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viruria&#44; and viremia only indicate viral replication&#44; not nephropathy&#44; but they are key tools for preventing and monitoring the disease&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The only clinical sign of BKVN is the deterioration of kidney function&#44; and when this occurs&#44; it is already too late to intervene&#44; since the renal damage has already been produced&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The diagnosis of the disease can only be performed with a graft biopsy in which the typical basophilic nuclear viral inclusions are found in the epithelial cells &#40;tubular&#44; Bowman&#8217;s capsule&#44; and&#47;or urothelium&#41;&#44; and signs of inflammation with tubulitis &#40;Figure 1A&#41;&#44; similar findings to those that appear in acute transplant rejection by T-cells&#46; Only by using the immunohistochemical technique for SV-40 LTAg can we observe a positive nuclear staining and identify the polyomavirus &#40;BK&#44; JC&#41; as that responsible for the inflammation&#44; thus discarding the diagnosis of acute T-cell rejection &#40;Figure 1B&#41; and confirming the diagnosis of BKVN&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">BKVN histological lesions are focal and heterogeneous&#44; and so a negative biopsy cannot exclude the diagnosis&#46; As such&#44; this test must be repeated if the viral load in the patient&#8217;s blood remains persistently high&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The histological patterns of BKVN<span class="elsevierStyleSup">2&#44;8&#44;9</span> are based on the identification and extension of the inflammatory infiltrate and viral infection-associated fibrosis&#44; which allows for three histological patterns to be established &#40;Figure 2&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CLINICAL EVOLUTION AND OPPORTUNITIES FOR EARLY PREVENTION AND DIAGNOSIS </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The common clinical evolution of BKVN<span class="elsevierStyleSup">9</span> is represented in Figure 3&#44; which shows how the development of the disease is predicted by the appearance of BK viruria &#40;BK Vr&#41;&#44; a consequence of viral reactivation and replication in the urinary tract&#44; with the appearance of typical <span class="elsevierStyleItalic">decoy</span> cells &#40;figure 4&#41;&#44; which are easy to identify using routine urine cytology tests&#46; However quantification of Vr using PCR techniques is more sensitive than using cytology&#44; and allows for distinguishing between BKV and JCV infections&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">When viruria is &#62;10<span class="elsevierStyleSup">5</span> copies&#47;ml and persists&#44; it is followed weeks or months later by the development of viremia &#40;Vm&#41; at &#62;10<span class="elsevierStyleSup">7</span> copies&#47;ml and&#44; finally&#44; BKVN&#46; BK Vr is not diagnostic of renal parenchymal damage&#44; but the simultaneous appearance of Vm and Vr is pathognomonic of renal parenchymal damage &#40;BKVN&#41;&#46; Maintained&#44; or more typical&#44; increasing Vm is a predictive factor for deteriorating kidney function&#44; and is correlated with the presence and severity of histological lesions&#46; In patients with normal or moderately low kidney function&#44; the probability of finding histological indicators of BKVN is directly proportional to the duration and severity of viremia&#46; Elevated and sustained viremia identifies those patients with uncontrolled viral replication that leads to kidney damage&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">In conclusion&#44; early diagnosis and intervention minimises the damage to the transplant&#46; Figure 5 demonstrates a diagnostic algorithm based on previous publications&#46;<span class="elsevierStyleSup">4&#44;9</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">BKVN TREATMENT</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The best treatment for BKVN is an early diagnosis of the disease in order to act before renal damage is caused&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">For this reason&#44; KDIGO Guides<span class="elsevierStyleSup">10</span> suggest using a screening process for all kidney transplant patients by testing monthly Vm levels during the first 3 months &#40;2D&#41; and every three moths until the end of the first year &#40;2D&#41;&#44; whenever renal dysfunction is produced with no visible alternative cause &#40;2D&#41;&#44; and after treatment for en episode of acute rejection &#40;2D&#41;&#46; A reduction in IS is also suggested when Vm is persistently greater than 10<span class="elsevierStyleSup">7</span> copies&#47;ml &#40;2D&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Regarding the reduction in IS&#44; the first step consists of implementing the standard protocol &#40;not giving CAN or antiproliferative treatments above the levels indicated for the therapeutic range&#41;&#44; followed by measuring viremia every 4 weeks&#44; reducing NAb by 15&#37;-20&#37;&#44; reducing MMF and&#47;or MMF suppression by 50&#37;&#44; and&#47;or substituting TAC by CsA or an ISP &#40;Figure 6&#41;&#46;<span class="elsevierStyleSup">11</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">With regard to antiviral treatments&#44; i&#46;v&#46; immunoglobulins&#44; ciclofovir&#44; leflunomide&#44; and quinolones have been used empirically&#44; and their efficacy is currently difficult to determine because they have not been administered in combination with a reduction in IS and because of the lack of controlled and randomised prospective studies&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Finally&#44; we would like to comment on kidney retransplantation in patients that have lost a graft due to BKVN&#46; The recurrence of the disease in short studies is 12&#37;&#46; The recommendations that must be taken into account in these situations are&#58; <span class="elsevierStyleItalic">1</span>&#41; inform the patient as to the increased potential risk of recurrence of BKVN&#59; <span class="elsevierStyleItalic">2</span>&#41; confirm the absence of viral replication &#40;blood and urine PCR when the patient is included on the transplant list and every 6 months thereafter&#41;&#44; the patient must receive the transplant with negative PCR results from blood samples&#44; and <span class="elsevierStyleItalic">3</span>&#41; adapt the IS to the pathology&#46;<span class="elsevierStyleSup">12-14</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">KEY POINTS</span></p><p class="elsevierStylePara">1&#46; The powerful and modern forms of immunosuppression could be responsible for the increasing prevalence of this infection</p><p class="elsevierStylePara">2&#46; BK virus infection in immunocompromised patients could affect the function and survival of kidney transplants</p><p class="elsevierStylePara">3&#46; Early diagnosis by strictly monitoring urine decoy cell count and&#47;or viruria and viremia is crucial for avoiding the negative impacts of this complication</p><p class="elsevierStylePara">4&#46; No evidence exists of a specific effective treatment for this infection&#46; Only a reduction in immunosuppression treatment can minimise virulence&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11151&#95;en&#95;figura&#95;1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11151_en_figura_1.jpg" alt=" Basophilic nuclear viral inclusions in epithelial cells and tubulitis in the BK-virus nephropathy &#40;a&#41; and immunohistochemistry for the antigen SV-40 LTAg &#40;b&#41; "></img></a></p><p class="elsevierStylePara">Figure 1&#46; Basophilic nuclear viral inclusions in epithelial cells and tubulitis in the BK-virus nephropathy &#40;a&#41; and immunohistochemistry for the antigen SV-40 LTAg &#40;b&#41; </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11167&#95;en&#95;f2&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11167_en_f2.jpg" alt="Histological patterns of the BK virus-associated nephropathy "></img></a></p><p class="elsevierStylePara">Figure 2&#46; Histological patterns of the BK virus-associated nephropathy </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11168&#95;en&#95;f3&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11168_en_f3.jpg" alt="Disperse decoy cells and cellular cylinders containing compacted decoy cells&#46; When they appear&#44; these cylinders are pathognomic of kidney damage "></img></a></p><p class="elsevierStylePara">Figure 3&#46; Disperse decoy cells and cellular cylinders containing compacted decoy cells&#46; When they appear&#44; these cylinders are pathognomic of kidney damage </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11169&#95;en&#95;f4&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11169_en_f4.jpg" alt="Phases of evolution of the BK virus-associated nephropathy"></img></a></p><p class="elsevierStylePara">Figure 4&#46; Phases of evolution of the BK virus-associated nephropathy</p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11170&#95;en&#95;f5&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11170_en_f5.jpg" alt="BKVN diagnostic algorithm "></img></a></p><p class="elsevierStylePara">Figure 5&#46; BKVN diagnostic algorithm </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11171&#95;en&#95;f6&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11171_en_f6.jpg" alt="BKVN treatment algorithm"></img></a></p><p class="elsevierStylePara">Figure 6&#46; BKVN treatment algorithm</p>"
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BK virus-associated Nephropathy
Nefropatía asociada a infección por poliomavirus BK
, D.. Burgosb, C.. Jirondab, M.. Martínb, M.. González-Molinab, D.. Hernándezb
b Servicio de Nefrología, Hospital Carlos Haya, Málaga
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along with the papillomavirus&#44; belongs to the papovavirus family of pathogens&#46; The BK virus &#40;BKV&#41; belongs to the polyomavirus family along with other polyomaviruses that have been detected in humans&#44; such as the JC virus &#40;JCV&#41;&#44; the KI virus&#44; the WU virus&#44; the Merkel cell carcinoma virus&#44; and the Simian virus 40 &#40;SV40&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">These are small&#44; <span class="elsevierStyleItalic">non-enveloped</span><span class="elsevierStyleItalic"> </span>viruses&#44; with a diameter of 42 nm&#46; The capsid has icosahedral symmetry and houses a double circular chain genome of DNA with over 5000 base pairs&#44; composed of an &#8220;early&#8221; region that is highly conserved and codes for the &#8220;T&#47;t antigen&#8221; &#40;TAg&#41;&#44; which is implicated in transformation&#44; viral replication&#44; and gene regulation and expression&#59; and a &#8220;late&#8221; region that codes for the three capsid proteins&#44; known as VP1&#44; VP2&#44; and VP3&#44; and for a protein called &#8220;agnoprotein&#44;&#8221; a non-coding regulatory region situated between the other two&#44; where the determinants for replication&#44; the TAg union&#44; and transcriptional regulation elements are located&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The polyomavirus possesses adaptation specificity to its host&#59; therefore&#44; its evolution is probably associated with the host species&#8217; evolution&#44; and so the natural infection occurs only in a limited number of closely related species&#44; constituting a marker for establishing the racial differences between humans&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Using gene-sequencing analysis&#44; different genotypes have been established&#58; European&#44; Asian&#44; and African&#46; The rest of the genotypes correspond to recombinations of these three&#44; and although its origin is difficult to establish&#44; the study of this virus could provide a tool for aiding in understanding the evolution of human migrations&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">BKV is associated with two complications observed in transplant recipients&#58; BK virus-associated nephropathy &#40;BKVN&#41; in kidney transplants&#44; and haemorrhagic cystitis in bone marrow transplants&#46; In contrast to the BKV&#44; although the JCV resides in the uroepithelium and normally reactivates&#44; it rarely produces nephropathy&#44; but is associated with multifocal leukoencephalopathy and encephalitis&#46; SV40&#44; which comes from simians&#44; was introduced into the human population through vaccines contaminated with polio and adenovirus&#44; and although its presence has been detected in transplanted kidney biopsies&#44; its importance in kidney transplantation is not yet well defined&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">EPIDEMIOLOGY AND RISK FACTORS</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The primary infection occurs subclinically during the first decade of life&#44; 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the prevalence of nephropathies associated with BK virus &#40;BKVN&#41; oscillates between 1&#37; and 10&#37;&#44;<span class="elsevierStyleSup">4</span> based more on the immunosuppression treatment and diagnostic methods than due to real epidemiological differences&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">In 2004&#44; the treatment of the BKV infection after kidney transplantation was included in the American database as a variable for post-transplant evolution &#40;TBKV&#41;&#59; the data were later analysed&#44; resulting in a total of &#62;48 000 transplants&#44; 1474 of which were treated within 24 months&#46; The cumulative incidence of TBKV increased with time&#44; going from 3&#46;45&#37; at 24 months to 6&#46;6&#37; at 60 months after the transplantation&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Graft failure secondary to BKVN occurs at a rate of 50&#37;&#8211;100&#37; at 24 months in centres with no screening programs&#44; which highlights the importance of an early diagnosis of the disease&#46;<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Different IS protocols have been identified as risk factors for the development of BKVN&#44; especially the use of triple therapies with anticalcineurinic drugs&#44; mycophenolate mofetil &#40;MMF&#41;&#44; and steroids&#44;<span class="elsevierStyleSup">5&#44;6</span> but BKVN cases have also been described when using other IS regimens&#44; which indicates that the intensity of IS treatment&#44; and not the specific drug itself&#44; is the risk factor in this case&#46; Other types risk factors also exist&#44; such as patient factors &#40;males &#62;50 years of age&#44; BKV seronegative recipient&#41;&#44; graft factors &#40;BKV seropositive donor&#44; HLA incompatibilities&#44; immunological or ischemic injury&#41;&#44; and viral factors &#40;latent viral load&#44; capsid serotype&#44; and capacity for replication&#41;&#46;<span class="elsevierStyleSup">7</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">BKVN HISTOLOGICAL DIAGNOSIS AND PROGRESSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Decoy</span> cells&#44; viruria&#44; and viremia only indicate viral replication&#44; not nephropathy&#44; but they are key tools for preventing and monitoring the disease&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The only clinical sign of BKVN is the deterioration of kidney function&#44; and when this occurs&#44; it is already too late to intervene&#44; since the renal damage has already been produced&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The diagnosis of the disease can only be performed with a graft biopsy in which the typical basophilic nuclear viral inclusions are found in the epithelial cells &#40;tubular&#44; Bowman&#8217;s capsule&#44; and&#47;or urothelium&#41;&#44; and signs of inflammation with tubulitis &#40;Figure 1A&#41;&#44; similar findings to those that appear in acute transplant rejection by T-cells&#46; Only by using the immunohistochemical technique for SV-40 LTAg can we observe a positive nuclear staining and identify the polyomavirus &#40;BK&#44; JC&#41; as that responsible for the inflammation&#44; thus discarding the diagnosis of acute T-cell rejection &#40;Figure 1B&#41; and confirming the diagnosis of BKVN&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">BKVN histological lesions are focal and heterogeneous&#44; and so a negative biopsy cannot exclude the diagnosis&#46; As such&#44; this test must be repeated if the viral load in the patient&#8217;s blood remains persistently high&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The histological patterns of BKVN<span class="elsevierStyleSup">2&#44;8&#44;9</span> are based on the identification and extension of the inflammatory infiltrate and viral infection-associated fibrosis&#44; which allows for three histological patterns to be established &#40;Figure 2&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CLINICAL EVOLUTION AND OPPORTUNITIES FOR EARLY PREVENTION AND DIAGNOSIS </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The common clinical evolution of BKVN<span class="elsevierStyleSup">9</span> is represented in Figure 3&#44; which shows how the development of the disease is predicted by the appearance of BK viruria &#40;BK Vr&#41;&#44; a consequence of viral reactivation and replication in the urinary tract&#44; with the appearance of typical <span class="elsevierStyleItalic">decoy</span> cells &#40;figure 4&#41;&#44; which are easy to identify using routine urine cytology tests&#46; However quantification of Vr using PCR techniques is more sensitive than using cytology&#44; and allows for distinguishing between BKV and JCV infections&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">When viruria is &#62;10<span class="elsevierStyleSup">5</span> copies&#47;ml and persists&#44; it is followed weeks or months later by the development of viremia &#40;Vm&#41; at &#62;10<span class="elsevierStyleSup">7</span> copies&#47;ml and&#44; finally&#44; BKVN&#46; BK Vr is not diagnostic of renal parenchymal damage&#44; but the simultaneous appearance of Vm and Vr is pathognomonic of renal parenchymal damage &#40;BKVN&#41;&#46; Maintained&#44; or more typical&#44; increasing Vm is a predictive factor for deteriorating kidney function&#44; and is correlated with the presence and severity of histological lesions&#46; In patients with normal or moderately low kidney function&#44; the probability of finding histological indicators of BKVN is directly proportional to the duration and severity of viremia&#46; Elevated and sustained viremia identifies those patients with uncontrolled viral replication that leads to kidney damage&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">In conclusion&#44; early diagnosis and intervention minimises the damage to the transplant&#46; Figure 5 demonstrates a diagnostic algorithm based on previous publications&#46;<span class="elsevierStyleSup">4&#44;9</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">BKVN TREATMENT</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The best treatment for BKVN is an early diagnosis of the disease in order to act before renal damage is caused&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">For this reason&#44; KDIGO Guides<span class="elsevierStyleSup">10</span> suggest using a screening process for all kidney transplant patients by testing monthly Vm levels during the first 3 months &#40;2D&#41; and every three moths until the end of the first year &#40;2D&#41;&#44; whenever renal dysfunction is produced with no visible alternative cause &#40;2D&#41;&#44; and after treatment for en episode of acute rejection &#40;2D&#41;&#46; A reduction in IS is also suggested when Vm is persistently greater than 10<span class="elsevierStyleSup">7</span> copies&#47;ml &#40;2D&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Regarding the reduction in IS&#44; the first step consists of implementing the standard protocol &#40;not giving CAN or antiproliferative treatments above the levels indicated for the therapeutic range&#41;&#44; followed by measuring viremia every 4 weeks&#44; reducing NAb by 15&#37;-20&#37;&#44; reducing MMF and&#47;or MMF suppression by 50&#37;&#44; and&#47;or substituting TAC by CsA or an ISP &#40;Figure 6&#41;&#46;<span class="elsevierStyleSup">11</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">With regard to antiviral treatments&#44; i&#46;v&#46; immunoglobulins&#44; ciclofovir&#44; leflunomide&#44; and quinolones have been used empirically&#44; and their efficacy is currently difficult to determine because they have not been administered in combination with a reduction in IS and because of the lack of controlled and randomised prospective studies&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Finally&#44; we would like to comment on kidney retransplantation in patients that have lost a graft due to BKVN&#46; The recurrence of the disease in short studies is 12&#37;&#46; The recommendations that must be taken into account in these situations are&#58; <span class="elsevierStyleItalic">1</span>&#41; inform the patient as to the increased potential risk of recurrence of BKVN&#59; <span class="elsevierStyleItalic">2</span>&#41; confirm the absence of viral replication &#40;blood and urine PCR when the patient is included on the transplant list and every 6 months thereafter&#41;&#44; the patient must receive the transplant with negative PCR results from blood samples&#44; and <span class="elsevierStyleItalic">3</span>&#41; adapt the IS to the pathology&#46;<span class="elsevierStyleSup">12-14</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">KEY POINTS</span></p><p class="elsevierStylePara">1&#46; The powerful and modern forms of immunosuppression could be responsible for the increasing prevalence of this infection</p><p class="elsevierStylePara">2&#46; BK virus infection in immunocompromised patients could affect the function and survival of kidney transplants</p><p class="elsevierStylePara">3&#46; Early diagnosis by strictly monitoring urine decoy cell count and&#47;or viruria and viremia is crucial for avoiding the negative impacts of this complication</p><p class="elsevierStylePara">4&#46; No evidence exists of a specific effective treatment for this infection&#46; Only a reduction in immunosuppression treatment can minimise virulence&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11151&#95;en&#95;figura&#95;1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11151_en_figura_1.jpg" alt=" Basophilic nuclear viral inclusions in epithelial cells and tubulitis in the BK-virus nephropathy &#40;a&#41; and immunohistochemistry for the antigen SV-40 LTAg &#40;b&#41; "></img></a></p><p class="elsevierStylePara">Figure 1&#46; Basophilic nuclear viral inclusions in epithelial cells and tubulitis in the BK-virus nephropathy &#40;a&#41; and immunohistochemistry for the antigen SV-40 LTAg &#40;b&#41; </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11167&#95;en&#95;f2&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11167_en_f2.jpg" alt="Histological patterns of the BK virus-associated nephropathy "></img></a></p><p class="elsevierStylePara">Figure 2&#46; Histological patterns of the BK virus-associated nephropathy </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11168&#95;en&#95;f3&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11168_en_f3.jpg" alt="Disperse decoy cells and cellular cylinders containing compacted decoy cells&#46; When they appear&#44; these cylinders are pathognomic of kidney damage "></img></a></p><p class="elsevierStylePara">Figure 3&#46; Disperse decoy cells and cellular cylinders containing compacted decoy cells&#46; When they appear&#44; these cylinders are pathognomic of kidney damage </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11169&#95;en&#95;f4&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11169_en_f4.jpg" alt="Phases of evolution of the BK virus-associated nephropathy"></img></a></p><p class="elsevierStylePara">Figure 4&#46; Phases of evolution of the BK virus-associated nephropathy</p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11170&#95;en&#95;f5&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11170_en_f5.jpg" alt="BKVN diagnostic algorithm "></img></a></p><p class="elsevierStylePara">Figure 5&#46; BKVN diagnostic algorithm </p><p class="elsevierStylePara"><a href="grande&#47;10587&#95;108&#95;11171&#95;en&#95;f6&#46;jpg" class="elsevierStyleCrossRefs"><img src="10587_108_11171_en_f6.jpg" alt="BKVN treatment algorithm"></img></a></p><p class="elsevierStylePara">Figure 6&#46; BKVN treatment algorithm</p>"
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