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<p>Since March 2024, many cases of renal dysfunction have been reported in Japan among individuals taking a supplement containing red yeast rice. We present the case of a 51-year-old woman who developed renal dysfunction and Fanconi syndrome after taking the supplement. The patient was referred to our hospital with hypouricemia, hypokalemia, hypophosphatemia, and glucosuria. Following a renal biopsy broadcast reports of kidney damage caused by the red yeast rice supplement and the patient’s declaration of taking this supplement, we diagnosed her with supplement-induced acute kidney injury and Fanconi syndrome. Renal pathological findings revealed acute tubular necrosis, including brush border loss and mitochondrial fragmentation in the proximal tubular cells. These were consistent with the clinical and pathological findings of previous cases involving the red yeast rice supplement. Additionally, a reduction in sodium-glucose co-transporter 2 (SGLT2) expression was observed in the proximal tubules, supporting that the red yeast rice supplement damaged the proximal tubular cells. The reduction of SGLT2 protein expression may be linked to supplement-induced glucosuria. After supplement intake was ceased, renal function recovered and laboratory findings including glucosuria returned to normal within 6&#xa0;months. The loss of glucosuria suggests that SGLT2 protein expression may be reversible. In consideration of our case and previous cases, it is probable that the nephrotoxicity of red yeast rice supplement is primarily affecting the proximal tubules, particularly the S1 and S2 segments.</p>

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Tubular damage and SGLT2 expression in a patient with Beni-koji tablet-associated acute kidney injury and Fanconi syndrome

  • 期刊论文

  • 发表日期：

    2025年3月24日

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  • Ayaka Kamada,
  • Takuo Hirose,
  • Hideaki Hashimoto,
  • Yukari Konya,
  • Fumiya Sato,
  • Katsuya Ishiyama,
  • Kensuke Joh,
  • Wako Yumura,
  • Takefumi Mori

摘要

Since March 2024, many cases of renal dysfunction have been reported in Japan among individuals taking a supplement containing red yeast rice. We present the case of a 51-year-old woman who developed renal dysfunction and Fanconi syndrome after taking the supplement. The patient was referred to our hospital with hypouricemia, hypokalemia, hypophosphatemia, and glucosuria. Following a renal biopsy broadcast reports of kidney damage caused by the red yeast rice supplement and the patient’s declaration of taking this supplement, we diagnosed her with supplement-induced acute kidney injury and Fanconi syndrome. Renal pathological findings revealed acute tubular necrosis, including brush border loss and mitochondrial fragmentation in the proximal tubular cells. These were consistent with the clinical and pathological findings of previous cases involving the red yeast rice supplement. Additionally, a reduction in sodium-glucose co-transporter 2 (SGLT2) expression was observed in the proximal tubules, supporting that the red yeast rice supplement damaged the proximal tubular cells. The reduction of SGLT2 protein expression may be linked to supplement-induced glucosuria. After supplement intake was ceased, renal function recovered and laboratory findings including glucosuria returned to normal within 6 months. The loss of glucosuria suggests that SGLT2 protein expression may be reversible. In consideration of our case and previous cases, it is probable that the nephrotoxicity of red yeast rice supplement is primarily affecting the proximal tubules, particularly the S1 and S2 segments.