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Volume: 17 Issue: 1 January 2019 - Supplement - 1


Screening for BK Viremia/Viruria and the Impact of Management of BK Virus Nephropathy in Renal Transplant Recipients

Objectives: The prevalence of BK-induced nephritis in renal transplant recipients is estimated to be 1% to 10%; the rate of graft loss within 1 year is 30% to 65%. We conducted this study to evaluate screening of BK virus in blood and/or urine among renal transplant recipients and to assess the effects of different therapeutic modalities in renal transplant recipients with BK nephropathy.

Materials and Methods: Kidney transplant recipients were screened at the time of transplant and then at 1, 2, 3, 6, 9, 12, 18, and 24 months posttransplant. Fifty-nine patients were diagnosed with BK virus viremia. Patients were divided into 2 groups according to treatment: group 1 (n = 29) received an active treatment and group 2 (n = 30) received minimized immunosuppression.

Results: Most patients required graft biopsies to confirm diagnosis (86.2% in group 1 vs 50% in group 2; P = .03). Both groups were comparable regarding demographic data. Initial posttransplant graft function was signifi-cantly better in group 1 (P = .017); ultimately, there was no significant difference between both groups regar-ding graft survival (P = .51). Fifty percent of patients had biopsy-proven acute T-cell-mediated rejection before BK virus-associated nephropathy diagnosis (significantly higher in group 1). Serum creatinine levels were significantly better in group 2 at 3, 4, and 5 years after BK nephropathy (P = .001, .017, and .003, respectively).

Conclusions: The prevalence of BK nephropathy in our renal transplant recipients was 5.9% with a rate of graft loss ranging from 43% to 51%. Regular screening, less intensive immunosuppressive therapy, and early intervention by reduction of immunosuppressive medications are advisable to obtain early diagnosis and to have better outcomes of BK virus-associated nephropathy with antiviral agents.

Key words : Immunosuppression, Kidney transplant recipients, Nephritis


Kidney transplant is the treatment of choice for end-stage renal disease.1 A successful kidney transplant improves the quality of life and reduces the mortality risk for most patients compared with maintenance on dialysis. However, patients require close follow-up after transplant since they are on complex immunosuppressive regimens that render them susceptible to infection, malignancy, and cardio-vascular disease.2

Patient survival after renal transplant varies based on the source of the allograft, patient age, and the presence and degree of severity of comorbid conditions. Other possible contributing factors include patient sex, race/ethnicity, and degree of immunosuppression.3

The prevalence of BK-induced nephritis in renal transplant recipients is estimated to be 1% to 10%; the rate of graft loss within 1 year is 30% to 65%. Viruria and viremia precede nephritis, which can occur as early as 6 days and up to 5 years posttransplant (mean of 10-13 months).4

Most cases of clinically significant nephropathy are thus preceded by a period of asymptomatic viruria followed by viremia. Viruria and viremia may be detected weeks to months before there is a detectable increase in serum creatinine levels, suggesting that routine screening and preemptive treatment may be an effective strategy among transplant recipients.4

Although urinary “decoy cells” have excellent sensitivity for the detection of overt BK virus-associated nephropathy (BKVN), polymerase chain reaction (PCR) is 4 times more sensitive than urine cytology for monitoring asymptomatic viruria. Quantitative nucleic acid-based viral load assays of urine or blood are becoming widely used for BK virus screening. Detectable virus in the blood is more predictive of BKVN than viruria alone.5

Donor-related risk factors include deceased-donor organs, active BK virus or cytomegalovirus (CMV) infection, seropositivity, and absence of HLA-C7.6 Recipient-related risk factors include old age, male sex, white ethnicity, diabetes mellitus, prior tubular injury, CMV infection, seropositivity, absence of HLA-C7, HLA-DR mismatch, procurement injury, cold ischemia time, delayed graft function, immuno-suppression, especially tacrolimus and mycop-henolate mofetil (MMF), treatment of rejection by antilymphocytes or steroids, drug toxicity, and HLA mismatch.6

Materials and Methods

Of 1000 renal transplant recipients screened for BK virus at the Hamed Al-Essa Organ Transplant Center of Kuwait between 2002 and 2012, 59 patients were included in this retrospective cohort. Kidney transplant recipients were screened for BK virus in urine and blood by qualitative and quantitative PCR at the time of transplantation, every month for 3 months posttransplant and then every 3rd month during the first 2 years posttransplant, when allograft dysfunction was noted (creatinine increase of > 25% over baseline), whenever allograft biopsy was performed, and whenever any viremia was noted.

Inclusion and exclusion criteria
All adult renal transplant recipients (male and females) with proven BK viremia and viruria were included in this retrospective cohort. All patients were followed up in our transplant center between 2002 and 2012. We excluded patients with negative BK virus in blood and urine.

Techniques used for diagnosis and treatment
A positive screening test was considered significant if the number of viral copies exceeded 107 copies/mL in urine or 104 copies/mL in blood; a positive test required confirmation within 4 weeks. Diagnosis of BK virus infection was considered if any viruria or viremia was present without graft dysfunction or BKVN. A diagnosis of presumptive BKVN meant twice positive test for viruria > 107 or viremia > 104 copies/mL without graft dysfunction. A diagnosis of definite BKVN meant a twice positive test for viruria > 107 or viremia > 104 with graft dysfunction or any positive graft biopsy for BKVN.

Indications for graft biopsy included high clinical suspicion, 2 measurements of viremia < 104 with graft dysfunction, 2 positive measurements of viremia > 104 or viruria > 107 with or without graft dysfunction, or unexplained serum creatinine increase during follow-up after diagnosis of BKVN.

BK virus-associated nephropathy was classified into 3 patterns: pattern A was defined as evidence of BKVN with minimal inflammation, pattern B was defined as BKVN with focal or diffuse interstitial fibrosis and tubular atrophy, and pattern C was defined as BKVN with significant graft sclerosis.

Treatment strategy
Patients who were enrolled in this study were subcategorized according to type of treatment: those with active treatment (group 1, n = 29) and those with minimization treatment (group 2, n = 30).

For those in the active treatment group (group 1), once they were diagnosed as definite or presumptive BKVN, MMF was discontinued and replaced with leflunomide as maintenance immunosuppression (loading dose of 100 mg/d for 3-5 d and then 20-60 mg/d). If significant adverse effects developed (eg, bone marrow suppression, acute hepatitis, or increased transaminases of more than double normal values), we held leflunomide and restarted a smaller dose when adverse effects improved (eg, 10 mg). A course of ciprofloxacin (500 mg twice daily for 2 weeks) was given, in addition to a course of intravenous immunoglobulin (IVIG; 2 g/kg to maximum of 125 g) over 3 to 5 days. Steroids were gradually reduced, and tacrolimus was either converted to cyclosporine or gradually reduced to a maintenance level of 4 to 5 ng/mL for tacrolimus and to 50 ng/mL for cyclosporine according to time of transplant. Conversion of calcineurin inhibitors (CNIs) to sirolimus was another approach, with maintenance of trough levels at 4 to 5 ng/dL to avoid CNI nephrotoxicity.

After this first step, with reduced viral load and stable graft function, we continued monitoring the same immunosuppression. However, in cases of sustained or rising viral load without further graft dysfunction, we reduced maintenance immunosup-pression further with close monitoring. If there was further unexplained graft dysfunction, we considered graft rebiopsy and proceeded with treatment according to the following results. If no evidence of BKVN was shown, we reduced immunosuppression and continued monitoring; if BKVN was evidenced alone without rejection, we tapered CNIs/sirolimus and continued close monitoring; if BKVN was associated with acute rejection, we treated rejection conventionally followed by reduction of maintenance immunosuppression; finally, if we could not dif-ferentiate BKVN from acute rejection, we considered another course of IVIG with further reduction of immunosuppression and continued monitoring.

For those in the immunosuppression minimization group (group 2), treatment followed 3 steps. First, once patients were diagnosed with definite or presumptive BKVN, maintenance immunosup-pression was gradually reduced with close monitoring and antirejection treatment was given as for group 1. Next, similar to group 1 but without antiviral therapy or IVIG, we considered treatment to be successful if the patient was without viremia with stable graft function. If BKVN and concurrent acute rejection were diagnosed, conventional antirejection treatment was considered according to the type of rejection, with IVIG (2 g/kg to maximum of 125 g over 5 days) preferred or pulse steroid (500-1000 mg daily for 3 days) followed by immediate reduction to previous steroid dose.

Data collection
We obtained information from a registered database of all kidney transplant recipients over a 5-year follow-up period. In particular, the following variables were collected: demographic data (age, sex, weight), associated comorbidities (diabetes mellitus, CMV, immediate graft function state), immunologic data, especially crossmatch and tissue typing data, type of immunosuppression (induction and maintenance), donor criteria (age, BK virus status, sex), number and type of rejection episode, patient and graft outcomes at last follow-up, and medical complications, especially hypertension, new-onset diabetes mellitus after transplant, CMV, malignancy, and other infections.

Immunosuppressive regimens
All patients received triple immunosuppressive regimens consisting of CNIs, MMF, and cortico-steroids. All induction therapy was based on our protocol guidelines and transplant risk factors. Patients at high risk for acute rejection (those who had retransplants and panel reactive antibodies of > 20%) received daily 1 mg/kg thymoglobulin for 5 days. Other patients received interleukin 2 receptor blockers as induction using basiliximab 20 mg intravenously on days 0 and 4. Corticosteroids were initiated intraoperatively, with 1000 mg methyl-prednisolone given initially, then 1 mg/kg to a maximum of 60 mg/day from day 1, and then low-dose prednisolone (0.1-0.5 mg/kg/d) by 3 months posttransplant.

Statistical analyses
Statistical analysis was conducted using SPSS software (version 20, Chicago, IL, USA). Qualitative data are presented as number and percentage, whereas quantitative data are presented as means and standard deviation. The t test was used to compare means and standard deviations of the groups. Categorical data were compared using the chi-square test. P < .05 was considered significant.


Most of the study patients were males in their 5th decade of life, with mean age of 40.12 ± 15.04 years for group 1 and 40.18 ± 17.38 years for group 2 (P = .989; Table 1). Group 1 patients had a slightly higher mean weight than group 2 patients (86.91 ± 18.19 vs 70.42 ± 17.63 kg; P = .431). More than 85% of the study patients were recipients of a first renal allograft with no significant difference between the 2 groups (P = .612), and most received grafts from living unrelated donors (44.8% in group 1 vs 53.3% in group 2; P = .163). Postoperative graft function was significantly better in group 1 than in group 2 (48.3% of patients in group 1 showed immediate graft function vs 20% in group 2); however, the number of patients with delayed graft function was significantly higher in group 1 (P = .017). Most patients in both groups received hemodialysis (no significant difference between groups, P = .585). We found no significant difference between the groups regarding the number of patients with diabetes mellitus (P = .3). There was a higher number of immuno-logically high-risk patients in group 1, and most patients in group 2 were immunologically low risk; however, these differences were not significant (P = .29; Table 1). Moreover, mean total HLA mis-matches were comparable in both groups (P = .344).

The original kidney disease was comparable between the 2 groups, although most patients had disease of unknown cause. Diabetic kidney disease and chronic glomerulonephritis represented the most common causes of end-stage kidney disease (P = .63; Table 1).

The number of patients who received induction was higher in group 1 than in group 2, although not significantly (P = .203). Moreover, most patients did not receive desensitization. Both groups were comparable regarding primary maintenance immunosuppression (P = .653, Table 1).

We observed that all patients had significant viremia (viral load of > 10 000 copies/mL) at the start of the study. However, the number of patients with BKVN was significantly higher in group 1 (25 patients) than in group 2 (15 patients) (P = .003; Table 2).

We found no significant differences between the 2 groups regarding the viral load at different time intervals during the study period until 1 year after BK virus diagnosis (P > .05; Table 2). However, in both groups, there was a significant reduction in the viral load compared with baseline values (P < .05).

We found no significant differences between groups regarding immunosuppression modification. Most patients in both groups underwent reduction of both CNIs and antiproliferative agents (P = .098; Table 3).

There were no significant differences between the study groups regarding mean serum creatinine levels at the time of BKVN diagnosis. We found that graft function, as shown by serum creatinine levels, was significantly better in group 2 at 3 years, 4 years, and 5 years (P = .001, .017, and .003, respectively). Graft function had significantly deteriorated in group 1, as shown by mean baseline serum creatinine (185 μmol/L) compared with levels at end of the study in both groups (Table 4).

We observed a significant deterioration in renal allograft estimated glomerular filtration rate (eGFR) in group 1 (P = .64) versus an improvement in group 2 (P = .050). There was no significant difference between the study groups regarding the number of patients with end-stage graft failure (P = .519; Table 5).

We found that the 2 groups were comparable regarding the total number of rejection episodes before and after BKVN diagnosis (P = .08 and .23, respectively). More than 50% of patients had biopsy-proven acute rejection before BKVN diagnosis. These were mainly episodes of acute cellular rejection, which were significantly higher in group 1. Both acute antibody-mediated rejection and steroid-resistant rejection were comparable in both groups (P > .05; Table 5).


With the development of effective immunosup-pressive regimens, renal transplant is considered the preferred treatment to extend expectancy and quality of life for patients with end-stage kidney disease.7 Human polyomaviruses, including BK virus and JC virus, are highly prevalent in humans but appear to cause clinical disease only in immunocompromised patients. BK virus primarily induces tubulointerstitial nephritis and ureteral stenosis in renal transplant recipients and hemorrhagic cystitis in bone marrow transplant recipients.8 BK virus infection is generally acquired at an earlier age (at 3-4 years).9,10

Since 2002, kidney transplant recipients have been screened at our center for possible BKVN using qualitative and quantitative PCR analyses of urine and blood. We started our routine mass screening of all kidney transplant recipients since 2006, with screening continued for 2 years posttransplant. In our study cohort, the prevalence of BK viremia was 5.9%; these results are similar to those reported by Dharnidharka and associates, in which the prevalence of BKVN was 4%.11 Schold and associates12 and van Aalderen and associates13 showed an estimated prevalence of BKVN of 1% to 10% with a mean of nearly 5%. In contrast, Chon and colleagues14 reported a higher prevalence of BK viremia in their cohort (52 of 361 patients [14.4%] were positive). Moreover, they showed a higher number of cases of biopsy-proven BKVN (46 of 248 patients, 18.6%). Both Dogan and associates15 and Boobes and associates16 reported a higher prevalence of BK viremia (15.8% and 14.7% in their cohorts, respectively).

The higher prevalence of BK viremia in other studies could be explained by the more prevalent risk factors, including more frequent use of thymo-globulin as induction, more patients with diabetes, and the use of a heavier maintenance tacrolimus-based immunosuppression strategy.14 Moreover, Pai and associates17 added that a higher mean cumulative dose of thymoglobulin as induction therapy was associated with higher prevalence of BKVN, although their results were not statistically significant (P = .07). Dogan and colleagues15 reported other risk factors in their cohort, including deceased-donor transplant and human leukocyte antigen matching (HLA-A24 and HLA-B55).

Quantitative or real-time PCR analysis for BK viral DNA of plasma or serum and less so of urine appears to be useful in monitoring kidney transplant recipients and significant viremia (> 104 copies/mL); this method can confirm BKVN diagnosis.18 In our study, we found that BK viral load was significantly positive at the time of diagnosis and became negative in almost all patients by the end of the study.

Initially, our patients had been screened for BK virus when unexplained graft dysfunction was noticed (> 20% of basal serum creatinine) or whenever graft biopsy was indicated. This practice is in accordance with that reported by Hirsch and associates,19 in which diagnosis of BKVN may be made in the absence of definitive findings on biopsy. In our study, most patients required graft biopsies to confirm the diagnosis of BKVN (86.2% in group 1 vs 50% in group 2; P = .003; Table 2).

Similar to that reported previously,20 our findings of sustained significant BK replication (plasma DNA PCR load > 10 000 copies/mL) with or without kidney dysfunction could be responsible for poor graft outcomes, especially in group 1. In addition, most patients were males and approximately in their 5th decade of life, which is similar to that reported previously by Chon and associates,14 who reported male preponderance (63.9%) in their cohort with mean age of 47.7 years. Multivariate analyses have shown that male sex is an independent risk factor.9-11,21,22

Both Wiseman and associates21 and Hirsch and associates19 hypothesized other risk factors, including older recipient age. The most reliable risk factor identified for the development of BKVN has been the overall degree of immunosuppression. In their prospective study, Brennan and associates5 found that incidences of BK viruria and viremia were similar in patients randomly assigned to tacrolimus or cyclosporine; BKVN has also been shown to develop in recipients receiving different combinations of cyclosporine, azathioprine, and sirolimus and even in those who had CNI-free regimens.23,24 In a US study10 of more than 1000 kidney transplant recipients, no specific form of immunosuppression, including tacrolimus and MMF, was identified as a risk factor. Moreover, no specific immunosup-pressive drug or combination has been conclusively associated with BKVN.25,26 An Indian report showed a high frequency of BK virus (30 cases, prevalence of 10%) in patients not receiving tacrolimus or MMF.27 Another stated that BKVN developed only rarely in patients who did not receive either tacrolimus or MMF.28 Others found that tacrolimus, but not MMF, was a risk factor.29 However, Hirsch and associates30 demonstrated that patients who received cyclosporine-based immunosuppression had a lower rate of BKVN at 6 and 12 months posttransplant than those who were maintained on tacrolimus-based therapy. Moreover, they added that high titer of BK virus and the overall median BK viral loads were higher in the tacrolimus group.

In our study, although most patients were not highly sensitized, they received intensive immuno-suppression therapy (thymoglobulin induction, MMF, and tacrolimus) possibly due to other immunologic risk factors, including number of HLA mismatches (total mean HLA mismatch was 3.88 ± 1.24; Table 1), more acute rejection episodes before BKVN diagnosis, and donor type. However, the 2 groups were matched regarding induction and primary maintenance immunosuppression. We observed higher numbers of immunologically high-risk patients in group 1 with more potent induction (thymoglobulin) and main-tenance immunosup-pression (tacrolimus based) (Table 1) than in group 2, although results were not significant (P = .29; Table 1). This lower prevalence of BK viremia and BKVN despite previous known risk factors could be due to early detection of cases by our mass screening and their earlier treatment by either active or minimization regimens.

Most of our study patients received grafts from living donors (> 60%) and more than 85% received a first renal allograft (with no significance between groups regarding donor type; P = .612). This finding may explain the lower prevalence of BKVN in our cohort as deceased-donor transplant has been shown to be a risk factor.15

Differentiating between cellular infiltrates of rejection and BKVN has been shown to be difficult.29,30 BK virus nephropathy could be distinguished from allograft rejection by the presence of BK virus inclusions and immune histologic or in situ hybridization evidence of virally infected cells, which were usually tubular epithelial cells, rather than podocytes or endothelial cells.21 It can also be possible that some patients with acute cellular rejection also have evolving BKVN.31-33

In our study, we found that most patients (> 80%) started treatment after histopathologic evidence of BKVN, with > 50% showing pattern B. Other studies have shown that most BKVN biopsies display pattern A, with subsequent deterioration to patterns B and C. This could be explained by the heterogenous nature of the histopathologic abnormalities of BKVN.18,29

Significant graft dysfunction at the time of diagnosis of BKVN is a major risk factor for graft failure.9,12 We observed high baseline serum creatinine levels and reduced eGFR in both groups at the start of the study (Table 4). These observations may be due to more adverse prognostic factors (more males, more tacrolimus-based regimens, more rejection episodes, and more histologic pattern B).

As shown by eGFR results, group 1 patients had significant deterioration of renal allograft function compared with baseline eGFR results and compared with group 2 eGFR results at end of study (P < .05). In line with this observation, we observed no significant differences between groups regarding mean serum creatinine levels at the time of BKVN diagnosis. However, we found that graft function, as represented by serum creatinine, was significantly better in group 2 at 3, 4, and 5 years of follow-up.

BK virus nephropathy has an aggressive course, resulting in graft failure in more than 40% of our kidney transplant recipients on long-term follow-up (28 of 59 cases over 5-year follow up; Table 5). A similar finding was reported by Balba and as-sociates34 who showed that renal allograft loss from BKVN can occur in up to 50% of affected recipients despite clearance of viremia with reduction of immunosuppressive agents. Better results have been reported in other studies, which could be explained by shorter follow-up, fewer enrolled patients, and early diagnosis of the disease in their cohorts.29,34,35 More than 50% of patients had biopsy-proven acute rejection before BKVN diagnosis (Table 5). Most rejection episodes were T-cell-mediated rejection, with results significantly higher in group 1. The total number of T-cell-mediated rejection episodes was significantly higher in group 1 before and after BKVN diagnosis, which could be a reason for worse graft outcomes in group 1 than in group 2.

A recent review of the published literature showed that certain patients with BK viremia or BKVN could benefit from cidofovir, leflunomide, and IVIG therapy, but these data were derived from case series or protocol-driven cohort studies.36 A com-bined therapy incorporating adjuvant IVIG was more effective in eliminating virus from BKVN than conventional therapy. Moreover, IVIG administration appeared to be safe and effective in treating BK viremia and BKVN and preventing graft loss in patients who had inadequate response to immuno-suppression reduction and leflunomide therapy. From our study, we observed that patients in group 1 who received high-dose IVIG treatment (23 patients) did not gain any benefit and had worse long-term graft outcomes (Table 3). This discrepancy in response to IVIG may be due to differences in patient characteristics, with possible hypogam-maglobulinemia in some patients and not in others.

An advantage of IVIG is that it could effectively treat both polyoma infection and allograft rejection. An IVIG treatment may contain antibodies against BK and JC virus, since these viruses are ubiquitous in the general population. However, these antibodies may not be neutralizing.37 In addition, anti-BK antibodies were not shown to be protective and may indicate an augmented humoral response to an inadequate cellular immune response.37

Treatment with leflunomide may be effective for BKVN.38 Leflunomide is a prodrug whose antime-tabolite has both immunosuppressive and antiviral activity.39 However, no well-designed randomized controlled studies have examined the efficacy of leflunomide in BKVN. Leflunomide has some limitations in its use in kidney transplant recipients due to unpredictable blood levels, difficulty in monitoring, and weak immunosuppressive effects. From our study, we observed that group 1 patients who received leflunomide treatment (23 patients) did not gain any benefit and had worse long-term graft outcome (Table 3). Our unfavorable results may be due to its late use and possible interrupted therapy due to its adverse effects.

Regarding the use of ciprofloxacin, Leung and colleagues40 showed that quinolones had anti-polyomavirus activity in vitro and observed resolution of BK virus replication in vivo in some transplant patients. A recent prospective, multicenter, double-blind, placebo-controlled trial showed that administration of 500 mg/day of levofloxacin or placebo for 30 days resulted in an equivalent percent reduction in BK viral load at 1, 3, and 6 months and no difference in graft outcome. Moreover, therapy with a quinolone was initiated because it was fairly inexpensive and easy to administer. Quinolone antibiotics may have anti-BK virus properties by inhibiting DNA topoisomerase activity and SV40 large T antigen helicase.41

Compared with cephalosporin, ciprofloxacin significantly lowered urinary BK viral loads. An observational study reported that the use of a fluoroquinolone was associated with prevention of BK viremia.42 These data supported a role for quinolones in prevention of BK viremia and BKVN. However, so far, data at present are insufficient to support the use of this agent in this setting. From our study, we observed no benefit, with patients in group 1 even having worse long-term graft outcomes (Table 3).

Vandercam and associates43 reported that cido-fovir had a significant in vitro effect regarding inhibition of nonhuman polyomaviruses. However, the pronounced nephrotoxicity limited its use, particularly in renal transplant recipients.9,44 Only 1 patient in group 1 received this treatment in our study group.

In a retrospective nonrandomized study of 21 patients with BKVN, 8 were administered weekly adjuvant low-dose cidofovir plus a reduction in immunosuppressive therapy, whereas 13 were treated with reduced immunosuppressive therapy alone. At a median period of 25 months, all allografts of those administered cidofovir survived. However, 8 of 13 allografts not given cidofovir were lost at a median period of 8 months.45 In one report of 4 patients, including 2 children, cidofovir was effective in all 4 patients.46

However, cidofovir has been shown to be highly nephrotoxic, resulting in proteinuria and renal failure in 20% of patients.44 Therefore, it should be used cautiously and under the supervision of a transplant center familiar with BKVN and cidofovir. An international panel also recommended that patients be enrolled in clinical studies, if possible.33 Until results of additional trials become available, cidofovir should only be used when all other interventions have failed after a trial period of 3 months.


The prevalence of BKVN in our renal transplant recipients was 5.9% with a rate of graft loss that ranged between 43% and 51%. Regular screening, less intensive immunosuppressive therapy, and early intervention by reduction of immunosuppressive medications are advisable to obtain early diagnosis and to have better outcomes of BKVN.


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Volume : 17
Issue : 1
Pages : 83 - 91
DOI : 10.6002/ect.MESOT2018.O17

PDF VIEW [159] KB.

From the 1Hamed Al-Essa Organ Transplant Center, Kuwait; the 2Internal Medicine Department, Faculty of Medicine, Zagazig University, Mansoura, Egypt; the 3Urology and Nephrology Center, Mansoura University, Mansoura, Egypt; and the 4Department of Internal Medicine and Nephrology, Ain Shams University.
Acknowledgements: The authors have no sources of funding for this study and have no conflicts of interest to declare.
Corresponding author: Osama A. Gheith, Hamed Al-Essa Organ Transplant Center, Ministry of Health – Ibn Sina Hospital, Kuwait
Phone: +96 566641967