Cardiac Remodeling in Chronic Kidney Disease

Kaesler, Nadine; Babler, Anne; Floege, Jürgen; Kramann, Rafael

doi:10.3390/toxins12030161

Cited by 95 publications

(77 citation statements)

References 106 publications

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“…Furthermore, as in rodents, accelerated senescence was confirmed in ADMSCs isolated from patients with CKD as compared to those from healthy kidney donors by the findings of higher expression of DNA damage markers γH2AX and 53BP1 as well as CDKN2A and higher percentage of SA‐β‐gal‐positive cells resulting in the upregulation in SASP genes. Our observations showing that CKD causes MSCs to undergo cellular senescence are in accordance with the findings that uremic toxin or hyperphosphatemia can induce senescence of vascular smooth muscle cells (Muteliefu et al, 2012; Takemura et al, 2011; Troyano et al, 2015) or myoblasts (Sosa et al, 2018), which have been suggested as potential mechanisms of cardio‐renal cross talk (Hénaut et al, 2018; Kaesler et al, 2020) or sarcopenia associated with CKD (Sosa et al, 2018).…”

Section: Discussionsupporting

confidence: 90%

Metformin inhibits chronic kidney disease‐induced DNA damage and senescence of mesenchymal stem cells

Kim

Yu²,

Lee

et al. 2021

Aging Cell

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Mesenchymal stem cells (MSCs) are promising source of cell‐based regenerative therapy. In consideration of the risk of allosensitization, autologous MSC‐based therapy is preferred over allogenic transplantation in patients with chronic kidney disease (CKD). However, it remains uncertain whether adequate cell functionality is maintained under uremic conditions. As chronic inflammation and oxidative stress in CKD may lead to the accumulation of senescent cells, we investigated cellular senescence of CKD MSCs and determined the effects of metformin on CKD‐associated cellular senescence in bone marrow MSCs from sham‐operated and subtotal nephrectomized mice and further explored in adipose tissue‐derived MSCs from healthy kidney donors and patients with CKD. CKD MSCs showed reduced proliferation, accelerated senescence, and increased DNA damage as compared to control MSCs. These changes were significantly attenuated following metformin treatment. Lipopolysaccharide and transforming growth factor β1‐treated HK2 cells showed lower tubular expression of proinflammatory and fibrogenesis markers upon co‐culture with metformin‐treated CKD MSCs than with untreated CKD MSCs, suggestive of enhanced paracrine action of CKD MSCs mediated by metformin. In unilateral ureteral obstruction kidneys, metformin‐treated CKD MSCs more effectively attenuated inflammation and fibrosis as compared to untreated CKD MSCs. Thus, metformin preconditioning may exhibit a therapeutic benefit by targeting accelerated senescence of CKD MSCs.

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Section: Discussionsupporting

confidence: 90%

Metformin inhibits chronic kidney disease‐induced DNA damage and senescence of mesenchymal stem cells

Kim

Yu²,

Lee

et al. 2021

Aging Cell

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“…Either the differences in residual gradients are too small to have a meaningful clinical relevance or other factors such as AF or baseline LVMI have a much greater effect on remodeling than these prosthesis parameters. In the present study, AF patients had more often chronic renal failure, which is known to be associated with LV hypertrophy and fibrosis [30]. This might be another factor for the limited reverse remodeling process in those with AF.…”

Section: Discussionmentioning

confidence: 53%

Impact of sinus rhythm versus atrial fibrillation on left ventricular remodeling after transcatheter aortic valve replacement

et al. 2021

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Aims Atrial fibrillation (AF) is associated with increased mortality after transcatheter aortic valve replacement (TAVR). Cerebrovascular complications and bleeding events associated with anticoagulation therapy are discussed to be possible causes for this increased mortality. The present study sought to assess whether AF is associated with impaired left ventricular (LV) reverse remodeling representing another possible mechanism for poor outcome. Methods All patients who underwent TAVR in our institution and had 1-year echocardiography follow-up were included. LV mass index (LVMI) at baseline and follow-up as well as LVMI change at 1 year were assessed with respect to the presence of AF (either at baseline or during hospitalization after TAVR) and sinus rhythm (SR). Results A total of 213 patients (n = 95 in AF; n = 118 in SR) were enrolled in the present study. Patients with AF had higher LVMI at 1 year compared to those with SR (173 ± 61 g/m2 vs. 154 ± 55 g/m2; p = 0.02) and they showed lower relative LVMI change at 1 year (− 2 ± 28% vs. − 9 ± 29%; p = 0.04). In linear regression analysis, AF was independently associated with relative LVMI change (regression coefficient ß 0.076 [95% CI 0.001–0.150]; p = 0.04). With respect to clinical outcome depending on AF and LVMI regression, the Kaplan–Meier estimated event-free of death or cardiac rehospitalization at 3 years was lowest among patients with AF and no LVMI regression. Conclusions The present study identified a significant association of AF with changes in LVMI after TAVR, which was also shown to be associated with clinical outcome.

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“…The QTpe interval at all leads and QRS duration were shortened after HD. Patients with a longer uremic toxins, and corrects electrolyte imbalance [30,32], and this might shorten the QTpe interval. A recent study reported no differences in QTpe intervals between the SCD and survivor groups among HD patients, similar to our results [33].…”

Section: Discussionmentioning

confidence: 99%

“…Our hypothesis to explain these ndings is as follows. Chronic kidney disease frequently causes cardiac remodeling with hypertrophy, capillary loss, and brosis [30]. Progression of myocardial brosis could lead to increased dispersion of repolarization and an increased QTpe interval on ECG [31].…”

Section: Comparison With Other Studies: An Explanatory Hypothesismentioning

confidence: 99%

Clinical Associations Between Serial Electrocardiography Measurements and Sudden Cardiac Death in Patients with End-Stage Renal Disease Undergoing Hemodialysis: Multi-Center, Retrospective Cohort Study

et al. 2020

Preprint

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BackgroundThe rate of sudden cardiac death (SCD) for hemodialysis (HD) patients is significantly higher than that observed in the general population and have the highest risk for arrhythmogenic death. In this study, we examined serial electrocardiography (ECG) data in patients undergoing HD and determined their associations with the occurrence of SCD.Method In the retrospective review of three tertiary referral hospitals from November 1986 to November 2016, Patients starting HD in each hospital were enrolled; they underwent regular check-ups at least twice a Measurements and Main Results Of 678 enrolled subjects who underwent serial ECG before and after HD, 291 died and 39 developed SCD. In the pre-HD ECG, SCD patients had significantly longer QT peak-to-end (QTpe) intervals in all leads (II, III, aVF, and V1-6, P<0.001) and a longer QRS duration (92.6±14.0 vs. 100.6±14.9 ms, P=0.015) than survivors. However, in the post-HD ECG, there were no significant differences in any of the variables (QTpe interval at all leads, QRS duration, and proportion of patients with atrial fibrillation) that showed differences in the pre-HD ECG analysis. Moreover, the SCD group showed a significant change in the QTpe interval of the inferior, anterior, and lateral leads before and after HD compared with the survivor group (all leads, P<0.001). A cut-off value of 148.1 ms for the QTpe interval at the V2 lead in pre-HD was determined using receiver operating characteristic curve analysis, and QTpe intervals >148.1 ms were significantly associated with SCD after adjusting for age and sex in multivariable analysis (hazard ratio: 5.675, confidence interval: 2.373–13.575).Conclusions In end-stage kidney disease patients, the QTpe interval at all leads and QRS duration were shortened after HD. Patients with a longer QTpe interval before HD and large changes in ECG parameters after HD might be at a higher risk of SCD. Therefore, changes in the ECG before and after HD could help to predict SCD.

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Cardiac Remodeling in Chronic Kidney Disease

Cited by 95 publications

References 106 publications

Metformin inhibits chronic kidney disease‐induced DNA damage and senescence of mesenchymal stem cells

Metformin inhibits chronic kidney disease‐induced DNA damage and senescence of mesenchymal stem cells

Impact of sinus rhythm versus atrial fibrillation on left ventricular remodeling after transcatheter aortic valve replacement

Clinical Associations Between Serial Electrocardiography Measurements and Sudden Cardiac Death in Patients with End-Stage Renal Disease Undergoing Hemodialysis: Multi-Center, Retrospective Cohort Study

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