The rise in BUN (azotemia) in AP patients are explained by a mechanism of acute renal injury consequence of (a) the loss of intravascular volume, due to interstitial extravasations related to the systemic inflammatory response (SIRS) [9, 12, 16] and (b) a direct renal injury mechanism, occurring in AP promoted by the releasing of activated enzymes such trypsin and chymotrypsin, inflammatory mediators, and cytokines (TNF-alpha, IL-8, IL-6, and IL-1 beta) [17]. Here, IL1B is linked to alkaline phosphatase measurement.