case_images: PMC9411007_01
case_images: Clinical features and course of case 1. Renal biopsy of case 1 was performed approximately 2 months after disease onset. Disease activity and effectiveness of treatment for acute tubulointerstitial nephritis were monitored by renal function (serum creatinine), inflammation (C-reactive protein), and tubular functional defects (urinary glucose, protein, beta2-microglobulin, and N-acetylglucosaminidase). Abbreviations: RBx, renal biopsy; RBCs, red blood cells; NA, not available; HPF, high-power field; NAG, N-acetylglucosaminidase.
case_images: CRIN2022-6203803.001.jpg
case_images: PMC9411007_01_CRIN2022-6203803.001.jpg
case_images: fig1
case_images: On day X-4, the laboratory data indicated severe tubulointerstitial nephritis with positive urine protein (1+) and urine sugar (1+), along with urine beta2-microglobulin of 56.73 mg/L and N-acetyl-beta-D-glucosaminidase (NAG) of 14.5 IU/L, with eosinophilia (11% of white blood cells, 7100/muL) (Figure 1).
case_images: Renal pathological findings of case 1. Light microscopy findings show minor glomerular changes in case 1. Periodic acid-Schiff staining (a, c) and periodic acid methenamine silver staining (b). Immunofluorescence studies show no specific staining for immunoglobulin, complement, and fibrinogen (d).
case_images: CRIN2022-6203803.002.jpg
case_images: PMC9411007_01_CRIN2022-6203803.002.jpg
case_images: fig2
case_images: The renal specimen contained 8 glomeruli and was found to show no global sclerosis and no proliferative lesions or membranous alterations in the glomeruli (Figures 2(a) and 2(b)). Diffuse areas of tubulitis were observed, with necrosis and desquamation of tubular epithelial cells (Figure 2(c)). Immunoglobulins and complement were not specifically stained in the glomeruli (Figure 2(d)).