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| LETTER TO EDITOR |
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| Year : 2018 | Volume
: 16
| Issue : 2 | Page : 61-62 |
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Recurrent nephropathy among immunocompromised persons could warrant BK polyomavirus testing
Idris Abdullahi Nasir1, Halima Ali Shuwa2, Hafsat Saidu Isiaka3
1 Department of Medical Laboratory Services, University of Abuja Teaching Hospital, Gwagwalada, FCT Abuja; Department of Medical Microbiology and Parasitology, College of Health Sciences, University of Ilorin, Ilorin, Nigeria
2 Department of Immunology, School of Medical Laboratory Science, Usmanu Danfodiyo University, Sokoto, Nigeria
3 Department of Medical Microbiology and Parasitology, College of Health Sciences, University of Ilorin, Ilorin, Nigeria
| Date of Web Publication | 5-Jul-2018 |
Correspondence Address:
Mr. Idris Abdullahi Nasir
Department of Medical Laboratory Services, University of Abuja Teaching Hospital, Gwagwalada, FCT Abuja
Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/NJGP.NJGP_1_18
How to cite this article:
Nasir IA, Shuwa HA, Isiaka HS. Recurrent nephropathy among immunocompromised persons could warrant BK polyomavirus testing. Niger J Gen Pract 2018;16:61-2 |
How to cite this URL:
Nasir IA, Shuwa HA, Isiaka HS. Recurrent nephropathy among immunocompromised persons could warrant BK polyomavirus testing. Niger J Gen Pract [serial online] 2018 [cited 2023 May 29];16:61-2. Available from: https://www.njgp.org/text.asp?2018/16/2/61/236058 |
Dear Editor,
BK virus (BKV) is a naked DNA virus, which belongs to the Polyomaviridae family. BK and JC polyomaviruses were the first human polyomaviruses isolated from immunosuppressed patients.[1],[2] BKV was first isolated in 1971 from the urine of an immunocompromised renal transplant patient with the initials B.K.[2] BKV causes interstitial nephritis in kidney transplant patients but has also been reported to cause renal diseases in nonrenal transplant patients and bone marrow transplant recipients.[3] The BKV seroprevalence stood as high as 81%, with the virus in latent/dormant stage embedded in the urothelium.[4] Intermittent reactivation with low-level viruria (106 virus copies/mL of urine) has been noted in approximately 5% of immunocompromised patients without clinical consequence.[5] Due to the detection of viral DNA in tonsillar tissue, BKV transmission is thought to occur via a respiratory route.[6] There is also evidence for other possible routes of transmission such as fecal-oral, urino-oral, transplacental, and blood transfusion.[6]
There are four BKV genotypes: designated I, II, III, and IV. After primary infection, BKV enters a latency phase and tends to persist indefinitely.[7] Autopsy studies have detected BKV mainly in kidney parenchyma, renal pelvis, ureter, and urinary bladder of immunocompetent individuals.[7] Reactivation of BKV replication is observed in states of relative or absolute immunodeficiency such as transplantation, pregnancy, diabetes, cancer, HIV infection, and systemic lupus erythematosus. Unchecked BKV replication can then lead to BKV nephropathy (BKVN) and other organ diseases.
Pathologically, BKV infection manifests by BK viruria, BK viremia, and BKVN. BK viruria precedes BK viremia by a median of 4 weeks and BKVN by an average of 6.5 months.[8] One of the earlier methods to detect BKV infection was by the detection of “decoy” cells in the urine. Decoy cells originate from infected renal tubular cells with nuclei altered by BKV inclusions.[8] They can be observed on urine cytology using Papanicolaou stains (Pap) or on phase-contrast microscopy. The urine Pap smear More Details, though sensitive for the diagnosis of BKVN, has a positive predictive value of only 29%.[8] The measurement of BK viral load by polymerase chain reaction in the urine is another method used to monitor BKV infection.[9] Low levels of viruria may reflect asymptomatic shedding during the latent phase, and increasing viral load is indicative of active BKV replication.
In two clinical studies on BKV pathology, 35% of kidney transplant recipients develop BK viruria, 11.1% develop BK viremia, and 6.4% develop BKVN.[8],[10] Although rarely tested in time, it is thought that BK reactivation in kidney transplant recipients occurred very infrequently in the 1970s–1980s. The increased prevalence in recent times is attributed, in part, to the use of a more potent calcineurin inhibitor (CNI)-based immunosuppressive regimens. It is important to acknowledge that better understanding of BKV infection has led to screening protocols in kidney transplantation that has resulted in the increased recognition of asymptomatic BKV infections.[11]
The definitive diagnosis of BKVN requires a kidney biopsy where intranuclear polyomavirus inclusion bodies in tubular epithelial and/or glomerular parietal cells can be identified.[11] Inclusion bodies are basophilic structures seen on light microscopy.[8] The cytopathic changes are often associated with epithelial cell necrosis resulting in denudation of tubular basement membranes and acute tubular injury.[8]
BKV reactivation following kidney transplant should be considered in the differential diagnosis of acute kidney injury (AKI) or chronic kidney disease. Other common causes of AKI in kidney transplant recipients are CNI nephrotoxicity and allograft rejection. A kidney biopsy is necessary to definitively differentiate these, although the specific clinical scenario can raise suspicion for BKVN. With the rising cases of recurrent kidney diseases among kidney transplant recipients and other immunocompromised persons, it is recommended that BKV viremia level and histological grading be considered to promptly ameliorate complication associated with BKVN.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Gardner SD, Field AM, Coleman DV, Hulme B. New human papovavirus (B.K.) isolated from urine after renal transplantation. Lancet 1971;1:1253-7.  |
| 2. | Padgett BL, Walker DL, ZuRhein GM, Eckroade RJ, Dessel BH. Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy. Lancet 1971;1:1257-60. |
| 3. | Kuppachi S, Kaur D, Holanda DG, Thomas CP. BK polyoma virus infection and renal disease in non-renal solid organ transplantation. Clin Kidney J 2016;9:310-8. |
| 4. | Knowles WA, Pipkin P, Andrews N, Vyse A, Minor P, Brown DW, et al. Population-based study of antibody to the human polyomaviruses BKV and JCV and the simian polyomavirus SV40. J Med Virol 2003;71:115-23. |
| 5. | Randhawa P, Uhrmacher J, Pasculle W, Vats A, Shapiro R, Eghtsead B, et al. A comparative study of BK and JC virus infections in organ transplant recipients. J Med Virol 2005;77:238-43. |
| 6. | Jiang M, Abend JR, Johnson SF, Imperiale MJ. The role of polyomaviruses in human disease. Virology 2009;384:266-73. |
| 7. | Sharma PM, Gupta G, Vats A, Shapiro R, Randhawa P. Phylogenetic analysis of polyomavirus BK sequences. J Virol 2006;80:8869-79. |
| 8. | Hirsch HH, Knowles W, Dickenmann M, Passweg J, Klimkait T, Mihatsch MJ, et al. Prospective study of polyomavirus type BK replication and nephropathy in renal-transplant recipients. N Engl J Med 2002;347:488-96. |
| 9. | Vats A, Shapiro R, Singh Randhawa P, Scantlebury V, Tuzuner A, Saxena M, et al. Quantitative viral load monitoring and cidofovir therapy for the management of BK virus-associated nephropathy in children and adults. Transplantation 2003;75:105-12. |
| 10. | Brennan DC, Agha I, Bohl DL, Schnitzler MA, Hardinger KL, Lockwood M, et al. Incidence of BK with tacrolimus versus cyclosporine and impact of preemptive immunosuppression reduction. Am J Transplant 2005;5:582-94. |
| 11. | Nickeleit V, Hirsch HH, Binet IF, Gudat F, Prince O, Dalquen P, et al. Polyomavirus infection of renal allograft recipients: From latent infection to manifest disease. J Am Soc Nephrol 1999;10:1080-9. |
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