Hypertrophy of Intramyocardial Arteriolar Smooth Muscle Cells in Experimental Renal Failure

Törnig, Johannes; Gross, Marie–Luise; Simonaviciene, Aurelia; Mall, Gerhard; Ritz, Eberhard; Amann, Kerstin

doi:10.1681/asn.v10177

Cited by 29 publications

(3 citation statements)

References 38 publications

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“…As parameters of CV disease, the average wall thickness of the left ventricle (LV), septum, aorta, and intramyocardial arteries was quantified by measuring either 10 different positions evenly distributed to the LV, septum, and aorta or the inner and outer diameters of intramyocardial arteries as described previously ( 19 ). All morphological analyses were performed in a blinded fashion, i.e., the investigator was unaware of the experimental group the animal belonged to.…”

Section: Methodsmentioning

confidence: 99%

Cardiovascular changes in the NZB/W F1 mouse model of lupus nephritis

Böhme¹,

Daniel²,

Ferrazzi³

et al. 2023

Front. Cardiovasc. Med.

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BackgroundPatients with systemic lupus erythematosus (SLE), an autoimmune disease, have a higher risk of cardiovascular (CV) disease and death. In addition, up to 40%–50% of SLE patients develop lupus nephritis (LN) and chronic kidney disease, which is an additional CV risk factor. Thus, the individual contributions of LN and other SLE-specific factors to CV events are unclear.MethodsIn this study, we investigated the effect of LN on the development of CV changes using the female NZBxNZW F1 (NZB/W) mouse model of lupus-like disease, with female NZW mice as controls. Standard serologic, morphologic, immunohistologic, and molecular analyses were performed. In a separate group of NZB/W mice, systolic blood pressure (BP) was measured during the course of the disease using tail plethysmography.ResultsOur data show marked CV changes in NZB/W mice, i.e., increased heart weight, hypertrophy of the left ventricle (LV) and septum, and increased wall thickness of the intramyocardial arteries and the aorta, which correlated with the progression of renal damage, but not with the age of the mice. In addition, systolic BP was increased in NZB/W mice only when kidney damage progressed and proteinuria was present. Pathway analysis based on gene expression data revealed a significant upregulation of the response to interferon beta in NZB/W mice with moderate kidney injury compared with NZB mice. Furthermore, IFI202b and IL-6 mRNA expression is correlated with CV changes. Multiple linear regression analysis demonstrated serum urea as a surrogate marker of kidney function and IFI202b expression as an independent predictor for LV wall thickness. In addition, deposition of complement factors CFD and C3c in hearts from NZB/W mice was seen, which correlated with the severity of kidney disease.ConclusionsThus, we postulate that the pathogenesis of CV disease in SLE is affected by renal impairment, i.e., LN, but it can also be partly influenced by lupus-specific cardiac expression of pro-inflammatory factors and complement deposition.

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Section: Methodsmentioning

confidence: 99%

Cardiovascular changes in the NZB/W F1 mouse model of lupus nephritis

Böhme¹,

Daniel²,

Ferrazzi³

et al. 2023

Front. Cardiovasc. Med.

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“…However, like diabetes, uraemic arterial changes occur in both large and small vessels. In hypertension, such small vessel disease is recorded and may play an important role in impairment of cardiac vasodilator reserve 99–101 . Cardiac and renal amyloid can often co‐exist, and arteriolar involvement by amyloidosis is a cause of ‘ischaemic’ chest pain 102 .…”

Section: Coronary Artery Diseasementioning

confidence: 99%

Coronary Artery Disease in Patients With Renal Failure

Goldsmith

Covic

2001

Int J Clinical Practice

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SUMMARYCardiovascular disease is prevalent in patients with advanced renal failure or on dialysis treatment, and after renal transplantation. The risk factors for the cardiovascular problems are a mixture of conventional and novel ones. Inflammation and oxidation may be especially important in the acceleration of atherosclerosis in chronic renal failure. This article discusses these factors and gathers together the evidence for cardiovascular intervention and treatment in a group of patients whose overall mortality is high.

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“…When Chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) cause progressive and potentially permanent chronic kidney disease this condition called chronic cardiorenal syndrome or Type 2 CRS, CKD has been observed in [45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63]25,26,[10]. The number of participants in the questionnaire is 100 and the questionnaire was distributed in two ways.…”

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confidence: 99%

Cardio-Renal Syndrome

2023

JPTCP

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The cardio-renal syndrome (CRS) can be generally defined as a pathophysiologic disorder includes a broad spectrum of diseases in which heart and kidney are both involved, the CRS classification essentially recognizes two main groups, cardio-renal and Reno-cardiac syndromes, on the basis of ''premium moves'' of disease (cardiac or renal); both cardio-renal and Reno-cardiac syndromes are then divided into acute and chronic, according to the disease's onset, Five subtypes of the syndromes were identified, abrupt worsening of cardiac function that lead to acute kidney injury called Acute Cardio-renal Syndrome or Type 1 CRS, this appears to be a syndrome of worsening renal function that frequently complicates hospitalized patients with acute heart failure and acute coronary syndrome. When Chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) cause progressive and potentially permanent chronic kidney disease this condition called chronic cardiorenal syndrome or Type 2 CRS, CKD has been observed in [45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63]25,26,[10]. The number of participants in the questionnaire is 100 and the questionnaire was distributed in two ways. In the first way, the questionnaire was published on social media and the number of participants was 79 and the number of pharmacists participating in the electronic questionnaire was 51 and the number of participating physicians was 28. In the second way, the questionnaire was distributed to a group of private pharmacies in Baghdad, which numbered 21 and purpose of the questionnaire was to find out if the participants had any information about Cardio-renal Syndrome. Heart and kidney interactions are complex and the subject of immense clinical and scientific interest and debate. In this article, we argue that without consensus on definitions and classification, clinicians will not be able to precisely phenotype the various forms of cardio-renal syndrome. Such phenotyping, in turn, forms the basis for in vitro and animal studies, as well as small translational studies in patients. Through the ADQI consensus on CRS, other processes will now be facilitated, including a better or clearer understanding of the epidemiology of these conditions, opportunities for early diagnosis through biomarkers, the development of preventive strategies and application of evidence-based management strategies

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Hypertrophy of Intramyocardial Arteriolar Smooth Muscle Cells in Experimental Renal Failure

Cited by 29 publications

References 38 publications

Cardiovascular changes in the NZB/W F1 mouse model of lupus nephritis

Cardiovascular changes in the NZB/W F1 mouse model of lupus nephritis

Coronary Artery Disease in Patients With Renal Failure

Cardio-Renal Syndrome

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