ABSTRACT
We report the first case of a ganciclovir-resistant cytomegalovirus (CMV) involving the gastrointestinal tract that was successfully treated with high-dose valganciclovir. A kidney transplant recipient developed drug-resistant CMV colitis which was initially treated with valganciclovir, but his CMV was found to have major resistance to ganciclovir and cidofovir due to UL97 and UL54 mutations. The patient was switched to intravenous foscarnet 40 mg/kg given every twelve hours. However, foscarnet had to be discontinued after 4 days of treatment due to acute kidney injury. Patient was restarted on valganciclovir at a higher target dose of 1800 mg twice a day based on the creatinine clearance. CMV became undetectable 2 weeks after valganciclovir treatment was completed. High-dose valganciclovir along with immune suppression reduction may be a treatment option for CMV colitis with ganciclovir resistance due to dual UL97 and UL54 gene mutations.
Subject(s)
Antiviral Agents/administration & dosage , Colitis/drug therapy , Cytomegalovirus Infections/drug therapy , Ganciclovir/analogs & derivatives , Viral Proteins/genetics , Adult , Cidofovir , Colitis/virology , Cytomegalovirus/drug effects , Cytomegalovirus/genetics , Cytomegalovirus Infections/virology , Cytosine/administration & dosage , Cytosine/analogs & derivatives , DNA-Directed DNA Polymerase/genetics , Drug Resistance, Viral/genetics , Foscarnet/administration & dosage , Ganciclovir/administration & dosage , Humans , Kidney Transplantation , Male , Mutation , Organophosphonates/administration & dosage , Phosphotransferases (Alcohol Group Acceptor)/genetics , Valganciclovir , Viral Proteins/drug effectsABSTRACT
Acute interstitial nephritis is a well-recognized cause of acute kidney injury in native kidneys. While the most common etiology being drug-induced, other causes are infectious, autoimmune, and idiopathic forms of disease. Drug-induced acute interstitial nephritis is not only uncommon in renal transplant recipients but is difficult to diagnose as it mimics acute cellular rejection histologically. We have described herein a renal transplant recipient with acute kidney injury to highlight the difficulties to distinguish acute interstitial nephritis from acute cellular rejection.
