Acute kidney injury (AKI) has been shown to be associated with unfavorable outcomes in patients with concurrent acute lung injury (ALI). ALI related to AKI was originally called “uremic lung, " and these conditions are currently also related to cardiac and noncardiac pulmonary edema. However, lung injuries, as well as mechanical ventilation used to treat respiratory failure, have been shown to induce AKI. Experimental evidences in animal models with AKI or ALI have demonstrated the tight and bidirectional interactions between kidney and lung injury and shown many structural and functional similarities. To date, the molecular mechanisms of the kidney-lung interaction have been shown to involve a number of inflammatory mediators and receptors, channels/transporters for water or electrolytes, and leukocytes. Thus, kidney-lung crosstalk is commonly present in certain pathological states and is clinically recognized as a critical condition requiring intensive management. In this chapter, we discuss the pathogenic and mechanistic associations of AKI with lung injury.
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