Biopsy-proven vancomycin-induced acute kidney injury: a case report and literature review

Abstract

Background: Vancomycin is the first-line antibiotic for methicillin-resistant Staphylococcus aureus and coagulase-negative strains. The risk of vancomycin-induced acute kidney injury increases with plasma vancomycin levels. Vancomycin-induced acute kidney injury is histologically characterized by acute interstitial nephritis and/or acute tubular necrosis. However, only 12 biopsy-proven cases of vancomycin-induced acute kidney injury have been reported so far, as renal biopsy is rarely performed for such cases. Current recommendations for the prevention or treatment of vancomycin-induced acute kidney injury are drug monitoring of plasma vancomycin levels using trough level and drug withdrawal. Oral prednisone and high-flux haemodialysis have led to the successful recovery of renal function in some biopsy-proven cases.

Case presentation: We present the case of a 41-year-old man with type 1 diabetes mellitus, who developed vancomycin-induced acute kidney injury during treatment for Fournier gangrene. His serum creatinine level increased to 1020.1 μmol/L from a baseline of 79.6 μmol/L, and his plasma trough level of vancomycin peaked at 80.48 μg/mL. Vancomycin discontinuation and frequent haemodialysis with high-flux membrane were immediately performed following diagnosis. Renal biopsy showed acute tubular necrosis and focal acute interstitial nephritis, mainly in the medullary rays (medullary ray injury). There was no sign of glomerulonephritis, but mild diabetic changes were detected. He was discharged without continuing haemodialysis (serum creatinine level, 145.0 μmol/L) 49 days after initial vancomycin administration.

Conclusions: This case suggests that frequent haemodialysis and renal biopsy could be useful for the treatment and assessment of vancomycin-induced acute kidney injury, particularly in high-risk cases or patients with other renal disorders.

Keywords: Acute interstitial nephritis; Acute kidney injury; Acute tubular necrosis; High-flux haemodialysis; Vancomycin.

Fig. 1

Clinical course for the treatment of Fournier gangrene and vancomycin-induced acute kidney injury in a 41-year-old man. The vertical biaxis shows the serum creatinine level (sCr, red), urinary volume (yellow), and plasma trough level of vancomycin (green). Intravenous vancomycin dosages were 3.0 g/day, then increased to 4.5 g/day. VCM, vancomycin; HD, haemodialysis, PIPC/TZA, Piperacillin/Tazobactam; ABPC/SBT, Ampicillin/Sulbactam; LVFX, Levofloxacin; CLDM, Clindamycin

Fig. 2

a Computed tomography image showing free air in the genital lesion (white arrow). b Computed tomography image showing no sign of hydronephrosis or renal atrophy. c Gallium scintigraphy showing significant accumulation in both kidneys (yellow arrows)

Fig. 3

Kidney biopsy slide specimen showing: a subcapsular and medullary ray fibrosis in 10% of the specimen, b mild mesangial expansion in the glomeruli, c focal but severe lymphocyte infiltration and tubulitis, d tubular epithelium injury with nuclear denudation or tubular dilatation, and e interstitial monocyte infiltration and tubulitis mainly distributed in the medullary ray lesion [a, Masson trichrome, × 2; b, c, Periodic acid–Schiff, × 40 and × 20, respectively; d, Periodic acid–methenamine–silver, × 40; e, Tamm–Horsfall protein staining added on Periodic acid–Schiff, × 10]