Table 1.
Clinical and laboratory findings on patients at the time of biopsy.
Fig 1.
Expression of CMIP in glomeruli from patients with class II lupus nephritis.
Representative immunohistochemistry analysis of class II positive biopsies. Top panel: CMIP and WT1 expression in controls (normal human kidney); WT1 labeling shows selective localization in podocytes. Right of the panel: CMIP expression in lupus nephritis class II. CMIP abundance is clearly increased in podocytes with same cellular distribution as WT1, while no detectable expression was seen in tubules. Scale bars, 20 μm. Middle and lower panels: Confocal microscopy analysis of nephrin (red) and CMIP (green) expression in control human kidney (Con) and Class II lupus nephritis (LN-II) biopsies. CMIP abundance is significantly increased in LN-II and colocalizes with nephrin. Scale bars, 10 μm.
Table 2.
Histological and immunohistochemistry findings in class II biopsies.
Fig 2.
Expression of CMIP in patients with different classes of lupus nephritis.
Upper panel, expression of CMIP in patients with class III lupus nephritis. In one class III-lupus nephritis (left panel), CMIP is highly detectable in glomeruli with a nuclear and cytoplasmic pattern, while it is not induced in other biopsies (represented by right panel). Scale bars, 20 μm. Middle panel, expression of CMIP in patients with class IV lupus nephritis. No significant signal was detected in podocytes, either in cytoplasm or in nucleus compartments. Scale bars, 20 μm. Lower panel, expression of CMIP in patients with class V lupus nephritis. Note that CMIP is mostly expressed in the cytoplasm of podocytes. Scale bars, 20 μm.
Table 3.
Histological and immunohistochemistry findings in class III biopsies.
Table 4.
Histological and immunohistochemistry findings in class IV biopsies.
Table 5.
Histological and immunohistochemistry findings in class V biopsies.
Fig 3.
Phenotype characterization of renal infiltrating cells.
Left panel, Representative immunohistochemistry analysis. Double immunolabeling of kidney biopsies with CMIP (red) and either CD3, CD20 or CD68 (brown) antibodies. Mononuclear cells infiltrating the glomeruli or the interstitium are mainly positive for CD68 (macrophage), CD3 (T cells) and CD20 (B cells) markers. CMIP colocalized with a subset of either CD3 or CD20 positive cells, but never with CD68. Some cells are exclusively positive for CMIP. Scale bars, 20 μm. Right panel, immunofluorescence double labeling analysis of kidney biopsies with CMIP (green), CD3 or CD20 (red) antibodies. The colocalisation CMIP and T or B cells is restricted to some lymphocyte subsets. Scale bars, 50 μm.
Fig 4.
CMIP abundance is significantly increased in non-proliferative lupus glomerulopathies.
A- Quantitative reverse transcription-PCR of laser-microdissected glomeruli from kidney biopsy specimens (Class II: n = 4 (30 glomeruli); class III: n = 4 (58 glomeruli); class IV: n = 4 (32 glomeruli); Class V: n = 4 biopsies (48 glomeruli) and control kidneys (n = 5 samples, 69 glomeruli). Relative -fold inductions were calculated as described in Methods. Kruskal-Wallis test, **P = 0.0025. B- The relative abundance of CMIP was measured by computer-assisted image analysis using X 400 magnification. Positive staining within each glomerulus was expressed as percentage of the immunostained area over total glomerular area using the image analysis software (Image J). Kruskal-Wallis test, ****P< 0.0001.