PMC5577077_01
Clinical course. The kidney function deteriorated rapidly, and the creatinine kinase concentration was markedly elevated after admission. Cre: creatinine, UA: uric acid, CK: creatine kinase
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On the third day, the concentrations of serum creatinine, uric acid, and CK rose to 3.91 mg/dL, 11.0 mg/dL, and 24,640 U/L, respectively (Fig. 1).
(a) Contrast-enhanced computed tomography with 40 mL of iodine contrast agent performed during an episode of acute kidney injury. A nephrographic-phase image at 120 s after contrast administration shows patchy areas of hypoattenuation in both kidneys. (b) Computed tomography 24 h after contrast administration demonstrates persistent enhancement in the patchy areas, which correspond to the hypoattenuated areas on nephrographic-phase CT. The wedge-shaped areas comprise multiple linear bands of contrast enhancement. (c) Diffusion-weighted imaging shows signal hyperintensity in the hypoattenuated areas on contrast-enhanced computed tomography.
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Wedge-shaped areas of decreased enhancement in both kidneys were noted on contrast-enhanced CT with 40 mL of iopamidol (300 mg iodine/mL) at the time serum creatinine was 1.88 mg/dL (eGFR, 38.2 mL/min/1.73 m2) during the recovery phase of AKI (Fig. 2a). Twenty-four hours later, unenhanced CT revealed residual contrast medium in the corresponding areas (Fig. 2b). Renal MRI showed multifocal wedge-shaped areas of signal hyperintensity on diffusion-weighted imaging (DWI) (Fig. 2c), with the same areas appearing slightly hyperintense on T2-weighted imaging.
Pathological findings of the renal biopsy specimen. Cellular injury of the tubular epithelial cells (arrows) and the loss of brush borders (arrowheads) are evident. In contrast, at least one glomerulus appears normal. Periodic acid-Schiff staining (400x), Scale bar 200 microm.
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A renal biopsy revealed acute tubular necrosis with normal glomeruli showing no deposition of urate crystals (Fig. 3).