Cardiorenal Syndrome and the Role of the Bone-Mineral Axis and Anemia

Charytan, David M.; Fishbane, Steven; Małyszko, Jolanta; McCullough, Peter A.; Goldsmith, David

doi:10.1053/j.ajkd.2014.12.016

Cited by 41 publications

(35 citation statements)

References 106 publications

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“…Phosphate is considered as one of the principal uremic toxin and the crucial importance to control phosphatemia in CKD patients has been deeply investigated [11]. During the last decades, increasing evidence supports the idea that vascular calcification strongly associates with cardiovascular morbidity and mortality in patients affected by advanced CKD.…”

Section: Discussionmentioning

confidence: 99%

A new in vitro model to delay high phosphate-induced vascular calcification progression

et al. 2015

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An increasing amount of patients affected by advanced chronic kidney disease suffer from vascular calcification (VC) that associates with cardiovascular morbidity and mortality. In this study, we created a new experimental in vitro model, trying to better elucidate high phosphate (Pi)-induced VC pathogenic mechanisms. Rat aortic vascular smooth muscle cells (VSMCs) were challenged for 7-10 days with high Pi with a repeated and short suspensions of high Pi treatment (intermittent suspension, IS) that was able to induce a significant inhibition of high Pi calcification, maximal at 5 h. Interestingly, the delay in calcification is a consequence of either the absence of free Pi or calcium-phosphate crystals being comparable to the total effect obtained during the 5 h-IS. The protective effect of IS was mediated by the reduction of apoptosis as demonstrated by the action of 20 μmol/L Z-VAD-FMK and by the preservation of the pro-survival receptor Axl expression. Furthermore, autophagy, during IS, was potentiated by increasing the autophagic flux, evaluated by LC3IIB western, while treating VSMCs with 1 mmol/L valproic acid did not affect VC. Finally, IS prevented VSMC osteoblastic differentiation by preserving smooth muscle lineage markers expression. Our data support the hypothesis that to delay significantly VC is necessary and sufficient the IS of high Pi challenge. The IS was able to prevent significantly apoptosis, to induce a potentiation in autophagy, and to prevent osteoblastic differentiation by preserving SM lineage markers.

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Section: Discussionmentioning

confidence: 99%

A new in vitro model to delay high phosphate-induced vascular calcification progression

et al. 2015

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“…From the point of view of the kidneys, the main task is the reduction of CKD progression through the control of intraglomerular hemodynamics and hyperfiltration, the limitation of protein and salt intake, neurohormonal modulation, and control of blood pressure [37]. Recent evidence has pointed out that chronic inflammation, anemia, and metabolic alterations typical of uremia (e.g., hyperuricemia) [38,39] even at its early stages may influence the rate of vascular calcification, myocardial fibrosis, aortic and mitral calcification, and the propensity for atrial and ventricular arrhythmias [40,41]. In this syndrome, there appears to be opportunities to improve the micronutrient status of patients with the goal of reducing frailty and complications over time [42,43].…”

Section: Crs Typementioning

confidence: 99%

A Call to Action to Develop Integrated Curricula in Cardiorenal Medicine

Ronco

McCullough

2017

Blood Purif

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With the adoption of the new definition and classification of cardiorenal syndrome (CRS) and its relevant subtypes, much attention has been placed on elucidating the mechanisms of heart and kidney interactions. Of great interest are the pathophysiological pathways by which acute heart failure may result in acute kidney injury (AKI; type 1), chronic heart failure accelerating the progression of chronic kidney disease (CKD; type 2), AKI provoking cardiac events (type 3), and CKD increasing the risk and severity of cardiovascular disease (type 4). A remarkable interest has also been placed on the acute and chronic systemic conditions, such as sepsis and diabetes, which simultaneously affect heart and kidney function (type 5). Furthermore, the physiology of acute and chronic heart-kidney cross talk is drawing attention to hemodynamics (fluids, pressures, flows, resistances, perfusion), physiochemical (electrolytes, pH, and toxins), and biological (inflammation, immune system activation, neurohormonal signals) processes. Common clinical scenarios call for recognition, knowledge, and skill in managing CRS. There is a clear need for medical and surgical specialists that are well versed in the pathophysiology and the clinical manifestations that arise in the setting of CRS. With this editorial, we are making a call to action to stimulate universities, medical schools, and teaching hospitals to create a core curriculum for cardiorenal medicine to better equip the physicians of the future for these common, serious, and frequently fatal syndromes.

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“…The elegant work of Wolf and colleagues has identified the phosphaturic hormone fibroblast growth factor (FGF)-23 as a kidney-specific mediator of left ventricular hypertrophy [9] and predictor of HF in CKD [10]. Anemia is an important risk factor, and iron deficiency may be an important link between anemia, bone metabolism, and cardiovascular disease in CKD [11]. At all stages of CKD, deranged mineral metabolism contributes to vascular calcification, leading to accelerated atherosclerotic disease characterized by medial and intimal plaque calcification.…”

Section: Pathways Leading To Hf In Patients With Cardiorenal Syndromesmentioning

confidence: 99%

Soluble Guanylate Cyclase Stimulators: a Novel Treatment Option for Heart Failure Associated with Cardiorenal Syndromes?

Dubin

Shah

2016

Curr Heart Fail Rep

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Heart failure in the setting of chronic kidney disease (CKD) is an increasingly common scenario and carries a poor prognosis. Clinicians lack tools for primary or secondary heart failure prevention in patients with cardiorenal syndromes. In patients without CKD, angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB) and statins mitigate cardiovascular risk in large part due to salutary effects on the endothelium. In the setting of CKD, use of these therapies is limited by adverse effects of hyperkalemia in pre-dialysis CKD (ACE-I/ARB), or potential increased risk of stroke in end-stage renal disease (statins). The soluble guanylate cyclase (sGC) stimulators are a novel class of medications that promote endothelial and myocardial function with no known risk of hyperkalemia or stroke. In this review, we discuss the evidence emerging from recent clinical trials of sGC stimulators in pulmonary hypertension and heart failure, the diseased pathways involved in cardiorenal syndromes likely to be restored by sGC stimulators, and several strategies for designing future clinical trials of cardiorenal syndromes that might shorten the timeline for discovery and approval of effective cardiovascular therapies in these high-risk patients.

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Cardiorenal Syndrome and the Role of the Bone-Mineral Axis and Anemia

Cited by 41 publications

References 106 publications

A new in vitro model to delay high phosphate-induced vascular calcification progression

A new in vitro model to delay high phosphate-induced vascular calcification progression

A Call to Action to Develop Integrated Curricula in Cardiorenal Medicine

Soluble Guanylate Cyclase Stimulators: a Novel Treatment Option for Heart Failure Associated with Cardiorenal Syndromes?

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