Cardio-renal syndrome

Gnanaraj, Joseph

doi:10.12688/f1000research.8004.1

Cited by 20 publications

(44 citation statements)

References 64 publications

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“…The complete shutdown of vitamin D synthesis would consequently enhance an uncontrolled reaction over accumulation of Ang-II that, in turn, scatters the high viability of pro-inflammatory cytokine and interleukins, such as IL-6, followed by a sudden regression of kidney, heart, and lung axis functionality (7).…”

Section: Discussionmentioning

confidence: 99%

“…The pathophysiology that underlies the complex loop of lungheart-kidney interactions is a well-accepted assumption, a kind of respiratory-cardio-renal syndrome condition that gives rise to a susceptibility to many primary and secondary dysfunctions, such as infections, auto-immune reactions, sepsis, and declined endocrine activity (low level of erythropoietin (EPO)). In COVID-19 patients, there is often seen a long-term clinical history of kidney/heart deficit advocated by a compromised renin angiotensin system (RAS) [1][2][3][4][5][6][7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

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The Vitamin D, IL-6 and the eGFR Markers a Possible Way to Elucidate the Lung–Heart–Kidney Cross-Talk in COVID-19 Disease: A Foregone Conclusion

et al. 2021

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Background: Based on recent findings, we speculated the existence of the lung, heart, and kidney axis as the main pathway for the COVID-19 disease progression. Methods: This paper reports on an observational study conducted by a team of researchers and doctors of the 118-Pre-Hospital and Emergency Department of SG Moscati of Taranto City in Italy. The study was conducted on a totality of 185 participants that were divided into three groups. The study group included COVID-19 affected patients (PP n = 80), the first control group included patients with different pathologies (non-COVID-19 NNp n = 62) of the SG Moscati Hospital, and the second control group included healthy individuals (NNh n = 43). The core of the current trial was focused on assessing the level of the vitamin D (serum 25(OH) D concentration), IL-6, and the renal glomerular filtrate (eGFR) in COVID-19 disease and non-COVID-19 patients in both groups. Results: It was observed that the majority of COVID-19-infected patients showed a progressive multi-organ involvement, especially in regard to the lung, kidney, and heart. The majority of the COVID-19 patients exhibited preexisting comorbidities which include cardiovascular, respiratory, and renal disorders accompanied by a severely low level of vitamin D, extremely high level of IL-6, and low glomerular filtration rate (eGFR). The significant overall damages exerted by the immune-mediated responses under the hyper-expression of proinflammatory cytokines and interleukins, such as IL-6, may be facilitated by either a decreased level of vitamin D or the ageing process. The reduced presence of vitamin D was often found together with a reduced functionality of renal activity, as revealed by the low eGFR, and both were seen to be concomitant with an increased mortality risk in patients with lung disorders and heart failure (HF), whether it is showed at baseline or it develops during manifestation of COVID-19. Therefore, the documentation of the modifiable risk factors related to SARS-CoV-2 and lung impairment in older patients with kidney and heart disease may help the clinician to better manage the situation. Conclusions: This paper addresses how a low level of vitamin D and older age may be indicative of systemic worsening in patients with COVID-19, with a goal of providing a broader context in which to view a better therapeutic approach.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Vitamin D, IL-6 and the eGFR Markers a Possible Way to Elucidate the Lung–Heart–Kidney Cross-Talk in COVID-19 Disease: A Foregone Conclusion

et al. 2021

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“…CKD is also an independent risk factor for CVD [7] and CVD progression directly contributes to kidney function decline [8]. These multiple interactions between the heart and kidneys have led to the concept of the cardiorenal syndrome (CRS), in which acute or chronic dysfunction of either the heart or the kidneys leads to dysfunction of the other organ [9,10]. The molecular mechanisms underlying these interactions remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

TWEAK–Fn14 as a common pathway in the heart and the kidneys in cardiorenal syndrome

et al. 2021

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There is a complex relationship between cardiac and renal disease, often referred to as the cardiorenal syndrome. Heart failure adversely affects kidney function, and both acute and chronic kidney disease are associated with structural and functional changes to the myocardium. The pathological mechanisms and contributing interactions that surround this relationship remain poorly understood, limiting the opportunities for therapeutic intervention. The cytokine tumor necrosis factor‐like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor‐inducible 14 (Fn14), are abundantly expressed in injured kidneys and heart. The TWEAK–Fn14 axis promotes responses that drive tissue injury such as inflammation, proliferation, fibrosis, and apoptosis, while restraining the expression of tissue protective factors such as the anti‐aging factor Klotho and the master regulator of mitochondrial biogenesis peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α). High levels of TWEAK induce cardiac remodeling, and promote inflammation, tubular and podocyte injury and death, fibroblast proliferation, and, ultimately, renal fibrosis. Accordingly, targeting the TWEAK–Fn14 axis is protective in experimental kidney and heart disease. TWEAK has also emerged as a biomarker of kidney damage and cardiovascular outcomes and has been successfully targeted in clinical trials. In this review, we update our current knowledge of the roles of the TWEAK–Fn14 axis in cardiovascular and kidney disease and its potential contribution to the cardiorenal syndrome. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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“…When using the TAC model to study heart failure it is important to take the cardiorenal axis into account, patients with reduced cardiac function often also experience CKD ( Harada et al, 2018 ; Kumar and Seth, 2019 ; Patel et al, 2019 ; Zaleska-Kociecka et al, 2019 ), as it has been suggested that a decline in kidney function directly contributes to further deterioration of cardiac function in patients ( Hewitson et al, 2015 ; Gnanaraj and Radhakrishnan, 2016 ). Several papers have indicated that a good animal model that properly represents the clinical manifests of CRS is lacking ( Szymanski et al, 2012 ; Tan et al, 2018 ; Liu, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Mildly Increased Renin Expression in the Absence of Kidney Injury in the Murine Transverse Aortic Constriction Model

et al. 2021

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Cardiorenal syndrome type 2 is characterized by kidney failure as a consequence of heart failure that affects >50% of heart failure patients. Murine transverse aortic constriction (TAC) is a heart failure model, where pressure overload is induced on the heart without any systemic hypertension or its consequences. Whether renal function is altered in this model is debated, and if so, at which time post-TAC renal dysfunction starts to contribute to worsening of cardiac function. We therefore studied the effects of progressive heart failure development on kidney function in the absence of chronically elevated systemic blood pressure and renal perfusion pressure. C57BL/6J mice (N = 129) were exposed to TAC using a minimally invasive technique and followed from 3 to 70 days post-TAC. Cardiac function was determined with 3D ultrasound and showed a gradual decrease in stroke volume over time. Renal renin expression and plasma renin concentration increased with progressive heart failure, suggesting hypoperfusion of the kidney. In addition, plasma urea concentration, a surrogate marker for renal dysfunction, was increased post-TAC. However, no structural abnormalities in the kidney, nor albuminuria were present at any time-point post-TAC. Progressive heart failure is associated with increased renin expression, but only mildly affected renal function without inducing structural injury. In combination, these data suggest that heart failure alone does not contribute to kidney dysfunction in mice.

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Cardio-renal syndrome

Cited by 20 publications

References 64 publications

The Vitamin D, IL-6 and the eGFR Markers a Possible Way to Elucidate the Lung–Heart–Kidney Cross-Talk in COVID-19 Disease: A Foregone Conclusion

The Vitamin D, IL-6 and the eGFR Markers a Possible Way to Elucidate the Lung–Heart–Kidney Cross-Talk in COVID-19 Disease: A Foregone Conclusion

TWEAK–Fn14 as a common pathway in the heart and the kidneys in cardiorenal syndrome

Mildly Increased Renin Expression in the Absence of Kidney Injury in the Murine Transverse Aortic Constriction Model

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