Medicine (Austin & Northern Health) - Research Publications

Permanent URI for this collection

http://hdl.handle.net/11343/211

Filters

2011 1
1
Reset filters

Settings
Statistics
Citations
Subject: Diseases and Abnormal Conditions) not elsewhere classified × Subject: Clinical Sciences not elsewhere classified; Clinical Health (Organs × Start date: 2010 × End date: 2012 × Author: Bellomo, Rinaldo × Type: Journal Article ×

Search Results

Now showing 1 - 1 of 1
  • Item
    Thumbnail Image
    Septic Acute Kidney Injury: The Glomerular Arterioles
    Bellomo, R ; Wan, L ; Langenberg, C ; Ishikawa, K ; May, CN ; Kellum, JA ; Ronco, C ; Vincent, JL (KARGER, 2011-01-01)
    Acute kidney injury (AKI) is a serious condition that affects many intensive care unit (ICU) patients. The most common causes of AKI in the ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite our increasing ability to support vital organs. This is partly due to our poor understanding of the pathogenesis of sepsis-induced renal dysfunction. However, new concepts are emerging to explain the pathogenesis of septic AKI, which challenge previously held dogma. Throughout the past half century, septic AKI has essentially been considered secondary to tubular injury, which, in turn, has been considered secondary to renal ischemia. This belief is curious because the hallmark of septic AKI and AKI in general is the loss of glomerular filtration rate (GFR). It would seem logical, therefore, to focus on the glomerulus in trying to understand why such loss of GFR occurs. Recent experimental observations suggest that, at least in the initial phases of septic AKI, profound changes occur which involve glomerular hemodynamics and lead to loss of GFR. These observations imply that changes in the vasoconstrictor tone of both the afferent and efferent arterioles are an important component of the pathogenesis of septic AKI.