Low Erythropoietin Production in Familial Amyloidosis TTR V30M Is Not Related with Renal Congophilic Amyloid Deposition

Hypoxia plays a role in ischemic, toxic and sepsis-induced acute kidney injury. Evolving hypoxia triggers renal adaptive responses that may mitigate the insult, leading to sublethal forms of cell injury. The unique capability of the kidney to downregulate oxygen consumption for tubular transport could represent one such adaptive response which promotes maintenance of renal oxygenation, thereby preserving cellular integrity. Tran et al. recently explored a novel mechanism that might prevent tubular damage by downregulation of mitochondrial biogenesis and oxygen consumption. Using expression profiling of kidney RNA in endotoxemic rodents and complementary studies in vitro and in PGC-1α knockout mice, they found a sepsis-related decline in PPARγ coactivator-1α (PGC-1α) expression and of PGC-1α-dependent genes involved in oxidative phosphorylation. This response may explain their observation of a paradoxical preservation of kidney oxygenation and structural integrity in sepsis, despite reduced renal blood flow and oxygen delivery. Thus, resetting of mitochondrial respiration and oxygen consumption during sepsis might be added to the growing list of adaptive responses that occur during hypoxic stress. This review will focus on these mechanisms that mitigate evolving hypoxic injury, even at the expense of transient renal dysfunction.

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Cellular adaptive changes in AKI: mitigating renal hypoxic injury

Heyman

Evans

Rosen

et al. 2012

Nephrology Dialysis Transplantation

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Emerging role of Lipopolysaccharide binding protein in sepsis-induced acute kidney injury

Stasi

Intini

Divella

et al. 2016

Nephrol. Dial. Transplant.

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Sepsis remains a serious cause of morbidity and mortality in critically ill patients, with limited therapeutic options available. Of the several disorders connected with sepsis, acute kidney injury (AKI) is one of the major complications. The pathophysiology of sepsis-induced AKI is characterized by severe inflammation in renal parenchyma with endothelial dysfunction, intra-glomerular thrombosis and tubular injury. Endothelial dysfunction is regulated by several mechanisms implicated in cellular de-differentiation, such as endothelial-to-mesenchymal transition (EndMT). Gram-negative bacteria and their cell wall component lipopolysaccharides (LPSs) are frequently involved in the pathogenesis of AKI. The host recognition of LPS requires a specific receptor, which belongs to the Toll-like receptor (TLR) family of proteins, called TLR4, and two carrier proteins, namely the LPS-binding protein (LBP) and cluster of differentiation 14 (CD14). In particular, LBP is released as a consequence of Gram-negative infection and maximizes the activation of TLR4 signalling. Recent findings regarding the emerging role of LBP in mediating sepsis-induced AKI, and the possible beneficial effects resulting from the removal of this endogenous adaptor protein, will be discussed in this review.

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Acute Kidney Injury in Neonates Requiring ECMO

et al. 2012

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Acute kidney injury (AKI) is common in neonates requiring extracorporeal membrane oxygenation (ECMO). Despite the strong association between AKI and worse outcome in patients requiring ECMO, there is considerable variation in how this morbidity is managed. We will address the pathophysiology and epidemiology of AKI in the neonatal ECMO patient. We will also discuss the indications and technical aspects of providing renal replacement therapy (RRT) for the neonate on ECMO.Objectives After completing this article, readers should be able to:1. Describe the pathophysiology of acute kidney injury (AKI) in neonates requiring extracorporeal membrane oxygenation (ECMO). 2. Identify the indications for renal replacement therapy (RRT) in the neonatal ECMO patient. 3. Describe the different forms of RRT that can be utilized on ECMO. 4. Identify the issues that are unique to providing RRT for the neonatal ECMO patient.Extracorporeal membrane oxygenation (ECMO) has been used as rescue therapy for critically ill neonates for over 35 years. Critically ill neonates who require ECMO are at risk for multiple organ failure, including acute kidney injury (AKI). Despite the many advances in extracorporeal technology, there is still no uniform method of treating AKI and fluid overload for the ECMO patient. Renal replacement therapy (RRT) can alleviate AKI and volume overload in critically ill patients by providing gradual and consistent clearance of solutes and removal of excess fluids. Among different ECMO centers, there is a great deal of variation on the use of RRT. In this review, we will discuss the pathophysiology of AKI and fluid overload in the neonatal ECMO patient, the role of RRT, and the different methods of providing RRT to the neonatal ECMO patient. Pathophysiology of AKI in Neonates Requiring ECMONeonates requiring ECMO often represent the sickest patients, with varied underlying conditions including meconium aspiration, persistent pulmonary hypertension, congenital heart disease, congenital diaphragmatic hernia (CDH), and sepsis. AKI in these patients is often multifactorial with contributions from their underlying illness as well as from ECMO itself. The pathophysiology of AKI can be due to altered renal perfusion, vasomotor nephropathy from the release of vasoactive substances, systemic inflammation, hypoxic and oxidative injury during ischemia-reperfusion, and nephrotoxic medications.(1) Further complicating this pathophysiology is the interplay between the kidneys and organs such as the heart and lungs that contributes to multiorgan dysfunction.(2)(3)

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Low Erythropoietin Production in Familial Amyloidosis TTR V30M Is Not Related with Renal Congophilic Amyloid Deposition

Cited by 5 publications

References 32 publications

Cellular adaptive changes in AKI: mitigating renal hypoxic injury

Cellular adaptive changes in AKI: mitigating renal hypoxic injury

Emerging role of Lipopolysaccharide binding protein in sepsis-induced acute kidney injury

Acute Kidney Injury in Neonates Requiring ECMO

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