Sepsis & AKI

Figure 1a. A simplified illustration of the traditional model of sepsis induced renal failure. Despite the vasodialtory effect of nitric oxide (NO) synthase, sepsis induced hypovloalemia and hypotension activates the sympathetic and renin-angiotensin-aldosterone system (RAAS) resulting in net renal vasoconstriction, decrease in glomerular filtration rate, and if severe and persistent enough, ischaemia induced tissue damage (ATN).

Figure 1b. A simplified illustration of the proposed contemporary, resuscitated model of sepsis induced renal failure. Sepsis induced hypovloalemia and hypotension, when treated early and aggressively results in reduced activation the sympathetic and renin-angiotensin-aldosterone system (RAAS) causing less renal vasoconstriction. The net effect of vasodilatation from unopposed NO may result in a decrease in glomerular filtration rate because of the loss of afferent - efferent renal arteriolar control rather than decreased renal blood flow. Despite adequate renal blood flow, with time inflammatory mechanisms and apoptosis are likely to contribute to tissue damage.

Figure 1c. A simplified diagram of inflammatory mechanisms leading to endothelial and renal tissue damage.