Abstract: FR-PO087
Role of Macrophages in Human AKI
Session Information
- AKI: Mechanisms - Inflammation/Sepsis/Remote Injury
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Kim, Myung-Gyu, Korea University Anam Hospital, Seoul, Seoul, Korea (the Republic of)
- Lim, Kijoon, Korea University Anam Hospital, Seoul, Seoul, Korea (the Republic of)
- Lee, Kyungmi, Korea University Anam Hospital, Seoul, Seoul, Korea (the Republic of)
- Jo, Sang-Kyung, Korea University Anam Hospital, Seoul, Seoul, Korea (the Republic of)
Background
Macrophages are an important player in the injury and repair of experimental ischemia/reperfusion injury (IRI). While M1 macrophage contribute to IRI, phenotypic shift from pro-inflammatory M1 to anti-inflammatory M2 macrophages is important in repair process. However, emerging evidence also show persistence of M2 macrophages is associated with fibrosis. The purpose of this study is to examine the role of macrophages in human acute kidney injury (AKI).
Methods
We retrospectively reviewed the medical records of 72 patients with biopsy proven acute tubular necrosis (ATN) without chronic lesions, including 29 cases of native kidneys and 43 cases of deceased donors. M1 and M2 macrophage infiltration was determined by immunohistochemistry of CD68 and CD163 respectively. Healthy kidney sections obtained from nephrectomy was used as control.
Results
CD163+ macrophage outnumbered CD68+ cells in control kidneys and both of these macrophage subtypes increased significantly in ATN. The number of CD68+ M1 macrophage was significantly higher in stage 3 AKI compared to stage 1 or 2. However, there was no difference in the number of CD163+ M2 macrophages according to different stages of AKI.
During the mean follow up period of 35.4 ± 30.9 months, 72.2% showed renal functional recovery defined as eGFR≥60ml/min/1.73m2. In contrast to CD68+ M1 macrophage that showed no association with renal recovery, the number of CD163+ M2 macrophage was significantly lower in patients with renal recovery (3.34 ± 2.3 vs 5.23±2.92 cells/HPF, X200, p=0.005). This association was evident especially in native kidney ATN, more advanced stage AKI and also in late biopsy groups. The number of CD168+ M2 macrophage was found to be an independent predictor of no recovery of renal function at 3 months in advanced stage AKI.
Conclusion
This is a first human study demonstrating the possible important role of macrophages with heterogenous phenotypes in injury and repair of AKI.