case_images: PMC10601886_01
case_images: Renal histopathology of RPDN. a: PAS, b, c: PAM, d: IgG, e: IgA, f: C3, magnification, x400. Light microscopy revealing endothelial enlargement and inflammatory cell infiltration in the glomeruli and PTCs and a moderately enlarged mesangial area (a). Mesangiolysis, and some GBM doubling were observed (b, c). Immunofluorescent staining of paraffin-embedded kidney tissue showing that IgG was 1+ to 2+ in granular form on the GBM (d), a finding consistent with DN, IgA was 1+ to 2+ in the mesangium (e) and C3 was 1+ in the mesangium (f), suggesting a complication of IgA nephropathy, but the increase in mesangial cells was not noticeable on light microscopy.
case_images: cnd-2023-0013-0001-531015_F01.jpg
case_images: PMC10601886_01_cnd-2023-0013-0001-531015_F01.jpg
case_images: F1
case_images: Light microscopy showed mild mesangial expansion (Fig. 1a: periodic acid-Schiff stain [PAS], Fig. 1b, c: periodic acid-methenamine-silver stain [PAM]) and neovascularization at the glomerular vascular pole (Fig. 1a, arrow), but no lesions of nodular sclerosis were observed. DN class IIb was made. Despite the absence of thrombotic findings, pathologic TMA findings such as glomerular and PTC endothelial enlargement (Fig. 1b, asterisk), mesangiolysis (Fig. 1b, arrow), and GBM doubling (Fig. 1c, arrow head) were observed. IgG in granular form on the GBM (Fig. 1d), a finding consistent with DN. IgA (Fig. 1e) and C3 (Fig. 1f) deposits were found in the mesangial area, suggesting
case_images: VEGF staining results (a: normal kidney glomerulus, b, c: DN control glomerulus, d: RPDN glomerulus, e normal kidney interstitium, f, g: DN control interstitium, h: RPDN interstitium, magnification, x400) and HB-EGF staining results (i: normal kidney, j: DN control, k: RPDN, magnification, x400). Immunohistological examination results showing VEGF staining on the glomerular epithelial cells and CD31 staining on the vascular endothelial cells and PTCs in the normal control (Normal 1) (a). VEGF is rarely expressed in the tubular interstitium (a). In the DN controls (DN 1, 2), there is a marked expression of VEGF in the glomeruli and tubulointerstitium and a decrease in the number of CD31-positive endothelial cells in the glomerular and tubulointerstitium (b, c). In the RPDN case, a marked decrease in VEGF expression was only present in the glomerular epithelial cells, and the expression of VEGF in the tubulointerstitium was higher than that in the normal control (Normal 1) (d). HB-EGF immunostaining showing high expression in mesangium in the RPDN case (g), weak positivity in the DN control (DN 2) (f), and no expression in the normal control (Normal 2) (e). VEGF and HB-EGF are stained green, CD31-positive vascular endothelium is stained red, and nuclei are stained blue with DAPI. PAS, periodic acid-Schiff stain; PAM, periodic acid-methenamine-silver stain; PTCs, peritubular capillaries; DN, diabetic nephropathy; GBM, glomerular basement membrane; RPDN, rapidly progressive diabetic nephropathy; VEGF, vascular endothelial growth factor; HB-EGF, heparin-binding epidermal growth factor-like growth factor; GBM, glomerular basement membrane.
case_images: cnd-2023-0013-0001-531015_F02.jpg
case_images: PMC10601886_01_cnd-2023-0013-0001-531015_F02.jpg
case_images: F2
case_images: IgA nephropathy, but the absence of mesangial cell proliferation suggested that the disease was inactive. Immunohistochemical staining results showed markedly decreased VEGF expression only in glomeruli (Fig. 2d, h) and markedly increased heparin-binding epidermal growth factor-like growth factor (HB-EGF) expression in mesangial regions (Fig. 2k) in the RPDN case compared to DN class IIb (Fig. 2b, c, f, g) and normal (Fig. 2a, e) controls. In DN class IIb controls, VEGF expression in the glomerular (Fig. 2b, c) and tubular interstitium (Fig. 2f, g) was markedly upregulated compared to that in the normal controls (Fig. 2a, e), and HB-EGF expression in the mesangial region was slightly enhanced (Fig. 2j). Moreover, HB-EGF expression was not observed in the normal control (Fig. 2i).