Toshihiro Nakano

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.

Abstract Circulating levels of fibroblast growth factor-21 (FGF21) start increasing in patients with chronic kidney disease (CKD) since early stages during the cause of disease progression. FGF21 is a liver-derived hormone that induces responses to stress through acting on hypothalamus to activate the sympathetic nervous system and the hypothalamus-pituitary-adrenal endocrine axis. However, roles that FGF21 plays in pathophysiology of CKD remains elusive. Here we show in mice that FGF21 is required to survive CKD but responsible for blood pressure dysregulation. When introduced with CKD, Fgf21 −/− mice died earlier than wild-type mice. Paradoxically, these Fgf21 −/− CKD mice escaped several complications observed in wild-type mice, including augmentation of blood pressure elevating response and activation of the sympathetic nervous system during physical activity and increase in serum noradrenalin and corticosterone levels. Supplementation of FGF21 by administration of an FGF21-expressing adeno-associated virus vector recapitulated these complications in wild-type mice and restored the survival period in Fgf21 −/− CKD mice. In CKD patients, high serum FGF21 levels are independently associated with decreased baroreceptor sensitivity. Thus, increased FGF21 in CKD can be viewed as a survival response at the sacrifice of blood pressure homeostasis.

We demonstrate immunoglobulin-complexed aspartate aminotransferase (macro-AST) in a 14-year-old boy with rectitis-type ulcerative colitis by using both gel filtration and electrophoresis methods. The immunoglobulin complexed with AST in this case was identified as an IgG kappa both by electrosyneresis and immunoprecipitation reactions. The present case was noted to have a concomitant elevation of macro-AST associated with deterioration of ulcerative colitis. However, macro-AST has continued to exist when the activity of ulcerative colitis subsided, and the serum level of AST became normal. Thus, macro-AST might be related to an immunological component of ulcerative colitis as well as to the activity of the disease.

As immunotactoid glomerulopathy (ITG) is a very rare primary glomerular disease, no standard treatment has been established. It has been reported that ITG progresses to end-stage renal disease at a high rate. Here, we report a case of ITG exhibiting nephrotic syndrome treated by administration of a single dose of rituximab every 6 months for 4 years. In this case, complete remission (CR) was not achieved with steroids alone, but was achieved through long-term depletion of B cells by administration of rituximab. This is the first report that single-dose rituximab every 6 months for 4 years not only achieved CR of ITG, but also allowed steroid tapering. .