JC virus‐associated nephropathy in a post‐heart and ‐kidney transplantation patient

Abstract

Transpl Infect Dis. 2020;22:e13288.| 1 of 4 https://doi.org/10.1111/tid.13288 wileyonlinelibrary.com/journal/tid | INTRODUC TI ONPolyomavirus-associated nephropathy in solid organ transplantations is rarely caused by JC virus, with BK viremia being the more common cause. There are few cases of JC virus-associated nephropathy in kidney transplant patients, and even fewer cases in recipients of other solid organ transplants. We present a case of JC virus-associated nephropathy in a dual heart-kidney transplant recipient, which to our knowledge is the first case reported in the literature. | C A S E REP ORTA 79-year-old Caucasian male with a history of left nephrectomy in 1981 for an infected congenital atrophic kidney underwent a heart-kidney transplant in October 2011 for restrictive cardiomyopathy secondary to wild-type TTR amyloidosis and end-stage renal disease from presumed cardiorenal syndrome. As per our program's protocol with dual organ transplants, the patient received rabbit anti-thymocyte globulin (rATG) dosed at 1.5 mg/kg daily with standard premedication for 5 days immediately after surgery. A month after his transplantation, the patient had a negative serum polyoma BK virus PCR as part of routine screening after transplantation.The patient did well after heart-kidney transplantation with no episodes of rejection or infection requiring hospitalization. By 1-year post-transplant, his immunosuppressive regimen consisted of tacrolimus 1 mg twice daily titrated to a goal level 5-10 ng/mL and mycophenolate mofetil 500 mg twice daily. The patient was weaned to prednisone 10 mg daily at 3 months and 5 mg daily at 6 months. However, 7 years after heart-kidney transplantation, he presented with progressive renal dysfunction, with creatinine rising from 1.3 to 2.0 mg/dL over the course of 2 months. A urinalysis revealed a bland sediment without protein or leukocytes. Screening for decoy cells in urine is not routinely done at our center and thus was not done for our patient. The patient had no complaints of dysuria, flank pain, or hematuria. He denied use of NSAIDs, had not recently received intravenous iodinated contrast, and was on no new medications. Tacrolimus trough level was 7.3 ng/mL. A renal biopsy was performed.The renal biopsy showed tubulointerstitial inflammation and evidence of polyomavirus (SV40) in tubular epithelial cells by immunohistochemical (IHC) staining (Figure 1), changes consistent with polyomavirus nephropathy. There was also acute tubular injury with focal isometric cytoplasmic vacuolization ( Figure 1B) and a "striped" pattern of interstitial fibrosis (Figure 2A) suggestive of acute and chronic calcineurin inhibitor toxicity, respectively. Electron microscopy demonstrated paracrystalline array arrangement of polyomavirus particles ( Figure 2B). Despite the positive IHC staining for SV40, AbstractJC virus-associated nephropathy is rare in kidney transplant recipients, and even rarer in recipients of other solid organ transplants. We present a case of JC virus-associated nephropathy in ...

A Case of John Cunningham Virus Induced Rhombencephalitis after Rituximab Therapy for Idiopathic Thrombocytopenic Purpura

“…Polyomavirus JC (JCV) has a sero-prevalence of 50-86% among healthy adults, but remains dormant in immunocompetent persons. Conditions of immunosuppression such as AIDS [2], organ transplant recipients [3], autoimmune diseases treated by immuno-modulatory medications [4,5], and hematological malignancies [6] tend to cause reactivation of the endemic virus. Clinical presentation can be subacute to chronic symptoms with nonspecific findings on CSF and imaging.…”

JC Virus in Kidney Transplant Population: Are We Cautious Enough?

“…However, there are some more severe cases described in the literature. Aguilar et al reported a case of a heart and kidney transplant patient whose kidney function worsened seven years post-transplant with bland urinary sediment, and diagnosis of polyomavirus nephropathy was made based on kidney biopsy result that demonstrated positive immunohistochemical staining for SV40 polyomavirus in the tubular epithelial cells and tubulointerstitial inflammation [14]. Electronic microscopy confirmed the presence of polyomavirus particles in the paracrystalline array arrangement.…”

“…Subsequently, the patient's urine and serum PCR samples came back positive for JCV. The patient's kidney function stabilized despite JC viremia variation after stopping mycophenolate mofetil (MMF) and multiple intravenous immunoglobulins (IVIG) courses [14]. Rasonable et al investigated 263 solid organ transplant recipients and found JCV in blood in 2.7% of kidney transplant recipients [15].…”

“…Some authors interpret JCV infection as a sign of excessive immunosuppression [26]. Based on the literature data, the initial therapeutic steps typically involve reducing the tacrolimus dose (trough levels between 3-5 ng/mL) and mycophenolate mofetil dose (MMF) [10,11,14]. Some authors also suggest switching from MMF to azathioprine, given the similar longterm outcomes of MMF and azathioprine in kidney transplant patients [31,32].…”

Virus-Associated Nephropathies: A Narrative Review

“…Of note, some have reported the possibility of JC-virus-related nephropathy; the incidence is estimated to be between 0.2 and 0.4% in allograft biopsies. JC-virus-related nephropathy can occur both early and late following transplantation, unlike BKPyVAN, which typically occurs in the early post-transplant period [ 239 , 240 , 241 ]. All cases presented polyomavirus cytopathic changes and/or SV40 positive staining with JC virus blood replication, in the absence of BKPyV viremia.…”