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Updated: Sep 12, 2025
Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
Relationship between macrophage phenotype and kidney survival in patients with lupus nephritis
Ozcan Uzun1, Cihan Heybeli2, Fatma Sema Anar Kutlu3
1Yalova Research and Training Hospital, Yalova, Turkey.
Insights
Increased CD163-positive cells in kidney interstitium predict lupus nephritis progression. CD68-positive cells also indicate progression in specific lupus nephritis classes.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus.
- Understanding the role of macrophage phenotypes in LN progression is crucial for targeted therapies.
Purpose of the Study:
- To investigate the association between macrophage phenotypes (CD68+, CD163+) and kidney disease progression in lupus nephritis patients.
Main Methods:
- Immunohistochemistry was used to quantify CD68+ and CD163+ cells in kidney biopsies.
- Kidney disease progression was defined by serum creatinine doubling or end-stage kidney disease.
Main Results:
- Higher interstitial CD163+ cell counts were significantly associated with kidney disease progression (p=0.016).
- Interstitial CD163+ cells predicted progression with 80% sensitivity and 75% specificity.
- In class III-IV LN, increased interstitial CD68+ cells correlated with progression (p=0.012).
Conclusions:
- Interstitial CD163+ macrophages are a potential biomarker for kidney disease progression in lupus nephritis.
- CD68+ macrophages may also indicate progression in specific subtypes of lupus nephritis.
Aims:
To determine the possible relationship between macrophage phenotypes and the progression of kidney disease in patients with lupus nephritis (LN).
Methods:
Using immunohistochemistry, CD68+ and CD163+ cells were counted per glomerulus and per high-power field in the tubulointerstitium. Progression was defined as a doubling of the serum creatinine level and/or progression to end-stage kidney disease.
Results:
Among the 21 patients, 52% had class III or IV LN. During the median follow-up of 88 months, 5 (23.8%) patients experienced progression. In terms of clinical and pathological markers, the only significant difference between progressors and nonprogressors was the number of interstitial CD163+ cells (median 4 versus 2.4, respectively; p=0.025). A cutoff value of 2.7 for the mean number of CD163+ cells in the interstitium yielded a sensitivity of 80% and specificity of 75% for progression. The estimated median time to progression among patients with ≥2.7 CD163+ cells was shorter (median 136 versus 202 months, p=0.023). A greater number of CD163+ cells in the kidney interstitium was associated with the progression of kidney disease (HR 2.88, 95% CI 1.22-6.80; p=0.016). Class III-IV LN was associated with a higher median number of glomerular CD163+ cells (OR 1.96, 95% CI 1.1-3.49, p=0.023). Endocapillary hypercellularity and extracapillary proliferation were associated with greater number of CD163+ cells in the glomerular area. Among patients with class III-IV LN, the number of interstitial CD68+ cells was greater in those who experienced progression of kidney disease (p=0.012).
Conclusion:
A greater number of CD163+ cells in the kidney interstitium was associated with the progression of kidney disease in patients with LN, while a greater number of CD68+ cells in the interstitium was associated with progression in the subgroup of patients with class III-IV LN.
