case_images: PMC6304482_01
case_images: Serum creatinine trend. Serum creatinine at baseline was 91 umol/L (reference range: 40-100 umol/L). It increased to 177 umol/L on day of admission (arrow) to peak of 800 umol/L during admission. On day of discharge, serum creatinine was 554 umol/L (box). Dabigatran was started two years before this episode.
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case_images: fig1
case_images: Her serum creatinine rose from a baseline of 91 umol/L (reference value: 40-100 umol/L) to 177 umol/L on day of admission and reached 618 umol/L within 7 days of hospitalization (Figure 1).
case_images: Kidney biopsy histopathology I. (a) Kidney biopsy shows presence of abundant RBCs (box) and RBC casts (arrows) (Periodic Acid Schiff stain, Light Microscopy, Magnification: X200). (b) Kidney biopsy shows acute tubular injury with loss of brush borders, attenuated tubular epithelium, and reactive epithelial changes. RBC casts (arrows) indicate significant hemorrhage in tubules. The mesangium of glomerulus is minimally expanded with no evidence of proliferation. (Periodic Acid Schiff Stain, Light Microscopy, Magnification: X200.)
case_images: CRIN2018-7381505.002.jpg
case_images: PMC6304482_01_CRIN2018-7381505.002.jpg
case_images: fig2
case_images: The patient underwent a diagnostic kidney biopsy, which showed extensive red blood cell casts within tubular lumen as well as tubular epithelial cell injury on light microscopy (Figures 2(a) and 2(b)), without evidence of acute glomerulonephritis (Figures 3(a) and 3(b)).
case_images: Kidney biopsy histopathology II. (a) Periodic Acid Schiff (Magnification: X200) staining of glomeruli shows minimal mesangial expansion with no evidence of mesangial and endocapillary proliferation. Chronic ischemic damage is also evident by thickening of Bowman capsule membrane (blue arrow). The damaged tubules (black arrow) are also shown. (Light Microscopy.) (b) Hematoxylin and Eosin staining (Magnification: X100) shows damaged tubules with RBC casts (arrows) being seen. There is an absence of active glomerulonephritis.
case_images: CRIN2018-7381505.003.jpg
case_images: PMC6304482_01_CRIN2018-7381505.003.jpg
case_images: fig3
case_images: The patient underwent a diagnostic kidney biopsy, which showed extensive red blood cell casts within tubular lumen as well as tubular epithelial cell injury on light microscopy (Figures 2(a) and 2(b)), without evidence of acute glomerulonephritis (Figures 3(a) and 3(b)).
case_images: Kidney Biopsy Electron microscopy. Small subepithelial electron dense deposit shown in the mesangial notch (box) (Electron Microscopy).
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case_images: fig4
case_images: Electron microscopy showed subepithelial "hump-like" deposits most of which were located within the mesangial notch areas, and thus, thought to be resolving postinfectious glomerulonephritis (Figure 4).
case_images: Kidney biopsy immunofluorescence. Immunofluorescence microscopy probing for IgA, IgG, Kappa light chains, Lambda light chains, C3, and C1Q deposits. Trace focal deposition of C3 is present. IgA, IgG, Kappa light chains, Lambda light chains, and C1Q deposits are not visualized.
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case_images: PMC6304482_01_CRIN2018-7381505.005.jpg
case_images: fig5
case_images: Immunofluorescence microscopy was negative for IgA and IgG, but trace positive for C3 (Figure 5).