The Cardiorenal Syndrome: Making the Connection

Viswanathan, Gautham; Gilbert, Scott J.

doi:10.4061/2011/283137

Cited by 40 publications

(36 citation statements)

References 77 publications

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“…The heart and the kidney are closely interconnected with each other in terms of their functions and communication between these organs occurs through a variety of pathways [1,2] . It has been suggested that the overlap between cardiovascular disease and kidney dysfunction represents common pathophysiological processes that interact in deleterious ways to promote the vicious cycle of organ dysfunction.…”

Section: Introductionmentioning

confidence: 99%

“…The critical, dynamic, and bidirectional connections between both acute and chronic cardiac dysfunction and acute and chronic kidney disease (CKD) are well recognized and classified as Cardiorenal Syndromes [1,2,9] . Cardiorenal Syndrome classification system has five subtypes whose etymology reflects the primary and secondary pathology, the time frame, and simultaneous cardiac and renal co-dysfunction secondary to systemic disease [1] .…”

Section: Introductionmentioning

confidence: 99%

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Pro-Apoptotic Effects of Plasma from Patients with Cardiorenal Syndrome on Human Tubular Cells

et al. 2015

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Background: The pathophysiology of Cardiorenal Syndrome Type 1 (CRS1) is widely studied, although the mechanisms by which renal tubular epithelial cells (TECs) cease to proliferate and embark upon terminal differentiation, following the initial insult of heart failure (HF), remain a key target. This study seeks to provide insight into the pathophysiological pathways in CRS1; we evaluated in vitro the effects of CRS1 plasma on TECs. Methods: We enrolled 40 acute HF patients and 15 controls (CTR) without HF or acute kidney injury (AKI). Ten out of 40 HF patients exhibited AKI at the time of admission for HF or developed AKI during hospitalization and were classified as CRS1. In vitro, cell viability, DNA fragmentation and caspase-3 levels were investigated in TECs incubated with HF, CRS1, and CTR plasma. We assessed inflammatory cytokines and NGAL expression at the gene and protein levels. Results: We observed a marked pro-apoptotic activity and a significantly increased in vitro level of apoptosis in TECs incubated with plasma from CRS1 patients compared to HF and CTR (p < 0.01). In the CRS1 group, the mRNA expression of IL-6, IL-18 and NGAL resulted significantly higher in TECs incubated with CRS1 plasma compared with those incubated with plasma from HF and CTR (p < 0.01). IL-6, IL-18, NGAL, and RANTES levels were significantly higher in TECs supernatant incubated with CRS1 plasma compared with HF patients and CTR plasma (p < 0.01). Conclusion: In vitro exposure to plasma from CRS1 patients altered the expression profile of TECs characterized by increases in proinflammatory mediators, release of tubular damage markers, and apoptosis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pro-Apoptotic Effects of Plasma from Patients with Cardiorenal Syndrome on Human Tubular Cells

et al. 2015

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“…18,19 Kidney and heart functions are inter-related and implicated in maintaining the hemodynamic stability and the organ perfusion via a strict relationship that controls the volume status, the vascular tone, and the cardiac output. 21 The cardiorenal connection between these 2 organs ensures that subtle physiological changes in 1 system are compensated by the other through the activation of a cascade of mediators and pathways. 21 As a consequence, any perturbation in cardiac or renal functions may impair the ability of the other organ to compensate.…”

Section: Discussionmentioning

confidence: 99%

“…21 The cardiorenal connection between these 2 organs ensures that subtle physiological changes in 1 system are compensated by the other through the activation of a cascade of mediators and pathways. 21 As a consequence, any perturbation in cardiac or renal functions may impair the ability of the other organ to compensate.…”

Section: Discussionmentioning

confidence: 99%

cGMP-Dependent Protein Kinase 1 Polymorphisms Underlie Renal Sodium Handling Impairment

et al. 2013

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6However, the role of PRKG1 in the PNat mechanism has not yet been demonstrated in humans. Therefore, here we investigated the effects of an acute saline load in an expanded cohort of newly discovered never-treated (naive) hypertensive Abstract-Defective pressure-natriuresis related to abnormalities in the natriuretic response has been associated with hypertension development. A major signaling pathway mediating pressure natriuresis involves the cGMP-dependent protein kinase 1 (PRKG1) that, once activated by Src kinase, inhibits renal Na + reabsorption via a direct action on basolateral Na-K ATPase and luminal Na-H exchanger type 3, as shown in renal tubuli of animals. Because a clear implication of PRKG1 in humans is still lacking, here we addressed whether PRKG1 polymorphisms affect pressurenatriuresis in patients. Naive hypertensive patients (n=574), genotyped for PRKG1 rs1904694, rs7897633, and rs7905063 single nucleotide polymorphisms (SNPs), underwent an acute Na + loading, and the slope of the pressure-natriuresis relationship between blood pressure and Na + excretion was calculated. The underlying molecular mechanism was investigated by immunoblotting protein quantifications in human kidneys. The results demonstrate that the PRKG1 risk haplotype GAT (rs1904694, rs7897633, rs7905063, respectively) associates with a rightward shift of the pressurenatriuresis curve (0.017±0.004 μEq/mm Hg per minute) compared with the ACC (0.0013±0.003 μEq/mm Hg per minute; P=0.001). In human kidneys, a positive correlation of protein expression levels between PRKG1 and Src (r=0.83; P<0.001) or α1 Na-K ATPase (r=0.557; P<0.01) and between α1 Na-K ATPase and Na-H exchanger type 3 (r=0.584; P<0.01) or Src (r=0.691; P<0.001) was observed in patients carrying PRKG1 risk GAT (n=23) but not ACC (n=14) variants. A functional signaling complex among PRKG1, α1 Na-K ATPase, and Src was shown by immunoprecipitation from human renal caveolae. These findings indicate that PRKG1 risk alleles associate with salt-sensitivity related to a loss of the inhibitory control of renal Na + reabsorption, suggestive of a blunt pressure-natriuresis response. (Hypertension. 2013;62:1027-1033.) • Online Data Supplement

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“…An extension to this model, however, was projected by Bongartz et al [29] to explain the accelerated atherosclerosis, the cardiac remodeling and hypertrophy, and the progression of renal disease observed in the severe CRS. When the heart or the kidney fails, a vicious cycle, called the cardiorenal connection [81,82] in a scheme depicted by Bongartz et al [29], progresses: the RAAS, the NO-ROS balance, the sympathetic nervous system, and inflammation interact and synergize.…”

Section: Free Radicals: Key Biomarkers In Experimental Models To Explmentioning

confidence: 99%

Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome

Restini¹,

Pereira²,

Geleilete³

2016

Free Radicals and Diseases

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The National Heart, Lung, and Blood Institute Working Group has postulated the cardiorenal syndrome (CRS) as an interaction between the kidneys and the cardiovascular system in which therapy to relieve congestive heart failure (HF) symptoms is limited by the further worsening renal function. CRS is classified from type I to V, taking into account the progression of the symptoms in terms of mechanisms, clinical conditions, and biomarkers. Experimental and clinical studies have shown the kidney as both a trigger and a target to sympathetic nervous system (SNS) overactivity. Renal damage and ischemia, activation of the renin angiotensin aldosterone system (RAAS), and dysfunction of nitric oxide (NO) system are associated with kidney adrenergic activation. Indeed, the imbalances of RAAS and/or SNS share an important common process in CRS: the activation and production of free radicals, especially reactive oxygen species (ROS). The present chapter addresses connections of the free radicals as potential biomarkers as the imbalances in the RAAS and the SNS are developed. Understanding the involvement of free radicals in CRS may bring knowledge to design studies in order to develop accurate pharmacological interventions.

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The Cardiorenal Syndrome: Making the Connection

Cited by 40 publications

References 77 publications

Pro-Apoptotic Effects of Plasma from Patients with Cardiorenal Syndrome on Human Tubular Cells

Pro-Apoptotic Effects of Plasma from Patients with Cardiorenal Syndrome on Human Tubular Cells

cGMP-Dependent Protein Kinase 1 Polymorphisms Underlie Renal Sodium Handling Impairment

Free Radicals and Biomarkers Related to the Diagnosis of Cardiorenal Syndrome

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