<scp>JC</scp> polyomavirus nephropathy, a rare cause of transplant dysfunction: Case report and review of literature

Yang, Doyle; Keys, Brandon J.; Conti, David; Foulke, Llewellyn; Stellrecht, Kathleen A.; Cook, Linda; Lopez‐Soler, Reynold I.

doi:10.1111/tid.12654

Cited by 25 publications

(25 citation statements)

References 21 publications

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“…Several case reports describe manifestations of JC‐PyVAN after KT, but most were detected in adults, in whom the seroprevalence is high and the risk of significant JCPyV exposure would be presumably lower or mitigated . In support of this notion, a recent case‐control study of the Swiss transplant cohort study reported a significant increase only in BKPyV‐specific IgG activity in BKPyV‐DNAemic patients, whereas their JCPyV‐IgG activities remained unchanged .…”

Section: Discussionmentioning

confidence: 98%

“…Accordingly, the nOD of >0.100 of JCPyV‐IgG at a serum dilution of 1:200 was defined as positive. JCPyV‐specific IgM were measured as detailed and validated previously, whereby a nOD > 0.100 at 1:400 dilution was considered positive. Serologically significant exposure was defined as IgG seroconversion, or occurrence of JCPyV‐specific IgM, or as an increase of >0.5 nOD units in serially tested sera post‐transplant.…”

Section: Methodsmentioning

confidence: 99%

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JC polyomavirus‐specific antibody responses in pediatric kidney transplant recipients

Ylinen

Miettinen

Jalanko

et al. 2019

Pediatric Transplantation

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BKPyV is widely recognized in KTRs, but little is known about rates of primary and secondary JCPyV exposure in pediatric KTRs. We evaluated JCPyV exposure in pediatric KTRs using antibody responses in the first 12 months post‐transplant. Of 46 children transplanted between 2009 and 2014, 6 lacked any samples for serologic testing, leaving 40 KTRs for study. JCPyV‐specific IgG and IgM antibodies were measured using a normalized VLP ELISA. Significant JCPyV exposure was defined as IgG seroconversion, increasing IgG levels of >0.5 nOD units, or IgM detection. Of 40 recipients (median age 3.2 years), 11 (27.5%) were seropositive, 20 (50%) seronegative for JCPyV‐IgG, while 9 (22.5%) had no specimen at the time of transplantation, but were confirmed as seronegative in post‐transplant samples. Of 29 (72.5%) at risk, JCPyV‐IgG seroconversion occurred in 15/29 (51.7%) including JCPyV‐IgM in 6 patients (20.7%). Two patients (6.9%) developed only JCPyV‐IgM. Among JCPyV‐IgG‐positive KTRs, six (12.5%) had significant IgG increases. Altogether 23 of 40 patients (57.5%) had serological evidence of primary or secondary JCPyV exposure. In these patients, kidney function tended to be lower during the 2 years of follow‐up, but only one patient lost the graft due to JCPyV nephropathy. Thus, JCPyV exposure is common in pediatric KTR and may present serologically as primary or secondary infection. Although only one case of JC‐PyVAN occurred, a trend toward lower renal function was seen. Dedicated studies of larger cohorts are warranted to define impact of JCPyV in pediatric KTR.

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Section: Discussionmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

JC polyomavirus‐specific antibody responses in pediatric kidney transplant recipients

Ylinen

Miettinen

Jalanko

et al. 2019

Pediatric Transplantation

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“…For a suspicion of JC virus nephropathy, there should be high urine JC viral loads in the absence of BK virus in either blood or urine along with SV40 positive staining and JC virus DNA in the biopsy, 1,5,6 as JC virus in the blood is usually low or undetectable. Interestingly, it seems that BK virus nephropathy often occurs earlier than JC virus nephropathy, usually within 1‐2 years of transplant, 1 while JC virus nephropathy has been reported further out from transplant, with cases reported at 4 years, 7 6 years, 8 and, in a pediatric case, 7 years after transplant 9 . Asymptomatic JC viremia has been documented in solid organ transplant recipients.…”

Section: Discussionmentioning

confidence: 98%

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

Aguilar

Chang

Lin

et al. 2020

Transplant Infectious Dis

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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 ...

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“…Tubulointerstitial nephritis due to JC polyomavirus (JCPyVAN) presents histologically with the same features as BKPyVAN but in comparison is exceeding rare . A diagnosis of JCPyVAN should be considered when histological features of BKPyVAN are present but BK viremia is negative .…”

Section: Introductionmentioning

confidence: 99%

“…10 Tubulointerstitial nephritis due to JC polyomavirus (JCPyVAN) presents histologically with the same features as BKPyVAN but in comparison is exceeding rare. [11][12][13] A diagnosis of JCPyVAN should be considered when histological features of BKPyVAN are present but BK viremia is negative. 12 The diagnosis can be confirmed with evaluation of JC viral loads (viremia, viruria) and also with performance of histological studies specific for the JC virus (ie, in situ hybridization).…”

Section: Introductionmentioning

confidence: 99%

Granulomatous inflammation in BK polyomavirus–associated nephropathy

Zhang

Ahmed

Haririan

et al. 2018

Transplant Infectious Dis

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Evolving BK polyomavirus-associated nephropathy (BKPyVAN) is characterized by tubulointerstitial inflammation that closely resembles acute T-cell-mediated allograft rejection if tubulitis is significant. The cellular composition of the inflammation varies during the course of BKPyVAN, and clusters of plasma cells may herald resolution of the infection. Less commonly, BKPyVAN can present with a predominance of histiocytes and granuloma formation. Granulomatous interstitial nephritis is uncommon in biopsies of either native or transplant kidneys. In both settings, this distinctive type of inflammatory response requires a systematic approach with careful clinicopathological assessment to determine its etiology. We present three patients with granulomatous BKPyVAN in the first year post-transplantation. These allograft biopsies at 4, 6, and 12 months post-transplant exemplify spontaneously resolving BKPyVAN, resolving infection after immunosuppression reduction, and early BKPyVAN, respectively. In immunosuppressed patients, BKPyVAN should be added to the relatively broad differential diagnosis of granulomatous tubulointerstitial nephritis.

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JC polyomavirus nephropathy, a rare cause of transplant dysfunction: Case report and review of literature

Cited by 25 publications

References 21 publications

JC polyomavirus‐specific antibody responses in pediatric kidney transplant recipients

JC polyomavirus‐specific antibody responses in pediatric kidney transplant recipients

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

Granulomatous inflammation in BK polyomavirus–associated nephropathy

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