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Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
Quantification and localization of M2 macrophages in human kidneys with acute tubular injury
Matthew B Palmer1, Alfred A Vichot2, Lloyd G Cantley2
1Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Abstract:
This study addresses for the first time the question whether there is significant macrophage population in human kidney sections from patients with acute tubular injury (ATI). We examined therefore the interstitial macrophage population in human kidney tissue with biopsy-proven diagnosis of ATI, minimal change disease (MCD), and MCD with ATI. Kidney biopsies from patients with the above diagnoses were stained with antibodies directed against CD68 (general macrophage marker), CD163 (M2 marker), and HLA-DR (M1 marker) and their respective electron microscopy samples were evaluated for the presence of interstitial macrophages. Our study shows that patients with ATI have significantly increased numbers of interstitial CD68(+) macrophages, with an increase in both HLA-DR(+) M1 macrophages and CD163(+) M2 macrophages as compared to patients with MCD alone. Approximately 75% of macrophages were M2 (CD163(+)) whereas only 25% were M1 (HLA-DR(+)). M2 macrophages, which are believed to be critical for wound healing, were found to localize close to the tubular basement membrane of injured proximal tubule cells. Ultra structural examination showed close adherence of macrophages to the basement membrane of injured tubular epithelial cells. We conclude that macrophages accumulate around injured tubules following ATI and exhibit predominantly an M2 phenotype. We further speculate that macrophage-mediated repair may involve physical contact between the M2 macrophage and the injured tubular epithelial cell.
Insights
Macrophages increase in human kidneys with acute tubular injury (ATI), predominantly showing an M2 healing phenotype near damaged tubules. This suggests macrophages play a key role in kidney repair following ATI.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Acute tubular injury (ATI) is a major cause of kidney dysfunction.
- The role of interstitial macrophages in ATI pathogenesis and repair remains unclear.
Purpose of the Study:
- To investigate the presence and phenotype of interstitial macrophages in human kidney tissue with ATI.
- To determine the relationship between macrophage populations and tubular injury.
Main Methods:
- Immunohistochemical staining of kidney biopsies for macrophage markers (CD68, CD163, HLA-DR).
- Evaluation of electron microscopy samples for interstitial macrophages.
- Comparison of macrophage populations in ATI, minimal change disease (MCD), and MCD with ATI.
Main Results:
- Significantly increased interstitial CD68(+) macrophages in ATI patients compared to MCD patients.
- Increased M1 (HLA-DR+) and M2 (CD163+) macrophages in ATI, with M2 macrophages predominating (~75%).
- M2 macrophages localized near injured proximal tubule basement membranes, with close adherence observed ultrastructurally.
Conclusions:
- Macrophages accumulate around injured tubules in ATI, exhibiting a predominantly M2 phenotype.
- M2 macrophages, associated with wound healing, may be involved in tubular repair following ATI.
- Physical contact between M2 macrophages and injured tubular cells might be crucial for repair mechanisms.

