Abstract
Acute kidney injury (AKI) corrupts the outcome of about 50% of all critically ill patients. We investigated the possible contribution of the pathology acidemia on the development of AKI. Pigs were exposed to acidemia, acidemia plus hypoxemia or a normal acid-base balance in an experimental setup, which included mechanical ventilation and renal replacement therapy to facilitate biotrauma caused by extracorporeal therapies. Interestingly, extensive histomorphological changes like a tubular loss of cell barriers occurred in the kidneys after just 5 hours exposure to acidemia. The additional exposure to hypoxemia aggravated these findings. These ‘early’ microscopic pathologies opposed intra vitam data of kidney function. They did not mirror cellular or systemic patterns of proinflammatory molecules (like TNF-α or IL 18) nor were they detectable by new, sensitive markers of AKI like Neutrophil gelatinase-associated lipocalin. Instead, the data suggest that the increased renal proton excretion during acidemia could be an ‘early’ first hit in the multifactorial pathogenesis of AKI.
Highlights
Plasma IL-6 levels increased in tendency in all groups during the experiment, except in the normoventilated control-group, which was exposed to the highest inspiratory pressures
Mean arterial pressure (MAP) values decreased during the induction of acidemia, but remained above 65 mmHg
A moderate positive end-expiratory airway pressure (PEEP) of 5 mmHg did most likely not result in a compromised kidney perfusion, since diuresis remained above clinically accepted cut offs for oliguria (0.5 ml/kg/hr) (Table 1, Fig 3)
Summary
Acute kidney injury (AKI) complicates the course of disease of up to 50% of all patients admitted to an intensive care unit [1,2,3] and contributes to the failure of further organs, especially the lungs [4]. This ‘kidney-lung cross-talk’ seems to take place bidirectional [5,6,7,8,9] and the pathophysiological mechanisms include the release of proinflammatory mediators due to mechanical ventilation, impaired circulation due to positive end-expiratory airway pressure (PEEP), as well as hypercapnia and hypoxia due to acute lung injury (ALI) or lung protective. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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