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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2019  |  Volume : 30  |  Issue : 3  |  Page : 597-605
Incidence and risk factors of common viral infections among renal transplant recipients during the first year post-transplant in North-eastern Iran


1 Kidney Transplantation Complication Research Center, Mashhad University of Medical Sciences, Mashhad; Department in Biostatistics, Faculty of Paramedical Science, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Kidney Transplantation Complication Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
3 Norwegian Center for e-health Research, University hospital of North Norway, Tromsø, Norway
4 Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran
5 Cancer Molecular Pathology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

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Date of Web Publication26-Jun-2019
 

   Abstract 


Despite major therapeutic advances, management of viral infections in renal transplant recipients is still a major challenge. Hence, it is urgently needed to establish protocols for appropriate control and the prevention of viral infection. We evaluated demographic/clinical characteristics, frequency, and risk factors of symptomatic viral infections in renal transplant recipients during the 1st year posttransplant, in northeastern Iran. We retrospectively reviewed medical files of 247 patients including 146 males and 101 females who had undergone renal transplantation at Montaserie organ transplantation hospital of Mashhad during 2012–2014. These patients were followed up for one year after transplantation for the detection of any symptomatic viral infection. Demographic and clinical characteristics of recipients were collected and analyzed using the Statistical Package for Social Sciences version 18 software; P < 0.05 was considered as statistically significant. Data were presented using descriptive statistics. Furthermore, logistic regression analysis was used to determine risk factors for infection. The mean age of the patients was 34.94 ± 13.89 years. During the 1st year posttransplant, 68 episodes of viral infections were detected in 64 patients (25.9%). Cytomegalovirus (CMV, 21.9%), Varicella Zoster virus (2.8%), herpes simplex virus (2.0%), and human polyomavirus BK virus (0.8%) were the most common symptomatic viral infections found. Age of the patients was the only significant risk factor for viral infections (odds ratio = 1.066; 95% confidence interval: 1.002–1.134; P = 0.042). The incidence of symptomatic viral infections, particularly CMV disease, is high in our center. Hence, it is recommended to use appropriate prophylaxis and monitor the patients during the first six months post-transplant.

How to cite this article:
Eidgahi ES, Lotfi Z, Tayefi M, Bahrami A, Shams SF, Shakeri S, Sheikhi M. Incidence and risk factors of common viral infections among renal transplant recipients during the first year post-transplant in North-eastern Iran. Saudi J Kidney Dis Transpl 2019;30:597-605

How to cite this URL:
Eidgahi ES, Lotfi Z, Tayefi M, Bahrami A, Shams SF, Shakeri S, Sheikhi M. Incidence and risk factors of common viral infections among renal transplant recipients during the first year post-transplant in North-eastern Iran. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2019 Sep 20];30:597-605. Available from: http://www.sjkdt.org/text.asp?2019/30/3/597/261332



   Introduction Top


Organ transplantation is presently known to be the best therapeutic choice for curing variety of end-organ diseases.[1] Short-term graft survival has remarkably increased by applying new anti-rejection prophylaxis.[1] Clinical outcomes of the kidney allograft recipients have improved significantly during the past decade. However, renal allograft recipients are exposed to more intensive immunosuppressive therapy, which would make them susceptible to develop infectious complications.[2]

Viral infections are responsible for morbidity and mortality after transplant, and hence need to be evaluated early. Viral infections are related to impaired host immune defense, and cause severe clinical illness, dissemination to other end-organs and contribute to developing acute and chronic rejection in transplant recipients.[3]

Viral infections, such as cytomegalovirus (CMV), human BK polyomavirus (BKV), and hepatitis C virus (HCV), cause injury to the allograft organs by stimulating pro-inflammatory cytokine secretion.[4] Viral infections have immunomodulatory effects which lead to diabetes, cardiovascular disease, and chronic allograft nephropathy after transplant.[5] The infection can occur for the first time after transplantation or by reactivation of latent virus.

CMV, BKV, Epstein–Barr virus (EBV), varicella zoster virus (VZV), and herpes simplex virus (HSV) are common pathogens; severe clinical manifestations in transplanted patients are usually related to them.[6] This study was carried out because of high prevalence and major complications of symptomatic viral infections in the kidney transplant recipients which lead to the referral of patients to medical centers and lack of research regarding this issue in the northeastern part of Iran. In this study, we assessed the incidence, clinical characteristics, and associated patient risk factors of symptomatic viral infections during the 1st year after renal transplant.


   Material and Methods Top


This retrospective study was performed in Montaserie organ transplantation hospital in Mashhad involving kidney transplant recipients from 2012–2014, and they were followed up for one year. All renal transplant recipients, who had at least one year after transplantation were included in the study. Patients who had rejection episodes during the 1st year after transplantation and those with missing data in their medical records were excluded from the study. In our center, transplantation with marginal cadaveric kidney donors and complex living donors were not performed.

All donors older than 60 years, and those older than 50 years with any of the following comorbidities: (1) hypertension, (2) cerebro-vascular cause of brain-death, or (3) pre-retrieval serum creatinine (SCr) level >1.5 mg/dL, with a degree of glomerulosclerosis >15% and prolonged cold ischemia were considered as marginal cadaveric kidney donors.

The associated risk factors of complex living donor were as follows: evidence of current renal disease (e.g., hematuria, proteinuria, and nephrolithiasis), direct risk for chronic kidney disease [(CKD), e.g., hypertension and obesity], reduced nephron mass (e.g., age >65 years), genetic risk factors (e.g., family history of end-stage renal disease in first-degree relatives), risk factors for CKD (e.g., diabetes in a first-degree relative, impaired fasting glucose), cardiovascular risk factors (e.g., smoking, hyperlipidemia, and hypertension), and other causes (e.g., black race, and sickle trait).

Some variables such as gender, age, donor type, transplantation time, medical comorbi-dities, occurrence of infection, clinical manifestations, and duration posttransplant at diagnosis were extracted from medical records of patients and evaluated. Transplant procedures were performed by standard techniques. Standard immunosuppressive therapy and anti microbial prophylaxis were applied for all patients, which has been described previously.[7] All renal transplant recipients received cyclosporin (CyA), prednisolone (Pred) with myco-phenolate mofetil (MMF).

We monitored whole blood 12-h trough (CO) concentration of CyA: our CO target levels are:

  • 200–300 ng/mL at 1–3 months after transplant
  • 50–150 ng/mL for subsequent months


The dose of MMF was 1 g/12 h.

Prophylaxis for Pneumocystis jirovecii with co-trimoxazole and anti-microbial prophylaxis along with statins were administered for all cases. Ceftriaxone was used for surgical prophylaxis and Isoniazid was prescribed for recipients or donors who had a positive skin test. Methyl prednisolone/rabbit anti-thymocyte globulin was given for anti-rejection therapy. Prophylaxis against CMV was not given to recipients.

The common signs of CMV disease are fever, malaise, arthralgia, leukopenia, thrombocytopenia, pneumonitis, gastroenteritis and rarely, central nervous system, and retinal development.[8] CMV was diagnosed based on the gold standard method, quantitative realtime polymerase chain reaction (PCR) assay to determine the CMV DNA load in plasma with cutoff values of 5000 copies of CMV DNA/ml in the sample.[6] EBV infection was diagnosed by the presence of the EBV DNA in blood and/or tissue samples in relation with fever, leukopenia, malaise, and/or organ involvement; the diagnosis was established by biopsy and histopathology, to confirm EBV infection of suspected patients.[9]

Definitive laboratory testing including PCR, direct fluorescent assays, and viral culture can be used for atypical cases of VZV or HSV, in suspected disseminated or visceral diseases. However, generally, both primary VZV and HSV have typical clinical presentations that allow us to make a presumptive clinical diagnosis.[10] In the present study, VZV infection was diagnosed according to clinical features, including the appearance of classical papulovesicular rashes and verified by an expert dermatologist. HSV infection was defined according to clinical criteria. Known signs of HSV infection are small vesicles, vesico-pustular, vesicoulcerated lesions, and painful hyperemic ulcers in one or both lips or genital region.

Detection of BK virus in urine was done by quantitative nucleic acid-based viral load assay. BK urine load of 10[7]/mL was considered as positive test and confirmed by a virologist.[11]

Data were presented as frequencies, means, medians, standard deviations, and minimum and maximum values. Logistic regression analysis was used to determine infection risk factors. Data were analyzed using the Statistical Package for the Social Sciences (SPSS) software version 18 for Windows (SPSS, Inc., Chicago, III, US) and P <0.05 was considered statistically significant. The study was approved by the University’s ethics committee (Code: 940940).


   Results Top


Demographic and clinical parameters of 247 renal transplant recipients, including 101 women and 146 men were analyzed. The mean age of recipients was 34.94 ± 13.89 years (34.61 ± 13.86 years in males and 35.16 ± 13.95 in females). The median of age was 33 years and ranged between 6 and 66 years.

A total of 64 patients had 68 episodes of viral infection during the 1st year after transplant-tation. In 60 patients, one infection was detected and in four patients, two different viral episodes were diagnosed. Comparative characteristics of viral infected and noninfec-ted patients are summarized in [Table 1]. The highest age proportion of viral-infected patients was 15–29 years (36.8%). Age distribution of renal recipient patients is represented in [Table 2].
Table 1: Demographic and clinical characteristics of 247 renal transplant recipients with and without viral infection.

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Table 2: Age distribution of the studied renal recipients of northeastern Iran.

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For fitting logistic regression, we used backward elimination that first started with all of the variables such as gender, age, deceased donor and categorical variables (comorbidities) in the model and then nonsignificant variables (P >0.05) were excluded subsequently. Among all variables, only age was significant in the model (P = 0.001). It can be stated that age was an independent risk factor for viral infection (odds ratio = 1.066; 95% confidence interval: 1.002–1.134; P = 0.042; [Table 3]).
Table 3: The risk factors of symptomatic viral infections in transplant patients of northeastern Iran based on logistic regression analysis.

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The mean creatinine level was 1.7 ± 0.83 mg/dL at the time of diagnosis of viral infection. Based on Kolmogorov–Smirnov test, creatinine with minimum and maximum values of 0.5 and 8.3 is not normal (P <0.05) and hence, median of creatinine as 1.5 mg/dL was considered.

Following infection assessment, 35 symptomatic infection episodes (51.5%) were found during the first three months following the transplant, 18 (26.5%) in the period from 3rd to 6th month, and 15 (22%) after six months. Overall, there were 54 (79.4%), seven (10.3%), five (7.4%), and two (2.9%) episodes of viral infection attributed to CMV, VZV, HSV, and BKV, respectively. No EBV case was reported during one year follow-up.

Causative infective agents at different times after transplantation are shown in [Figure 1]. Themean duration between surgery and diagnosis of CMV disease was 122.4 ± 79.5 days (range: 8–343 days). Fifteen percent of CMV diseases occurred during the hospitalization period. The most common CMV manifestations were fever and constitutional symptoms and the least common was retinitis [Figure 2].
Figure 1: Type of viral infections in transplant recipients based on time elapsed after transplantation.
CMV: Cytomegalovirus, BK: Human BK polyomavirus.


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Figure 2: Frequency of clinical manifestations among renal transplant recipients with cytomegalovirus disease.

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Two patients developed BKV. The first patient was a 20-year-old male with SCr level of 1.8 mg/dL, who received graft from living donor; his infection was diagnosed 44-days postoperatively. The second was a 44-year-old woman, in whom BKV was detected 65 days postsurgery; she received kidney from deceased donor and her SCr level was 1.4 mg/dL at the time of diagnosis. Informed consent was obtained from both patients before reporting.


   Discussion Top


The findings of the present study revealed that 25.9% of recipients had one symptomatic viral infection episode during the 1st year of follow-up. Viral infections may induce graft failure by different ways, including immune system activation and cytokine stimulation which enforce interstitial inflammation, bacterial pyelonephritis, and tubulointerstitial nephritis. This process may also lead to renal graft damage and postoperative mortality.[12] Infection reactivation depends on the intensity of immunosuppression.[12]

In this study, the prevalence of symptomatic CMV was 21.9%. Clinical presentations of CMV may vary from asymptomatic infection to disseminated involvement.[3] CMV is transmitted via blood transfusion of the donor or through organ transplant.[13] It has direct and indirect effects on solid organ recipients. The incidence CMV is up to 65% in renal transplant population; 14%–46% of these infections are symptomatic.[14] It is estimated that almost 58%–80% of kidney transplant recipients develop active CMV disease, without suitable prophylaxis therapy.[15] The hallmark of our study is that none of the patients received any prophylaxis against CMV.

Other reports of Iran were consistent with the current study. Nafar et al, reported the prevalence of CMV infection as 16% among 427 Iranian kidney transplant recipients.[16] Results of a multi-center study including 3065 renal transplant recipients demonstrated that the prevalence of CMV infection was 21.9%.[17] Moreover, the prevalence of CMV infection was 17.6% in a single-center study in Tehran.[18] The average time of CMV detection was 122 days after transplantation among our patients; this finding was in agreement with other studies.[18] Fever and constitutional symptoms were the most common manifestations of CMV in this study, but retinitis was a rare manifestation; it is similar to other studies.[19],[20] In the present study, BKV was only observed in two patients and was detected during the first three months after transplantation. BKV was identified as a novel viral infection, in a study about common infections in kidney transplant recipients, in 1970.[21] In general, primary BKV infection emerges in childhood and remains in the genitourinary tract; it persists quiescent in most of the immuno-competent hosts. Latent BKV reactivates in allograft recipients which replicates and sheds in urine (viruria) and progresses to viremia; finally, it can cause allograft dysfunction because of tubulointerstitial nephritis.[22] The overall incidence of polyomavirus BK DNAuria was 40.7% in 76 studied transplant patients,[23] which is higher than our report. However, studies from Iran indicate that the rate of BKV in dialysis patients, kidney transplanted cases and BK virus-associated nephro-pathy (BKVAN) patients, is low. Sharif et al investigated BK viremia in dialysis patients. The authors reported BK viremia in 3.03% of peritoneal dialysis and none of the hemodialysis patients.[24] In a recent study in Tehran, BK viremia was not detected in any specimens of kidney transplant recipients.[25] Soleymanian and co-workers diagnosed BKVAN in 0.93% of biopsies and in 1.04% of renal allograft patients.[26] In another study, 2.5% of kidney transplant recipients had BK viremia within the 1st year after transplantation, but BKVAN did not develop among them.[27] Nasiri et al reported BK viremia in 3.3% of renal transplant recipients.[28] In a study performed in Ahvaz, BKV-DNA was found in 41.8% of urine specimens.[29] In another study from Iran, BKV replication was detected in 15.7% and 11% of plasma and tissue samples of renal transplant patients, respectively.[30] These disparity rates between different parts of Iran may be pertained to the environmental effects and population density, which are critical factors for BKV transmission.[31],[32]

The incidence of symptomatic VZV and HSV was 2.8% and 2.0% in our population, respectively. Infection usually occurred by reactivation of the latent virus in renal transplant recipients. HSV reactivation usually presents as oral or genital lesions; it can cause esopha-gitis, pneumonitis, encephalitis, or hepatitis in some patients.[33] VZV infection usually presents with dermatomal zoster; although it can be disseminated, leading to identical visceral involvement.[3] Pavlopoulou et al reported an incidence of 6.4% of herpes zoster, which is similar to our findings. The incidence of VZV was 4%–12% in kidney recipients in various studies.[3] Rostamzadeh et al reported a prevalence of 5.4% of HSV among kidney allograft recipients in Urmia, Iran.[3] Regarding the higher level of HSV incidence in developing countries, Iranian studies in both immuno-competent and immunodeficient patients demonstrated lower incidence compared to European studies.[35] Actually, the incidence of HSV-2 is the lowest in Asia in comparison with other regions.[36] This relatively low rate of HSV in this country may be due to the sexual behavior of the Iranian population, which is generally within the structure of the family.

In the present study, the risk of viral infections posttransplant increased with age. Gender (male subjects) has been considered as an independent risk factor for BK in some public-cations,[37],[38],[39] but we did not conclude this result from our analysis. In agreement with our findings, Dharnidharka et al showed no significant differences between males and females. In addition, they considered age as the most important risk factor for viral infection.[5] In the current study, medical comorbidities such as diabetes and hypertension were not recognized as risk factors for prevalence of viral infections, which is consistent with other studies.[20]

The limitations of the present study are related to the nature of retrospective studies. It was a single-center study, and hence, the results me be different depending on different donor characteristics. We assessed only symptomatic patients who were referred to the medical center; this kind of selection leads to exclusion of significant numbers of asymptomatic patients.


   Conclusion Top


The incidence of symptomatic viral disease in kidney transplant recipients in our center is relatively high (25.9%). Diabetes and hypertension were not risk factors for viral disease. The first six months posttransplantation are considered high-risk period for intense viral disease and therefore, intense monitoring of recipients in the cited duration is necessary. Due to the high prevalence of CMV disease, use of appropriate prophylaxis is indicated.


   Acknowledgments Top


This work was financially supported by the Mashhad University of Medical Sciences (Grant No. 940940). We are thankful to Dr. Mohammad Javad Mojahedi, Mr. Ghoncheh, Mr. Heidari and Mrs. Mirzakhani for their kind cooperation.

Conflict of Interest: None declared.



 
   References Top

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Pavlopoulou ID, Poulopoulou S, Melexopoulou C, Papazaharia I, Zavos G, Boletis IN. Incidence and risk factors of herpes zoster among adult renal transplant recipients receiving universal antiviral prophylaxis. BMC Infect Dis 2015;15:285.  Back to cited text no. 2
    
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Drachenberg CB, Papadimitriou JC, Ramos E. Histologic versus molecular diagnosis of BK polyomavirus-associated nephropathy: A shifting paradigm? Clin J Am Soc Nephrol 2006;1:374-9.  Back to cited text no. 11
    
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Lofaro D, Vogelzang JL, van Stralen KJ, Jager KJ, Groothoff JW. Infection-related hospitali-zations over 30 years of follow-up in patients starting renal replacement therapy at pediatric age. Pediatr Nephrol 2016;31:315-23.  Back to cited text no. 12
    
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Neumann AB, Daxbacher EL, Chiaratti FC, Jeunon T. Cutaneous involvement by cyto-megalovirus in a renal transplant recipient as an indicator of severe systemic infection. An Bras Dermatol 2016;91:80-3.  Back to cited text no. 13
    
14.
Gupta RK. Opportunistic infections in renal allograft recipients. Transplant Proc 2007;39: 731-3.  Back to cited text no. 14
    
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Nashan B, Gaston R, Emery V, et al. Review of cytomegalovirus infection findings with mammalian target of rapamycin inhibitor-based immunosuppressive therapy in de novo renal transplant recipients. Transplantation 2012;93:1075-85.  Back to cited text no. 15
    
16.
Nafar M, Roshan A, Pour-Reza-Gholi F, et al. Prevalence and risk factors of recurrent cytomegalovirus infection in kidney transplant recipients. Iran J Kidney Dis 2014;8:231-5.  Back to cited text no. 16
    
17.
Einollahi B. Cytomegalovirus infection following kidney transplantation: A Multicenter study of 3065 cases. Int J Organ Transplant Med 2012;3:74-8.  Back to cited text no. 17
    
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Pourmand G, Salem S, Mehrsai A, Taherimahmoudi M, Ebrahimi R, Pourmand MR. Infectious complications after kidney transplantation: A single-center experience. Transpl Infect Dis 2007;9:302-9.  Back to cited text no. 18
    
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Cordero E, Casasola C, Ecarma R, Danguilan R. Cytomegalovirus disease in kidney transplant recipients: Incidence, clinical profile, and risk factors. Transplant Proc 2012;44:694-700.  Back to cited text no. 19
    
20.
Díaz J, Henao J, Rodelo J, García A, Arbeláez M, Jaimes F. Incidence and risk factors for cytomegalovirus disease in a Colombian cohort of kidney transplant recipients. Transplant Proc 2014;46:160-6.  Back to cited text no. 20
    
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22.
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23.
Burgos D, Jironda C, Martín M, González-Molina M, Hernández D. BK-virus-associated nephropathy. Nefrologia 2010;30:613-7.  Back to cited text no. 23
    
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25.
Jozpanahi M, Ramezani A, Ossareh S, et al. BK viremia among Iranian renal transplant candidates. Iran J Pathol 2016;11:210-5.  Back to cited text no. 25
    
26.
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27.
Soleymanian T, Keyvani H, Jazayeri SM, et al. Prospective study of BK virus infection and nephropathy during the first year after kidney transplantation. Iran J Kidney Dis 2014;8:145-51.  Back to cited text no. 27
    
28.
Nasiri S, Ahmadi SF, Lessan-Pezeshki M, Seyfi S, Alatab S. Lack of cytomegalovirus and polyomavirus coexistence in Iranian kidney transplant recipients. Transplant Proc 2011;43:536-9.  Back to cited text no. 28
    
29.
Kaydani GA, Makvandi M, Samarbafzadeh A, Shahbazian H, Hamidi Fard M. Prevalence and distribution of BK virus subtypes in renal transplant recipients referred to golestan hospital in Ahvaz, Iran. Jundishapur J Microbiol 2015;8:e16738.  Back to cited text no. 29
    
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Pakfetrat M, Yaghobi R, Salmanpoor Z, Roozbeh J, Torabinezhad S, Kadkhodaei S. Frequency of polyomavirus BK infection in kidney transplant patients suspected to nephro-pathy. Int J Organ Transplant Med 2015;6:77-84.  Back to cited text no. 30
    
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33.
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34.
Rostamzadeh Khameneh Z, Sepehrvand N, Taghizadeh-Afshari A, Motazakker M, Ghafari A, Masudi S. Seroprevalence of herpes simplex virus-2 in kidney transplant recipients: A single-center experience. Iran J Kidney Dis 2010;4:158-61.  Back to cited text no. 34
    
35.
Kramer MA, Uitenbroek DG, Ujcic-Voortman JK, et al. Ethnic differences in HSV1 and HSV2 seroprevalence in Amsterdam, the Netherlands. Euro Surveill 2008;13. pii: 18904.  Back to cited text no. 35
    
36.
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37.
Boukoum H, Nahdi I, Sahtout W, et al. BK and JC polyomavirus infections in Tunisian renal transplant recipients. J Med Virol 2015;87: 1788-95.  Back to cited text no. 37
    
38.
Khamash HA, Wadei HM, Mahale AS, et al. Polyomavirus-associated nephropathy risk in kidney transplants: The influence of recipient age and donor gender. Kidney Int 2007;71: 1302-9.  Back to cited text no. 38
    
39.
Ramos E, Drachenberg CB, Papadimitriou JC, et al. Clinical course of polyoma virus nephro-pathy in 67 renal transplant patients. J Am Soc Nephrol 2002;13:2145-51.  Back to cited text no. 39
    

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Correspondence Address:
Afsane Bahrami
Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand
Iran
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DOI: 10.4103/1319-2442.261332

PMID: 31249223

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