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Specific COX-2 inhibition may induce renal ischemia, electrolyte imbalance and increased blood pressure, ultimately leading to fluid and sodium retention and decreased GFR [8].
However, this is the superimposition of renal hypoperfusion episodes in relation to other insults, such as sepsis or ischemia, which may induce renal failure.
Based on this pathogenesis, all hyperoncotic colloids may induce renal damage, whereas iso-oncotic tetra starch solutions, such as 6% HES 130/0.4, seem not to impair renal function [41, 46].
Collectively, our data indicate that the intravenous infusion of rhLK8 at therapeutic doses may induce renal toxicities, such as acute TIN, but these toxicities are clinically tolerable and reversible with close monitoring and a recovery period.
Although sepsis is the most frequent cause of AKI in the intensive care setting, a number of other clinical conditions may induce renal failure [ 1].
96 Subsequently, it has been found that long-term use in adults may induce renal toxicity and osteomalacia in some patients.
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Furthermore, the oncotic force of colloids may induce further renal function impairment by decreasing the renal filtration pressure [ 3].
Therefore, our findings suggest HGF gene therapy may induce a renal microenvironment that might promote macrophage-mediated renal tissue repair and regeneration.
Therefore Hippo signalling may regulate renal regeneration after AKI occurs, and the changes in the irreversible protein levels of the Hippo pathway components may induce persistent renal fibrosis.
Second, hyperuricemia may induce direct renal injury through the activation of the renin-angiotensin aldosterone system (RAS).
To validate if these studied polymorphisms may induce a renal injury in critically ill patients in ICU setting, a multicentric study with a larger sample size should be conducted.
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