PMC5437995_01
Axial CT source images. A: At the level of the renal hila. The swollen left kidney enhances poorly following intravenous contrast administration. There is calyceal distension and overlying cortical thinning. High attenuation calculus material is seen in the renal pelvis (white arrows). There is inflammatory stranding in the pararenal fat. B: Just inferior to the left kidney. Well-defined, low attenuation lesions are seen in both the enlarged left psoas and iliacus muscles (white arrows); the former contains a fleck of calcification. The rim of both lesions enhances with the administered intravenous contrast. Appearances are consistent with left-sided xanthogranulomatous pyelonephritis and secondary abscess formation. The psoas abscess contains an extruded calculus.
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Figure1
A CT abdomen was in keeping with unilateral XGP (Figure 1).
Gross nephrectomy specimen. A: Gross nephrectomy specimen - dilated renal pelvis filled with a large of amount of yellow pus-like material displaying regional areas of hemorrhage. B: Light microscopy of renal parenchyma with Hematoxylin and Eosin stain. Inflammatory infiltrate with foamy histiocytes and neutrophil clusters. Ziehl-Neelsen and auramine staining were negative for tuberculosis. C: Light microscopy of normal area of tissue from nephrectomy specimen showing no evidence of anti-GBM disease.
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Figure2
Proteus mirabilis isolated on microbiological culture (Figure 2). Postoperative contralateral renal ultrasound was normal and renal function preserved, creatinine pre-operatively was 0.57 mg/dL, with creatinine 0.53 mg/dL, and estimated glomerular filtration rate (eGFR), calculated by the modified Schwartz method, of 102 mls/min/1.73 m2 on discharge. 
Histopathological images. A: Hematoxylin and Eosin stain showing diffuse circumferential crescentic and necrotizing injury of the glomerulus, characteristic of anti-GBM disease. B and C: Methenamine silver stain shows remnants of the glomerular basement membrane (GBM) surrounded by a cellular crescent occupying bowman's space and focal fibrinoid necrosis. D: Immunofluorescence showing strong linear IgG of the GBM characteristic of anti-GBM disease. The glomerulus is compressed by a cellular crescent (not visible on immunofluorescence).
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Figure3
Histology revealed strong linear IgG deposition along the GBM with greater than 95% of glomeruli demonstrating crescents and evidence of acute tubular necrosis (Figure 3).