PGI2 is also a potent vasodilator and helps maintain renal perfusion in conditions of decreased actual or effective circulating volume; its inhibition in such patients can result in acute renal failure.
Because a MAP level of 65 mmHg is a survival factor in critically ill patients [88], especially during sepsis [89 91], this value is usually considered as the lowest acceptable level required for maintaining renal perfusion during AKI [92].
Intravenous fluids are widely administered to maintain renal perfusion and prevent acute kidney injury (AKI).
Maintaining renal perfusion and urine output can aid elimination of dabigatran, 80% of which is excreted through the kidneys unchanged.
In this model Male Sprague- Dawley rats are used, which are given NE and Ang II intravenously for 14 days, while an inflatable vascular occluder maintains renal perfusion pressure to the left kidney at baseline levels, and exposes the right kidney to elevated perfusion pressure [ 42].
If a patient receiving dabigatran presents with bleeding: omit/delay next dose of dabigatran; measure APTT and thrombin time (consider DTI assay if available); administer activated charcoal, with sorbitol, if within 2 h of dabigatran ingestion; give tranexamic acid (1 g intravenously if significant bleeding); maintain renal perfusion and urine output to aid dabigatran excretion.
Albumin-mediated renoprotection may be explained by several mechanisms, including maintaining renal perfusion [ 6, 31, 32], promoting proximal tubular integrity and function [ 22, 33- 38], binding of endogenous toxins and nephrotoxic drugs [ 39- 42], and preventing oxidative damage and binding and delivering protective lysophosphatidic acid [ 34, 36, 43, 44].
Our finding is in line with recent studies, which have demonstrated that higher MAP levels than previously recommended may be required to maintain adequate renal perfusion [ 14, 15].
Thus, maintaining adequate renal perfusion to overcome derangements caused by loss of autoregulation may be one of the few current therapeutic options for prevention and treatment of AKI.
In this concept, in chronic heart failure, an equilibrium exists where a certain degree of congestion is the price to be paid to maintain adequate renal perfusion and function.
