Microalbuminuria in Nondiabetic and Nonhypertensive Systolic Heart Failure Patients

Figueiredo, Estêvão Lanna; Leão, Fabiana Vieira Garcia; Oliveira, Lílian V.; Moreira, M.C.V.; Figueiredo, Amintas F. S.

doi:10.1111/j.1751-7133.2008.00008.x

Cited by 10 publications

(11 citation statements)

References 19 publications

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“…Although physicians have long recognized that dysfunction of either heart or kidney seldom occurs in isolation, only recently has the concept of the cardiorenal syndrome (CRS), along with a classification system, been proposed [1]. Studies have shown close heart-kidney interactions, for example chronic kidney dysfunction (CKD) increases risk for cardiovascular events, and patients with chronic heart failure (CHF) and microalbuminuria or CKD have worse outcomes than those with CHF alone [2-4]. However, the underlying mechanisms remain poorly understood and therapeutic options are limited.…”

Section: Introductionmentioning

confidence: 99%

Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress

Huang

Yan

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increased endoplasmic reticulum (ER) stress contributes to development of cardiorenal syndrome (CRS), and Silent Information Regulator 1 (SIRT1), a class III histone deacetylase, may have protective effects on heart and renal disease, by reducing ER stress. We aimed to determine if SIRT1 alleviates CRS through ER stress reduction. Methods: Wild type mice (n=37), mice with cardiac-specific SIRT1 knockout (n=29), or overexpression (n=29), and corresponding controls, were randomized into four groups: sham MI (myocardial infarction) +sham STNx (subtotal nephrectomy); MI+sham STNx; sham MI+STNx; and MI+STNx. To establish the CRS model, subtotal nephrectomy (5/6 nephrectomy, SNTx) and myocardial infarction (MI) (induced by ligation of the left anterior descending (LAD) coronary artery) were performed successively to establish CRS model. At week 8, the mice were sacrificed after sequential echocardiographic and hemodynamic studies, and then pathology and Western-blot analysis were performed. Results: Neither MI nor STNx alone significantly influenced the other healthy organ. However, in MI groups, STNx led to more severe cardiac structural and functional deterioration, with increased remodeling, increased BNP levels, and decreased EF, Max +dp/dt, and Max -dp/dt values than in sham MI +STNx groups. Conversely, in STNx groups, MI led to renal structural and functional deterioration, with more severe morphologic changes, augmented desmin and decreased nephrin expression, and increased BUN, SCr and UCAR levels. In MI+STNx groups, SIRT1 knockout led to more severe cardiac structural and functional deterioration, with higher Masson-staining score and BNP levels, and lower EF, FS, Max +dp/dt, and Max -dp/dt values; while SIRT1 overexpression had the opposite attenuating effects. In kidney, SIRT1 knockout resulted in greater structural and functional deterioration, as evidenced by more severe morphologic changes, higher levels of UACR, BUN and SCr, and increased desmin and TGF-β expression, while SIRT1 overexpression resulted in less severe morphologic changes and increased nephrin expression without significant influence on BUN or SCr levels. The SIRT1 knockout but not overexpression resulted in increased myocardial expression of CHOP and GRP78. Cardiac-specific SIRT1 knockout or overexpression resulted in increased or decreased renal expression of CHOP, Bax, and p53 respectively. Conclusions: Myocardial SIRT1 activation appears protective to both heart and kidney in CRS models, probably through modulation of ER stress.

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Section: Introductionmentioning

confidence: 99%

Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress

Huang

Yan

Chen

et al. 2018

Cell Physiol Biochem

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“…The prevalence of microalbuminuria was found to be significantly higher in CHF patients than in healthy individuals, even in the absence of diabetes mellitus and hypertension, and these patients had worse outcomes compared with CHF patients without microalbuminuria 7, 8 .…”

Section: Introductionmentioning

confidence: 91%

Renal Sympathetic Denervation Suppresses De Novo Podocyte Injury and Albuminuria in Rats With Aortic Regurgitation

Rafiq

Noma²,

Fujisawa³

et al. 2012

Circulation

115

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Background The presence of chronic kidney disease is a significant independent risk factor for poor prognosis in patients with chronic heart failure (CHF). However, the mechanisms and mediators underlying this interaction are poorly understood. In this study, we tested our hypothesis that chronic cardiac volume overload leads to de novo renal dysfunction by co-activating the sympathetic nervous system (SNS) and the renin-angiotensin system (RAS) in the kidney. We also examined the therapeutic potential of renal denervation and RAS inhibition to suppress renal injury in CHF. Methods and Results Sprague-Dawley rats underwent aortic regurgitation (AR) and were treated for 6 months with either vehicle, olmesartan [an angiotensin II (AngII) receptor blocker], or hydralazine. At 6 months, albuminuria and glomerular podocyte injury were significantly increased in AR rats. These changes were associated with increased urinary angiotensinogen excretion, kidney AngII and norepinephrine (NE) levels, as well as enhanced angiotensinogen and angiotensin type 1a receptor gene expression, and oxidative stress in renal cortical tissues. AR rats with renal denervation had decreased albuminuria and glomerular podocyte injury, which were associated with reduced kidney NE, angiotensinogen, AngII and oxidative stress. Renal denervation combined with olmesartan prevented podocyte injury and albuminuria induced by AR. Conclusions In this chronic cardiac volume overload animal model, activation of the SNS augments kidney RAS and oxidative stress, which act as crucial cardio-renal mediators. Renal denervation and olmesartan prevent the onset and progression of renal injury, providing new insight into the treatment of cardio-renal syndrome.

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“…Even higher percentages were found in the NHANES cohort from 1999–2004 [38]. In a case control study including non-diabetic and non-hypertensive patients it has been found that elevated ACR was significantly higher in patients with systolic heart failure, if compared to matched controls [39].…”

Section: Discussionmentioning

confidence: 93%

The Prevalence of Chronic Kidney Disease in a Primary Care Setting: A Swiss Cross-Sectional Study

et al. 2013

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Chronic kidney disease (CKD) often remains clinically silent and therefore undiagnosed until a progressed stage is reached. Our aim was to estimate the prevalence of CKD in a primary care setting in Switzerland. A multicenter, cross-sectional study with randomly selected general practitioners was performed. Adults visiting their general physician’s cabinet during defined periods were asked to participate. Baseline information was reported on a questionnaire, urine and blood samples were analyzed in a central laboratory. Renal status was assessed using the Kidney Disease: Improving Global Outcomes (KDIGO) classification. Extrapolation of results to national level was adjusted for age and gender. One thousand individuals (57% females) with a mean age of 57±17 years were included. Overall, 41% of the patients had normal estimated glomerular filtration rate (eGFR) and albumin creatinine ratio (ACR), whereas 36% of the subjects had slightly reduced excretory renal function with physiological albuminuria based on normal ACR. Almost one fourth of the subjects (23%) had either a substantially reduced eGFR or high levels of ACR. About 10% of the patients had a substantially reduced eGFR of <60 ml/min/1.73 m2, and 17% showed relevant proteinuria (ACR >30 mg/g creatinine). Extrapolation to national level suggests that about 18% of primary care patients may suffer from CKD. CKD prevalence in a primary care population is therefore high, and preventive interventions may be advisable, in particular as CKD prevalence is likely to rise over the next decades.

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Microalbuminuria in Nondiabetic and Nonhypertensive Systolic Heart Failure Patients

Cited by 10 publications

References 19 publications

Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress

Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress

Renal Sympathetic Denervation Suppresses De Novo Podocyte Injury and Albuminuria in Rats With Aortic Regurgitation

The Prevalence of Chronic Kidney Disease in a Primary Care Setting: A Swiss Cross-Sectional Study

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