Abstract
Acute kidney injury (AKI) is associated with widespread effects on distant organs, including the lungs. Surfactant protein (SP)-A and SP-D are members of the C-type lectin family, which plays a critical role in host defense and regulation of inflammation in a variety of infections. Serum levels of SP-A and SP-D are markers to reflect lung injury in acute respiratory distress syndrome, idiopathic pulmonary fibrosis, and sarcoidosis. We investigated the change of lung-specific markers, including SP-A and SP-D in an AKI mice model. We studied C57BL/6J mice 4 and 24 hours after an episode of ischemic AKI (23 min of renal pedicle clamping and then reperfusion); numerous derangements were present, including SP-A, SP-D, and lung tight-junction protein. Neutrophil infiltration and apoptosis in the lungs increased in ischemic AKI. Receptor for advanced glycation end products (RAGE) in the lungs, a marker of pneumocyte I, was not changed. Lung tight-junction proteins, particularly claudin-4, claudin-18, and anti-junctional adhesion molecule 1 (JAMA-1), were reduced in 24 hours after AKI. Serum SP-A and SP-D significantly increased in ischemic AKI. SP-A and SP-D in the lungs did not increase in ischemic AKI. The immunohistochemistry showed that the expression of SP-A and SP-D was intact in ischemic AKI. SP-A and SP-D in the kidneys were significantly higher in AKI than in the sham. These patterns of SP-A and SP-D in the kidneys were similar to those of serum. AKI induces apoptosis and inflammation in the lungs. Serum SP-A and SP-D increased in ischemic AKI, but these could have originated from the kidneys. So serum SP-A and SP-D could not reflect lung injury in AKI. Further study is needed to reveal how a change in lung tight-junction protein could influence the prognosis in patients with AKI.
Highlights
Acute kidney injury (AKI) is associated with high mortality and morbidity [1,2,3]
Serum creatinine levels and urea nitrogen were increased after ischemic AKI compared to the sham
The results showed that the amount of all three cytokines (IL-6, TNF-α, and monocyte chemoattractant protein-1 (MCP-1)) extremely increased in the serum of the AKI model, whereas the amount was significantly low in the sham (Fig 2)
Summary
Acute kidney injury (AKI) is associated with high mortality and morbidity [1,2,3]. Some reports suggest that AKI is a systemic disease that adversely affects other organs including bone, gut, brain, heart, and lungs [4,5,6,7]. The crosstalk between the kidneys and other organs could. Surfactant protein in acute kidney injury through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (HI17C-2059010017) and Soonchunhyang University Research Fund. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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