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 35-year-old man diagnosed with acute lymphoblastic leukemia achieved a second complete remission following salvage chemotherapy after a first relapse. Stem cell transplantation from an HLA-matched unrelated donor was performed following myeloablative conditioning. CMV serostatus was D−, R−. To prevent GvHD, cyclosporine with a short course of methotrexate was administered. Numerous complications occurred after transplantation, including an human herpesvirus 6 encephalitis. For the latter, ganciclovir was started and replaced after 24 hours by foscarnet because of concerns about known associated myelotoxicity with high doses of ganciclovir. Phosphonoformate crystalluria (proven by infrared spectrometry) was observed 7 days after onset of foscarnet associated with a nonglomerular hematuria but without renal tubular epithelial cells in urine sediment. Because of a stable kidney function, foscarnet administration was maintained at unchanged doses. Despite the human herpesvirus 6 encephalitis resolution, the patient died from acute respiratory failure due to uncontrolled bleeding.