RESUMEN
Introduction: JC polyomavirus (JCPyV) is a ubiquitous virus that can be latent in the brain and the kidney. It is the etiologic agent responsible for progressive multifocal leukoencephalopathy, a fatal, demyelinating disease of the central nervous system, and rarely causes polyomavirus nephropathy in immunocompromised kidney transplant recipients. Case description: We present the first case of JCPyV nephropathy in a simultaneous heart-kidney transplant patient, where viral-specific in situ hybridization staining of the kidney tissue was utilized to confirm the diagnosis. The patient was diagnosed 6 years after simultaneous heart-kidney transplantation and was treated with immunosuppression reduction and intravenous immunoglobulin. Discussion: JCPyV nephropathy should be considered in the differential diagnosis of kidney allograft injury, particularly, with suggestive light microscopy histologic features in the absence of BK polyomavirus viremia and/or viruria. In addition to obtaining JCPyV PCR in the blood, in situ hybridization staining may have a utility in confirming the diagnosis. To date, we lack effective JCPyV-specific therapies, and prompt initiation of immunosuppression reduction remains the mainstay of treatment.
RESUMEN
The use of allografts from hepatitis C virus (HCV) Nucleic Acid Testing (NAT)+ donors into HCV NAT- recipients has been reported to be efficacious in a handful of studies. However, these studies have not reflected real-world practice where the initiation of direct-acting antivirals (DAA) is dependent on insurance coverage. A single-center, retrospective chart review of HCV NAT- recipients who underwent solid organ transplantation (SOT) from a HCV NAT+ donor between April 1, 2019 and May 27, 2020 was conducted. Sixty-one HCV NAT- patients underwent SOT with a HCV NAT+ organ, with 59 transplant recipients included for evaluation: 22 kidney (KT), 18 liver (LiT), 10 heart (HT), nine lung (LuT). HCV transmission occurred in 100% of recipients. Average time to DAA initiation was POD 46.3 ± 25 days. SVR12 was achieved in 98% (56/57; two patients ineligible for analysis). Treatment failure occurred in one LuT on glecaprevir/pibrentasvir with P32del and Q80K mutations. No patients developed fibrosing cholestatic hepatitis. Two patients died, secondary to anastomotic complication (LuT) and pulmonary embolism (HT). Clinically significant rejection was diagnosed and treated in two HT (one patient with ACR2 and one with ACR2/pAMR2) and one LiT (RAI 5/9). Six patients (10.2%) had documented adverse effects attributed to DAA therapy, primarily gastrointestinal.
