Molecular determinants of acute kidney injury.

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