Holger Husi Christin Human


BACKGROUND: Acute kidney injury (AKI) is a condition that leads to a rapid deterioration of renal function associated with impairment to maintain electrolyte and acid balance, and, if left untreated, ultimately irreversible kidney damage and renal necrosis. There are a number of causes that can trigger AKI, ranging from underlying conditions as well as trauma and surgery. Specifically, the global rise in surgical procedures led to a substantial increase of AKI incidence rates, which in turn impacts on mortality rates, quality of life and economic costs to the healthcare system. However, no effective therapy for AKI exists. Current approaches, such as pharmacological intervention, help in alleviating symptoms in slowing down the progression, but do not prevent or reverse AKI-induced organ damage. METHODS: An in-depth understanding of the molecular machinery involved in and modulated by AKI induction and progression is necessary to specifically pharmacologically target key molecules. A major hurdle to devise a successful strategy is the multifactorial and complex nature of the disorder itself, whereby the activation of a number of seemingly independent molecular pathways in the kidney leads to apoptotic and necrotic events. RESULTS: The renin-angiotensin-aldosterone-system (RAAS) axis appears to be a common element, leading to downstream events such as triggers of immune responses via the NFkB pathway. Other pathways intricately linked with AKI-induction and progression are the tumor necrosis factor alpha (TNFa) and transforming growth factor beta (TGFb) signaling cascades, as well as a number of other modulators. Surprisingly, it has been shown that the involvement of the glutamatergic axis, believed to be mainly a component of the neurological system, is also a major contributor. CONCLUSION: Here we address the current understanding of the molecular pathways evoked in AKI, their interplay, and the potential to pharmacologically intervene in the effective prevention and/or progression of AKI. © 2014 KUMS, All rights reserved


How to Cite
HUSI, Holger; HUMAN, Christin. Molecular determinants of acute kidney injury. Journal of Injury and Violence Research, [S.l.], v. 7, n. 2, p. 75-86, sep. 2014. ISSN 2008-4072. Available at: <http://jivresearch.org/jivr/index.php/jivr/article/view/615>. Date accessed: 20 oct. 2018.
acute kidney injury; glutamate; NMDA receptor; death associated protein kinase; systems biology
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