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.
A 73-year-old man, previously diagnosed with myelodysplastic syndrome, underwent hematopoietic stem cell transplantation from an HLA-haploidentical donor. CMV serostatus: D−, R−. GvHD prophylaxis consisted of post-transplant cyclophosphamide, tacrolimus, and mycophenolate mofetil. In the post-transplantation phase, the patient presented several complications, including oral herpes (HSV1) infection. Because of proven in vitro valaciclovir resistance, foscarnet was introduced: phosphonoformate crystalluria was observed at day 11 after onset of therapy. Neither red blood cells nor any other cells were seen in the urine sediment. The patient developed AKI KDIGO stage 2 at day 12. The viral infection was effectively treated, but the patient died 2 months later due to an invasive fungal infection.