An increasing body of experimental evidence suggests that lung/kidney interactions are involved both in AKI-associated acute lung injury (ALI) and renal consequences of acute respiratory failure. Positive pressure ventilation, changes in PaCO2 and PaO2 levels along with systemic inflammation participate in the renal response to acute respiratory failure.
Positive pressure ventilation may modify venous return, cardiac after-load and may decrease cardiac output along with decreased renal blood flow, in glomerular filtration rate (GFR), and in osmolar and water clearance [1, 2]. Beyond hemodynamic consequences of mechanical ventilation, these effects were partly ascribable to an activation of the sympathetic and renin-angiotensin systems, suppress the atrial natriuretic peptide release, while anti-diuretic hormone concentration was demonstrated to play little role [1, 3–5]
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Changes in PaCO2 and PaO2 levels were shown to influence renal perfusion or sodium and water clearance.…