Influence of Coexisting Chronic Kidney Disease and Left Ventricular Hypertrophy on Changes in FGF23 and the Renin-Angiotensin-Aldosterone-System

2021 ◽  
Author(s):  
Kohei Okamoto ◽  
Hideki Fujii ◽  
Shunsuke Goto ◽  
Kentaro Watanabe ◽  
Keiji Kono ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Close Correlation ◽  
Left Ventricular ◽  
Heart Weight ◽  
Related Factors ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

Abstract Serum fibroblast growth factor 23 (FGF23) levels and the renin-angiotensin-aldosterone system (RAAS) are elevated in chronic kidney disease (CKD) patients, and their association with left ventricular hypertrophy (LVH) has been reported. However, whether the FGF23 elevation is the cause or result of LVH remains unclear. At 10 weeks, male C57BL/6J mice were divided into four groups: Sham, CKD (5/6 nephrectomy), LVH (transaortic constriction), and CKD/LVH group. At 16 weeks, the mice were sacrificed, and blood and urine, cardiac expressions of FGF23 and RAAS-related factors, and cardiac histological analyses were performed. Heart weight, serum FGF23 levels, and cardiac expression of FGF23 and RAAS-related factors, except for angiotensin-converting enzyme 2, more increased in the CKD/LVH group compared to the other groups. A significant correlation between LVH and cardiac expressions of FGF23 and RAAS-related factors was observed. Furthermore, there was a significantly close correlation of the cardiac expression of FGF23 with LVH and RAAS-related factors. The coexisting CKD and LVH increased serum and cardiac FGF23 and RAAS-related factors, and there was a significant correlation between them. A close correlation of cardiac, but not serum FGF23, with LVH and RAAS suggested that local FGF23 may be associated with LVH and the RAAS activation.

scholarly journals Changes of FGF23 and the Renin-Angiotensin-System in Male Mouse Models of Chronic Kidney Disease and Cardiac Hypertrophy

2021 ◽  
Author(s):  
Kohei Okamoto ◽  
Hideki Fujii ◽  
Kentaro Watanabe ◽  
Shunsuke Goto ◽  
Keiji Kono ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Renin Angiotensin System ◽  
Close Correlation ◽  
Left Ventricular ◽  
Heart Weight ◽  
Related Factors ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin

Abstract Serum fibroblast growth factor 23 (FGF23) levels and the renin-angiotensin-aldosterone system (RAAS) are elevated in chronic kidney disease (CKD) patients, and their association with left ventricular hypertrophy (LVH) has been reported. However, whether the FGF23 elevation is the cause or result of LVH remains unclear. At 10 weeks, male C57BL/6J mice were divided into four groups: Sham, CKD (5/6 nephrectomy), LVH (transaortic constriction), and CKD/LVH group. At 16 weeks, the mice were sacrificed, and blood and urine, cardiac expressions of FGF23 and RAAS-related factors, and cardiac histological analyses were performed. Heart weight, serum FGF23 levels, and cardiac expression of FGF23 and RAAS-related factors, except for angiotensin-converting enzyme 2, more increased in the CKD/LVH group compared to the other groups. A significant correlation between LVH and cardiac expressions of FGF23 and RAAS-related factors was observed. Furthermore, there was a significantly close correlation of the cardiac expression of FGF23 with LVH and RAAS-related factors. The coexisting CKD and LVH increased serum and cardiac FGF23 and RAAS-related factors, and there was a significant correlation between them. A close correlation of cardiac, but not serum FGF23, with LVH and RAAS suggested that local FGF23 levels may be associated with LVH and RAAS activation.

scholarly journals Echocardiographic assessment of left ventricular hypertrophy in patients of chronic kidney disease

2017 ◽  
Vol 5 (11) ◽  
pp. 4783 ◽  
Author(s):  
Bijaya K. Behera ◽  
Sanjay M.
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Serum Creatinine ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Mdrd Equation ◽  
Echocardiographic Assessment ◽  
Laboratory Investigations ◽  
Cardiovascular Evaluation

Background: Present study was conducted with an objective to study the prevalence of left ventricular hyper trophy (LVH) by echocardiography in patients with chronic kidney disease (CKD) and to find out correlation of left ventricular hypertrophy with severity of chronic kidney disease.Methods: From November 2012 to September 2014, 100 chronic kidney disease patients who were admitted in hospital or attended on OPD basis for dialysis were taken for study. Detailed history, clinical evaluation, laboratory investigations and echocardiography was carried out. The diagnosis of CKD was made on basis of serum creatinine more than 1.5 mg/dl which remained constantly for more than 3 months. Patients with mild, moderate and severe CKD were having serum creatinine level 1.5-3mg/dl, 3-6mg/dl and > 6mg/dl respectively. Glomerular filtration rate (GFR) was calculated by modification of diet in renal disease (MDRD) equation. Cut-off for CKD was taken to be <60ml/min / 1.73m2 as per existing guidelines.Results: Out of 100 patients studied, 67 were males and 33 were females. All patients were selected randomly. Majority of the patients were in the age group of 61 -70 years (41%). In the present study, it was found that left ventricular mass index (LVMI) which reflects LVH showed a progressive rise in severity of renal failure with 17 % of mild category of CKD having LVH as compared to 26% of moderate category and 57% of severe category of CKD.Conclusions: Patients with CKD have LVH, which is more marked in patients with severe CKD. So, these patients should have a thorough cardiovascular evaluation even if there were no symptoms, and efforts should be made to prevent LVH, during the early course of renal insufficiency, such as strict control of hypertension, anaemia.

scholarly journals MicroRNAs Regulating Renin–Angiotensin–Aldosterone System, Sympathetic Nervous System and Left Ventricular Hypertrophy in Systemic Arterial Hypertension

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1771
Author(s):  
Alex Cleber Improta-Caria ◽  
Marcela Gordilho Aras ◽  
Luca Nascimento ◽  
Ricardo Augusto Leoni De Sousa ◽  
Roque Aras-Júnior ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Left Ventricular Hypertrophy ◽  
Signaling Pathways ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Gene And Protein Expression ◽  
Sympathetic Nervous

MicroRNAs are small non-coding RNAs that regulate gene and protein expression. MicroRNAs also regulate several cellular processes such as proliferation, differentiation, cell cycle, apoptosis, among others. In this context, they play important roles in the human body and in the pathogenesis of diseases such as cancer, diabetes, obesity and hypertension. In hypertension, microRNAs act on the renin–angiotensin–aldosterone system, sympathetic nervous system and left ventricular hypertrophy, however the signaling pathways that interact in these processes and are regulated by microRNAs inducing hypertension and the worsening of the disease still need to be elucidated. Thus, the aim of this review is to analyze the pattern of expression of microRNAs in these processes and the possible associated signaling pathways.

scholarly journals Two in one: Neuregulin 1 improves cardiac diastolic and kindney funtcion in chronic kidney disease in rats

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Kiss ◽  
E Acar ◽  
S Watzinger ◽  
Z.S Kovacs ◽  
F Marvanykovi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Diastolic Dysfunction ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Low Grade ◽  
Funding Source ◽  
Neuregulin 1 ◽  
Expression Levels

Abstract Introduction The prevalence of chronic renal disease (CKD) is continuously increasing in developed countries. Uremic cardiomyopathy characterized by left ventricular hypertrophy (LVH) and diastolic dysfunction (DD) is a common cardiovascular complication of CKD. Cardiac microvascular low-grade inflammation and altered expression of endothelium derived Neuregulin-1 (NRG-1) are contributed to left ventricular DD. Our aim was to charachterize the effects of CKD on the expression of NRG-1 and 2) NRG-1 treatment on myocardial hypertrophy, diastolic dysfunction and renal function in the rat model of CKD. Methods Male Wistar rats were used and randomized into 3 groups: 1) Sham-operated,2) CKD induced by 5/6 nephrectomy (CKD) and 3) NRG-1-treated CKD group (CKD+NRG-1). In this group, 2 weeks after the CKD induction, the rats were treated with recombinant human NRG-1 (rhNRG-1) at the dose of 10 μg/kg/d for consecutive 10 days with tail vein injection of NRG-1. Serum and urea creatinine levels were measured to verify the development of CKD and transthoracic echocardiography was performed to monitor cardiac morphology and function. Furthermore, total RNA was isolated and RT-qPCR was performed to evaluate the expression levels of inflammatory chemokine and cytokines (TNF-α, TGF-β). In addition, NRG-1 protein levels were assessed in both kidney and heart tissue by ELISA. To clarify the underling anti-fibrotic mechanism, human ventricular cardiac fibroblasts (HCF) were cultured and treated with the TGF-β (20 ng/ml), and TGF-β + hrNRG-1 for 24 h, respectively. Confocal microscopy was used to detect α-smooth muscle actin (α-SMA) expression, marker for fibroblast to myofibroblast transtion. Results 10 weeks after the 5/6 nephrectomy, serum carbamide and creatinine levels were significantly increased and creatinine clearence was significantly decreased as compared to sham-operated animals proving the development of chronic kidney disease (CKD). This was accompanied by a significant decrease in NRG-1 protein expression levels in both cardiac and kidney tissue. Of note, NRG-1 treatment markedly reduced these changes, suggesting its renoprotective effects in CKD. In addition, In CKD animals, the significantly increased anterior, posterior and septal wall thicknesses with decreased end-diastolic and end-systolic diameters proved the development of concentric left ventricular hypertrophy. In CKD, the septal e' was significantly decreased and E/e' increased indicating the developemnt of diastolic dysfunction. These parameters were significantly improved by NRG-1 treatment. Mechanistically, NRG-1 treatment reduced the expression of inflammatory cytokines in compared to untreat group. Furthermore, TGF-β induced α-SMA and Col I upregulation was markedly reduced by hrNRG-1 treatment. Conclusions NRG-1 treatment improved both renal and cardiac funtion in CKD, via a mechansim including the anti-inflammatory and anti-fibrotic properties of NRG-1. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Österreichischer Austauschdienst

scholarly journals Left ventricular hypertrophy among chronic kidney disease patients in Ghana

2017 ◽  
Vol 28 ◽  
Author(s):  
Yaw Ampem Amoako ◽  
Dennis Odai Laryea ◽  
George Bedu-Addo ◽  
Bernard Cudjoe Nkum ◽  
Jacob Plange-Rhule
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular
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