 98%

“…Premature cardiovascular disease (CVD) is the leading cause of death in patients with kidney disease (CKD) [[1], [2], [3]], which is only partially explained by the effects of traditional CV risk factors and atherothrombotic coronary vascular complications. The non-atherosclerotic myocardial processes, which are intrinsically linked to marked structural and functional abnormalities include profound hypertrophic and interstitial remodeling and deposition of myocardial fibrosis [1], often referred to as ‘uremic cardiomyopathy’ [2]. Progression of CKD is associated with marked increase of risk of adverse events, including arrhythmia, sudden cardiac death and heart failure (HF) [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…The non-atherosclerotic myocardial processes, which are intrinsically linked to marked structural and functional abnormalities include profound hypertrophic and interstitial remodeling and deposition of myocardial fibrosis [1], often referred to as ‘uremic cardiomyopathy’ [2]. Progression of CKD is associated with marked increase of risk of adverse events, including arrhythmia, sudden cardiac death and heart failure (HF) [2,3]. Earlier recognition and timely management of structural myocardial changes represent essential steps towards improving the morbidity and mortality of CKD patients.…”

Section: Introductionmentioning

confidence: 99%

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Aortic stiffness is independently associated with interstitial myocardial fibrosis by native T1 and accelerated in the presence of chronic kidney disease

Chen

Arcari

Engel

et al. 2019

IJC Heart & Vasculature

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Background Patients with chronic kidney disease (CKD) have considerable cardiovascular morbidity and mortality. Aortic stiffness is an independent predictor of cardiovascular risk and related to left ventricular remodeling and heart failure. Myocardial fibrosis is the pathophysiological hallmark of the failing heart. Methods and results An observational study of consecutive CKD patients ( n = 276) undergoing comprehensive clinical cardiovascular magnetic resonance imaging. The relationship between aortic stiffness, myocardial fibrosis, left ventricular remodeling and the severity of chronic kidney disease was examined. Compared to age-gender matched controls with no known kidney disease ( n = 242), CKD patients had considerably higher myocardial native T1 and central aortic PWV ( p ≪ 0.001), as well as abnormal diastolic relaxation by E/e′ (mean) by echocardiography ( p ≪ 0.01). A third of all patients had LGE, with similar proportions for the presence and the (ischaemic and non-ischaemic) pattern between the groups. PWV was strongly associated with and age, NT-proBNP and native T1 in both groups, but not with LGE presence or type; the associations were amplified in severe CKD stages. In multivariate analyses, PWV was independently associated with native T1 in both groups ( p ≪ 0.01) with near two-fold increase in adjusted R 2 in the presence of CKD (native T1 (10 ms) R 2 , B(95%CI) CKD vs. non-CKD 0.28, 0.2(0.15–0.25) vs. 0.18, 0.1(0.06–0.15), p ≪ 0.01). Conclusions Aortic stiffness and interstitial myocardial fibrosis are interrelated; this association is accelerated in the presence of CKD, but independent of LGE. Our findings reiterate the significant contribution of CKD-related factors to the pathophysiology of cardiovascular remodeling.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Aortic stiffness is independently associated with interstitial myocardial fibrosis by native T1 and accelerated in the presence of chronic kidney disease

Chen

Arcari

Engel

et al. 2019

IJC Heart & Vasculature

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“…According to the glomerular filtration rate (GFR) test, CKD is classified into five stages and patients with CKD in the 5th stage, which is also known as end‐stage‐kidney‐disease (ESKD), may need kidney replacement therapy . The continued development of CKD results in the increased risk of cardiovascular (CV) disease and may even lead to sudden cardiac death and heart failure . The major challenge of the CKD treatment is that there were no early clinical symptoms before CKD develops to the irreversible damage phase .…”

Section: Introductionmentioning

confidence: 99%

microRNA‐206 overexpression inhibits epithelial‐mesenchymal transition and glomerulosclerosis in rats with chronic kidney disease by inhibiting JAK/STAT signaling pathway

Zhao

Shen

Gao

et al. 2019

J of Cellular Biochemistry

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Chronic kidney disease (CKD) is a traumatic disease with significant psychic consequences to the patient's overall physical condition. microRNA‐206 (miR‐206) has been reported to play an essential role in the development of various diseases. The purpose of the present study is to investigate the effect of miR‐206 through the JAK/STAT signaling pathway on epithelial‐mesenchymal transition (EMT) of renal tubular epithelial cells and glomerulosclerosis in rats with CKD. The targeting relationship between miR‐206 and ANXA1 was verified. To explore the role of miR‐206 in CKD, the model of CKD rats was established to detect glomerular sclerosis index (GSI), contents of interleukin‐6 (IL‐6) and transforming growth factor‐beta1 (TGF‐β1), and expression of type IV collagen. Moreover, to further determine the roles of both miR‐206 and the JAK/STAT signaling pathway in CKD, the gain‐ and loss‐of function approaches were performed with the expression of ANXA1, α‐SMA, E‐cadherin, vimentin, N‐cadherin, and the JAK/STAT signaling pathway‐related genes detected. miR‐206 negatively targeted ANXA1. Overexpressed miR‐206 inhibited the degeneration and interstitial fibrosis of renal tubular epithelial cells, decreased GSI of rats, and the expression of type IV collagen, TGF‐β1 and IL‐6. Overexpressed miR‐206 inhibited the degeneration of renal tubular epithelial cells, the expression of ANXA1, α‐SMA, TGF‐β1, p‐STAT3, STAT3, p‐STAT1, STAT1, p‐JAK2, and JAK2, while promoted the expression of E‐cadherin. Taken together the results, miR‐206 inhibits EMT of renal tubular epithelial cells and glomerulosclerosis by inactivating the JAK/STAT signaling pathway via ANXA1 in CKD.

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“… 6 Evidence from echocardiography and cardiac magnetic resonance (CMR) imaging studies suggests that adverse cardiac structural and functional change in CKD including elevated left ventricular (LV) mass begins early in CKD. 7 – 9 …”

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confidence: 99%

Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors at 5 Years

et al. 2021

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Kidney donation reduces renal function by ≈30% allowing study of the cardiovascular effects of a reduced estimated glomerular filtration rate without comorbidities. We report 5-year results of a longitudinal, parallel-group, blinded end-point study of living kidney donors (n=50) and healthy controls (n=45). The primary end point, left ventricular mass, was measured using cardiac magnetic resonance. Secondary end points, 24-hour ambulatory blood pressure, and pulse wave velocity were measured using validated blood pressure monitors and the SphygmoCor device. Effect sizes were calculated as differences between change from baseline in the donor and control groups. In donors, estimated glomerular filtration rate was 95±15 mL/min per 1.73 m2 at baseline (predonation) and 67±14 mL/min per 1.73 m2 at 5 years. In controls, there was a −1±2 mL/min per 1.73 m2 decline per annum. Change in left ventricular mass at 5 years was not significantly different between donors and controls (mean difference, +0.40 g [95% CI, −4.68 to 5.49] P =0.876), despite an initial increase in mass in donors compared with controls at 12 months. Pulse wave velocity, which increased in donors at 12 months, returned to levels not different from controls at 5 years (mean difference, −0.24 m/s [95% CI, −0.69 to 0.21]). Change in ambulatory systolic blood pressure was not different in donors compared with controls (mean difference, +1.91 mm Hg [95% CI, −2.72 to 6.54]). We found no evidence that the reduction in estimated glomerular filtration rate after kidney donation was associated with a change in left ventricular mass detectable by magnetic resonance imaging at 5 years.

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Characterizing Cardiac Involvement in Chronic Kidney Disease Using CMR—a Systematic Review

Cited by 15 publications

References 63 publications

Aortic stiffness is independently associated with interstitial myocardial fibrosis by native T1 and accelerated in the presence of chronic kidney disease

Aortic stiffness is independently associated with interstitial myocardial fibrosis by native T1 and accelerated in the presence of chronic kidney disease

microRNA‐206 overexpression inhibits epithelial‐mesenchymal transition and glomerulosclerosis in rats with chronic kidney disease by inhibiting JAK/STAT signaling pathway

Cardiovascular Effects of Unilateral Nephrectomy in Living Kidney Donors at 5 Years

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