Abstract
Human and experimental animal data support that AKI adversely affects the lungs. Experimental animal study could reveal that AKI itself affect to endothelial cell injury due to inflammation and apoptosis in lungs. Surfactant protein (SP)-A and SP-D are members of C-type lectin family, which play a critical role in host defense and regulation of inflammation in varitey of infections. Of lung specific markers, serum levels of SP-A and D have been reported to be increased in many lung diseases. Our hypothesis is AKI itself affect the injury of pneumocyte I and II, which could develop impairment of lung host defense mechanism.
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