This patient was a 70-year-old woman, diagnosed with high-grade myelodysplastic syndrome. After having achieved remission with systemic chemotherapy, she underwent a haploidentical stem cell transplantation. For GvHD prevention, she received post-transplant cyclophosphamide, tacrolimus, and mycophenolate mofetil. CMV serostatus: D−, R+. Despite anti-CMV prophylaxis with letermovir, CMV viral load increased from month 3 on, and a preemptive treatment with valganciclovir was introduced. Given a further increment of the viral load despite this treatment, foscarnet was subsequently started. Phosphonoformate crystalluria (proven by infrared spectrometry) was observed at day 9 after onset of foscarnet associated with a nonglomerular hematuria and renal tubular epithelial cells in urine sediment. The patient developed AKI KDIGO stage 1 at day 14.
This patient was a 63-year-old man who underwent liver transplantation for alcohol-induced cirrhosis. Despite anti-CMV (serostatus D+, R−) prophylaxis, the patient developed CMV infection against what he first received valganciclovir. The viral load of CMV further increasing, the patient was switched to foscarnet; however, phosphonoformate crystalluria (proven by infrared spectrometry) was observed 1 month after onset of the treatment with foscarnet and was accompanied by glomerular haematuria, leukocyturia, and renal tubular epithelial cells in urine sediment. The patient developed AKI KDIGO stage 1 47 days after onset of the treatment with foscarnet. CMV viral load decreased but remained present under bitherapy (foscarnet/ganciclovir, then ganciclovir/letermovir). Elevated creatinine persisted despite discontinuation of foscarnet.