Atrial natriuretic peptide attenuates kidney–lung crosstalk in kidney injury

Tulafu, Miniwan; Mitaka, Chieko; Hnin, May Khin; Abe, Shinya; Kitagawa, Masanobu; Ikeda, Satoshi; Eishi, Yoshinobu; Kurata, Shigeaki; Tomita, Makoto

doi:10.1016/j.jss.2013.07.033

Cited by 18 publications

(14 citation statements)

References 30 publications

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“…Considering the physiological ANP effects, an impairment of intrarenal blood flow regulation is likely in this situation. Moreover, in that ANP is thought to attenuate kidney-lung crosstalk [20], a particular potential corresponding risk of this ANP reduction with ECMO is a reduction in the renoprotective and anti-inflammatory effects of ANP in acute respiratory failure patients requiring ECMO [20]. Since atrial distention is the main stimulus to ANP release, the ANP reduction could be related to drainage of blood by the venous cannula in the right atrium.…”

Section: Ecmo-related Variablesmentioning

confidence: 99%

Extracorporeal Membrane Oxygenation and the Kidney

2015

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Background: Extracorporeal membrane oxygenation (ECMO) is an effective therapy for patients with reversible cardiac and/or respiratory failure. Acute kidney injury (AKI) often occurs in patients supported with ECMO; it frequently evolves into chronic kidney damage or end-stage renal disease and is associated with a reported 4-fold increase in mortality rate. Although AKI is generally due to the hemodynamic alterations associated with the baseline disease, ECMO itself may contribute to maintaining kidney dysfunction through several mechanisms. Summary: AKI may be related to conditions derived from or associated with extracorporeal therapy, leading to a reduction in renal oxygen delivery and/or to inflammatory damage. In particular, during pathological conditions requiring ECMO, the biological defense mechanisms maintaining central perfusion by a reduction of perfusion to peripheral organs (such as the kidney) have been identified as pretreatment and patient-related risk factors for AKI. Hormonal pathways are also impaired in patients supported with ECMO, leading to failures in mechanisms of renal homeostasis and worsening fluid overload. Finally, inflammatory damage, due to the primary disease, heart and lung crosstalk with the kidney or associated with extracorporeal therapy itself, may further increase the susceptibility to AKI. Renal replacement therapy can be integrated into the main extracorporeal circuit during ECMO to provide for optimal fluid management and removal of inflammatory mediators. Key Messages: AKI is frequently observed in patients supported with ECMO. The pathophysiology of the associated AKI is chiefly related to a reduction in renal oxygen delivery and/or to inflammatory damage. Risk factors for AKI are associated with a patient's underlying disease and ECMO-related conditions.

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Section: Ecmo-related Variablesmentioning

confidence: 99%

Extracorporeal Membrane Oxygenation and the Kidney

2015

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“…This is consistent with an earlier report that diabetes was a negative regulator of ANP. 18 Clinical studies also found that the ANP SNP 2238C allele was associated with a reduced severity of DN, 19 suggesting F I G U R E 5 The effect of ANP deficiency in HK-2 cells on EA.hy926 cells endothelial function and the mechanism. 17 Similar renoprotective effects of ANP were reported in the renal ischemia-reperfusion injury model.…”

Section: Xue Et Almentioning

confidence: 98%

“…17 Similar renoprotective effects of ANP were reported in the renal ischemia-reperfusion injury model. 18 Clinical studies also found that the ANP SNP 2238C allele was associated with a reduced severity of DN, 19 suggesting F I G U R E 5 The effect of ANP deficiency in HK-2 cells on EA.hy926 cells endothelial function and the mechanism. A,B, The silencing efficiency of ANP-siRNA sequence 1 and sequence 2 in HK-2 cells was measured by western blot (n = 6 in each group), compared with negative control-siRNA (NC-siRNA) group.…”

Section: Xue Et Almentioning

confidence: 98%

Corin plays a protective role via upregulating MAPK and downregulating eNOS in diabetic nephropathy endothelial dysfunction

et al. 2019

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Diabetic nephropathy (DN) is one of the leading causes of mortality in diabetic patients, but its pathogenesis is unclear. We aimed to study the role of the pro-ANP convertase Corin in the pathogenesis of DN. Corin and ANP expression in DN rat kidneys and high-glucose-treated HK-2 cells was analyzed by real-time PCR, western blotting, and immunohistochemical staining. The effect of Corin-siRNA or ANP-siRNA HK-2 cells on EA.hy926 cell migration was determined by scratch-wound healing assay. The expression of mitogen-activated protein kinase (MAPK) and endothelial NO synthase (eNOS) in EA.hy926 cells treated with conditioned medium from Corin-siRNA-or ANP-siRNA-transfected HK-2 cells was determined by western blotting. We found a significant reduction in Corin and ANP expression in DN rat kidneys. These results were recapitulated in HK-2 cells treated with high glucose.EA.hy926 cells treated with conditioned medium from Corin-deficient HK-2 cells had inhibited migration, increased MAPK activity, and decreased eNOS activity.Similar effects were observed with ANP-siRNA transfection. Finally, adding ANP to the Corin-deficient HK-2 conditioned medium rescued the above defects, indicating that Corin mediates its effects through ANP. In conclusion, Corin plays a renoprotective role through pro-ANP processing, and defects in Corin cause endothelial dysfunction through MAPK and eNOS signaling in DN. K E Y W O R D SCorin, diabetic nephropathy, endothelial dysfunction, eNOS, MAPK 96 |

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“…In a recent study by Mitaka et al (124), ANP pretreatment prevented kidney–lung cross talk in a rat model of renal ischemic reperfusion injury. Interestingly, this group has also shown that ANP posttreatment ameliorated injuries in kidney and lung by direct tissue protective effect and anti-inflammatory effects, which potentially inhibited interorgan cross talk (125). Zhu et al have shown that ANP reduced the levels pro-inflammatory cytokines such as IL-1β, IL-6, IL-10, and TNF-α in rats with oleic acid-induced ALI (126).…”

Section: The Contribution Of the Immune System To Heart Failurementioning

confidence: 99%

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

et al. 2017

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Congestive heart failure (CHF) has become a major medical problem in the western world with high morbidity and mortality rates. CHF adversely affects several systems, mainly the kidneys and the lungs. While the involvement of the renin–angiotensin–aldosterone system and the sympathetic nervous system in the progression of cardiovascular, pulmonary, and renal dysfunction in experimental and clinical CHF is well established, the importance of pro-inflammatory mediators in the pathogenesis of this clinical setting is still evolving. In this context, CHF is associated with overexpression of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1, and IL-6, which are activated in response to environmental injury. This family of cytokines has been implicated in the deterioration of CHF, where it plays an important role in initiating and integrating homeostatic responses both at the myocardium and circulatory levels. We and others showed that angiotensin II decreased the ability of the lungs to clear edema and enhanced the fibrosis process via phosphorylation of the mitogen-activated protein kinases p38 and p42/44, which are generally involved in cellular responses to pro-inflammatory cytokines. Literature data also indicate the involvement of these effectors in modulating ion channel activity. It has been reported that in heart failure due to mitral stenosis; there were varying degrees of vascular and other associated parenchymal changes such as edema and fibrosis. In this review, we will discuss the effects of cytokines and other inflammatory mediators on the kidneys and the lungs in heart failure; especially their role in renal and alveolar ion channels activity and fluid balance.

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Atrial natriuretic peptide attenuates kidney–lung crosstalk in kidney injury

Cited by 18 publications

References 30 publications

Extracorporeal Membrane Oxygenation and the Kidney

Extracorporeal Membrane Oxygenation and the Kidney

Corin plays a protective role via upregulating MAPK and downregulating eNOS in diabetic nephropathy endothelial dysfunction

Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure

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