Reduced Estimated GFR and Cardiac Remodeling: A Population-Based Autopsy Study

Izumaru, Kensuke; Hata, Jun; Nakano, Toshiaki; Nakashima, Yutaka; Nagata, Michio; Fukuhara, Mikio; Oda, Yoshinao; Kitazono, Takanari; Ninomiya, Toshiharu

doi:10.1053/j.ajkd.2019.02.013

Cited by 39 publications

(39 citation statements)

References 39 publications

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“…Because of the high prevalence of MF in patients with CKD and the direct correlation existing between the degree of impairment of kidney function and the severity of MF [9][10][11], it has been proposed that pro-fibrotic factors or pathways linked to CKD could exist [22]. Although we did not investigated mechanisms of mMF in the current study, some experimental and clinical evidence point to the matricellular protein osteopontin as a potential candidate.…”

Section: Discussionmentioning

confidence: 89%

“…In fact, a recent study has shown that CKD is related to cardiac remodeling, significantly impaired cardiac function and, worse outcomes in HFpEF patients, of whom > 80% were hypertensive [8]. Several post-mortem studies have shown MF in patients with CKD [9][10][11], and it has been proposed that the development of LV diastolic dysfunction (LVDD) and subsequent HFpEF in CKD patients is related to MF [12]. Although some studies have explored MF in patients with end-stage CKD using circulating collagen-related biomarkers [13,14], no information is available on serum PICP and CITP/MMP-1 ratio in CKD patients with HF.…”

Section: Introductionmentioning

confidence: 99%

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Does Chronic Kidney Disease Facilitate Malignant Myocardial Fibrosis in Heart Failure with Preserved Ejection Fraction of Hypertensive Origin?

Eirós

Romero‐González

Gavira

et al. 2020

JCM

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In hypertensive patients with heart failure (HF) a serum biomarker combination of high carboxy-terminal propeptide of procollagen type-I (PICP) and low carboxy-terminal telopeptide of collagen type-I to matrix metalloproteinase-1 (CITP:MMP-1) ratio identifies a histomolecular phenotype of malignant myocardial fibrosis (mMF) associated with severe diastolic dysfunction (DD) and poor outcomes. As chronic kidney disease (CKD) facilitates MF and DD, we investigated the influence of CKD on the mMF biomarker combination in HF patients with preserved ejection fraction (HFpEF). Hypertensives (n = 365), 232 non-HF and 133 HFpEF, were studied, and 35% non-HF and 46% HFpEF patients had CKD (estimated glomerular filtration rate < 60 mL/min/1.73 m2 or urine albumin-to-creatinine ratio ≥ 30 mg/g). Specific immunoassays were performed to determine biomarkers. Medians were used to establish the high PICP and low CITP:MMP-1 combination. A comparison with non-HF showed that the biomarker combination presence was increased in HFpEF patients, being associated with CKD in all patients. CKD influenced the association of the biomarker combination and HFpEF (p for interaction ≤ 0.019). The E:e’ ratio was associated with the biomarker combination in CKD patients. Among CKD patients with HFpEF, those with the biomarker combination exhibited higher (p = 0.016) E:e’ ratio than those without the pattern. These findings suggest that CKD facilitates the development of biomarker-assessed mMF and DD in hypertensive HFpEF patients.

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Does Chronic Kidney Disease Facilitate Malignant Myocardial Fibrosis in Heart Failure with Preserved Ejection Fraction of Hypertensive Origin?

Eirós

Romero‐González

Gavira

et al. 2020

JCM

View full text Add to dashboard Cite

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“…LVH can occur early in the course of CKD, even when the glomerular filtration rate (GFR) is still normal [16]. Once GFR is reduced, myocytes enlarge and cardiomyocytes expand, leading to LVH [17]. Cardiomyocytes are the major cell type, comprising about 70-85% of the total volume.…”

Section: Left-ventricular Hypertrophy In Ckdmentioning

confidence: 99%

“…Cardiomyocytes are the major cell type, comprising about 70-85% of the total volume. They generate contractility by cyclic calcium fluxes [17,18]. Fibroblasts secrete collagen precursors and matrix metalloproteinases (MMPs) and thereby actively remodel the ECM [17][18][19].…”

Section: Left-ventricular Hypertrophy In Ckdmentioning

confidence: 99%

Cardiac Remodeling in Chronic Kidney Disease

Kaesler

Babler

Floege

et al. 2020

Toxins

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Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.

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“…Multiple pathophysiological explanations have been proposed in favour of a causal link underlying the adverse cardiovascular profile of CKD patients [1,24]. These include increased intravascular calcium phosphate deposition and coronary artery calcification, [25][26][27] arterial stiffness, enhanced coagulability, endothelial dysfunction, increased subclinical inflammation, [28] volume overload [29], and left ventricular remodeling and dysfunction [30,31]. In addition, patients with CKD undergoing percutaneous coronary intervention for an acute coronary syndrome have been shown to have less complete revascularization, a condition associated with a poorer prognosis [32].…”

Section: Discussionmentioning

confidence: 99%

Chronic Kidney Disease Has a Graded Association with Death and Cardiovascular Outcomes in Stable Coronary Artery Disease: An Analysis of 21,911 Patients from the CLARIFY Registry

Vidal‐Petiot

Greenlaw

Kalra

et al. 2019

JCM

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Chronic kidney disease (CKD) is associated with an increased cardiovascular risk in a broad spectrum of populations. However, the risk associated with a reduced estimated glomerular filtration rate (eGFR) in patients with stable coronary artery disease receiving standard care in the modern era, independently of baseline cardiovascular disease, risk factors, and comorbidities, remains unclear. We analyzed data from 21,911 patients with stable coronary artery disease, enrolled in 45 countries between November 2009 and July 2010 in the CLARIFY registry. Patients with abnormal renal function were older, with more comorbidities, and received slightly lower-although overall high-rates of evidence-based secondary prevention therapies than patients with normal renal function. The event rate of patients with CKD stage 3b or more (eGFR <45 mL/min/1.73 m 2 ) was much higher than that associated with any comorbid condition. In a multivariable adjusted Cox proportional hazards model, lower eGFR was independently associated with a graded increased risk of cardiovascular mortality, with adjusted HRs (95% CI) of 0.98 (0., and <30 mL/min/1.73 m 2 , compared with eGFR ≥90 mL/min/1.73 m 2 . A strong graded independent relationship exists between the degree of CKD and cardiovascular mortality in this large cohort of patients with chronic coronary artery disease, despite high rates of secondary prevention therapies. Among clinical risk factors and comorbid conditions, CKD stage 3b or more is associated with the highest cardiovascular mortality.

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Reduced Estimated GFR and Cardiac Remodeling: A Population-Based Autopsy Study

Cited by 39 publications

References 39 publications

Does Chronic Kidney Disease Facilitate Malignant Myocardial Fibrosis in Heart Failure with Preserved Ejection Fraction of Hypertensive Origin?

Does Chronic Kidney Disease Facilitate Malignant Myocardial Fibrosis in Heart Failure with Preserved Ejection Fraction of Hypertensive Origin?

Cardiac Remodeling in Chronic Kidney Disease

Chronic Kidney Disease Has a Graded Association with Death and Cardiovascular Outcomes in Stable Coronary Artery Disease: An Analysis of 21,911 Patients from the CLARIFY Registry

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