JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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MIP-1α and NF-κB as indicators of acute kidney injury secondary to acute lung injury in mechanically ventilated patients.

OBJECTIVE: In this study the levels of macrophage inflammatory protein-1α and NF-κB were measured in patients suffering acute kidney injury secondary to acute lung injury induced by mechanical ventilation and in controls, to determine whether they are differentially expressed.

PATIENTS AND METHODS: 160 patients were enrolled in our study: 40 had acute kidney injury secondary to acute lung injury induced by mechanical ventilation (group A), 40 had acute lung injury induced by mechanical ventilation, but no secondary acute kidney injury (group B), 40 were treated with mechanical ventilation but suffered no complications (group C), and 40 were treated with a conventional nasal catheter or oxygen mask inhalation (group D). The seric levels of MIP-1α, NF-κB and hs-CRP were compared amongst the groups at time points of 6, 12, 24, and 72 hours and at 7 days after the start of the respiratory treatment.

RESULTS: The serum levels of MIP-1α, NF-κB and hs-CRP of groups A and B were significantly higher than those of groups C and D at each time point. Also, group A had higher levels than group B at each time point, and the differences were statistically significant (p < 0.05). No statistically significant differences were found while comparing levels in group C with those of group D (p > 0.05). In groups A and B, the levels of MIP-1α increased gradually to a peak at 72 hours and then fell again on the 7th day. Levels of NF-κB in groups A and B significantly increased at 6, 12 and 24 hours, and reached a peak level at 24 h, to then fall after 72 h. The levels in group A fell back to baseline at 7 days, while group B levels fell back to baseline faster, at 72 h. Finally, the levels of hs-CRP in groups A and B kept increasing even after 7 days.

CONCLUSIONS: Based on these results, it is possible that the levels of MIP-1α and NF-κB be used as early indicators of inflammation reflecting the occurrence of acute kidney injury secondary to acute lung injury induced by mechanical ventilation.

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