Risk Factors for BK Virus Infection and BK Virus–Associated Nephropathy Under the Impact of Intensive Monitoring and Pre-emptive Immunosuppression Reduction

BackgroundBK virus (BKV) nephropathy (BKVN) is an increasingly recognized cause of kidney allograft loss and is thought to be related to the newer, more potent immunosuppressive agents. However, the risk factors for different types of BKV infection under the impact of intensive monitoring and reduction of maintenance immunosuppression are not well understood.MethodsQuantitative BKV DNA surveillance in plasma/urine and cytological testing in urine were performed regularly within the first year post-transplantation in 229 kidney recipients. Patients with BK viremia and BKVAN treated with immunosuppression reduction were monitored for BKV every 3–6 months. All the patients were followed up for a minimum of 5 years to exclude later development of BKVAN. Potential variables were compared and analyzed using logistic regression model multivariate analysis to assess and rank the BKV infection-related factors.ResultsSeventy-eight (34.1%) patients had decoy cells, 99 (43.2%) BK viruria, 38 (16.6%) BK viremia, and 7 (3.1%) BKVAN. Risk for decoy cells, BK viruria, and viremia, and BKVAN in univariate analyses were higher with tacrolimus (Tac) and deceased kidney donation. Multivariate analysis showed that Tac ([HR, 2.7; P = .008], [HR, 2.3; P = .016], [HR, 2.9; P = .032]) and deceased kidney donation ([HR, 2.5; P = .004], [HR, 2.6; P = .002], [HR, 2.1; P = .071]) were risk factors for BK decoy cells, BK viruria, and viremia, respectively. BKVAN was inclined to the patients with the combination of Tac and mycophenolate mofetil and longer BKV clearance time.ConclusionsTac and deceased kidney donation are independent risk factors for BKV infection under the impact of therapeutic drug monitoring.     

Cytomegalovirus prevention strategies and the risk of BK polyomavirus viremia and nephropathy

Polyomavirus BK (BKV) is the cause of polyomavirus‐associated nephropathy resulting in premature graft loss. There are limited data regarding the role of cytomegalovirus (CMV) infection and its prevention in developing BKV viremia and PVAN. In a prospective study, we analyzed 207 consecutive renal transplant recipients previously enrolled in 2 randomized trials evaluating different CMV prevention regimens with routine screening for BKV and CMV. Of these, 59 received valganciclovir and 100 valacyclovir prophylaxis; 48 patients were managed by preemptive therapy. At 3 years, the incidence of BKV viremia and PVAN was 28% and 5%, respectively. CMV DNAemia developed in 55% and CMV disease in 6%. Both BKV viremia (42% vs 23% vs 21%, P = .006) and PVAN (12% vs 2% vs 2%, P = .011) were increased in patients treated with valganciclovir prophylaxis compared to valacyclovir and preemptive therapy. Using multivariate Cox proportional hazard regression, valganciclovir prophylaxis was independent predictor of BKV viremia (hazard ratio [HR] = 2.38, P = .002) and PVAN (HR = 4.73, P = .026). In contrast, the risk of subsequent BKV viremia was lower in patients with antecedent CMV DNAemia (HR = 0.50, P = .018). These data suggest valganciclovir prophylaxis may be associated with increased risk of BKV viremia and PVAN. CMV DNAemia did not represent a risk for BKV.     

Management of BK viremia is associated with a lower risk of subsequent cytomegalovirus infection in kidney transplant recipients

The risk of subsequent cytomegalovirus infection (CMV) in kidney transplant recipients (KTR) after diagnosis of BK polyomavirus viremia (BKV) is unclear, and current evidence is conflicting. We reviewed all KTR transplanted at our institution between 1/1/2005 and 12/31/2015. Follow-up began 3 months after transplantation to avoid confounding effects of prophylaxis. Clinically significant BKV, defined as detectable BK viremia >1000 copies/mL via molecular diagnostic testing (PCR), was treated as a time-varying exposure with 1-year follow-up. This viral load cutoff was chosen to ensure a more homogenous population that would be considered to have clinically significant BK viremia that necessitated management via immunosuppressive modification. Patients were then screened for subsequent CMV infection. 2435 RTX recipients met inclusion criteria; of these, 314 developed BKV during follow-up (BK+). Lymphocyte depletion, tacrolimus maintenance, and biopsy-proven rejection were significantly higher in the BK+ group. BK+ was associated with lower risk of subsequent CMV infection (BK+ HR 0.45, 95% CI 0.22-0.94, P = .03, relative risk reduction 55%). When adjusted for significant confounding factors, CMV incidence remained reduced in the BK+ population (HR 0.47, 95% CI 0.22-0.98, P = .04). This large series of KTR demonstrates that BKV is associated with lower risk of subsequent CMV infection.     

Surgical Wound Dehiscence in Kidney Transplantation: Risk Factors and Impact on Graft Survival

BackgroundSurgical wound dehiscence (SWD) is a frequent complication after kidney transplantation (KT) but there is not enough evidence of its impact on graft survival.MethodsA retrospective cohort study including all KT patients with SWD in our center from January 2015 to July 2020 was performed. A case–control study was performed and for each case of SWD, 2 controls were selected (2:1). To identify risk factors for SWD, a logistic regression analysis was carried out and a multivariable Cox regression was used to describe risk factors for graft survival.ResultsIn our center, 503 KT were performed, and 39 patients presented SWD. They were older (62.1 vs 57.1 years; P = .030), most had diabetes mellitus (59% vs 28.6%; P = .002) and their body mass index was higher (31 vs 26.9 kg/m²; P < .001). In multivariable logistic regression analysis, diabetes mellitus (P = .024) and a body mass index ≥30 kg/m² at time of transplantation (P = .018) were predictors of SWD. A higher rate of delayed graft function was described in SWD (P = .013) and it was associated with a longer hospital stay (20.9 vs 15 days; P = .004). Graft survival was lower in patients with SWD (P = .036). In multivariable Cox regression analysis, time in renal replacement therapy (P = .020) and SWD (P = .028) were predictors of shorter graft survival.ConclusionSWD is a risk factor for graft survival. The presence of diabetes mellitus and a higher body mass index are predictors for the appearance of this complication.     

Retrospective Analysis of the Kidney Donor Profile Index to Predict Patient and Graft Survival at 5 Years Posttransplantation in a Colombian Cohort

BackgroundThe Kidney Donor Profile Index (KDPI) has been used to predict patient and graft outcomes in deceased donor kidney transplantation. We aimed to evaluate the impact of KDPI on transplantation major outcomes applied to a Colombian cohort.MethodsWe retrospectively assessed 260 adult patients who underwent kidney transplantation (KT) from January 2011 to June 2014 at our center and compared their KDPIs with graft and patient outcomes at 5 years posttransplantation. Kaplan-Meier survival method and Cox analysis were fitted to analyze the impact of the 3 KDPI categories on graft and patient outcomes.ResultsA total of 18.4% of transplants were from donors with a KDPI ≥75%. There was a significant decrement in renal function with increasing KDPI at 5 years posttransplantation (P < .05). The final model indicates that donor diabetes was associated with elevated risk for graft loss (hazard ratio [HR], 6.5; 95% confidence interval [CI] 1.35-31.8; P = .019) at 5 years posttransplantation. Recipient age (HR, 2.3; 95% CI, 1.1-4.5; P = .001), diabetes status (HR, 2.17; CI, 1.04-5.5; P = .003), dialysis duration (HR, 1.08; 95% CI, 1.00-1.16; P = .003), and operating room time (HR, 1.47; 95% CI, 1.02-2.12; P = .003) were associated with elevated risk for death at 5 years posttransplantation. KDPI categories were not significantly associated with graft loss or death.ConclusionsWe found limited KDPI power to predict graft and patient survival when applied to a Latin American population in Colombia. Our findings highlight the importance of analyzing the application of KDPI in different populations. Therefore, our findings may not be generalizable to other regions outside of Colombia.     

Impact of Recipient Obesity on Kidney Transplantation Outcome: A Retrospective Cohort Study with a Matched Comparison

BackgroundThe aim of this study was to evaluate the effect of a recipient's obesity on posttransplant complications and patient and graft survival.MethodsA single-institution, retrospective study was performed on obese renal transplant recipients (BMI ≥ 30 kg/m², n = 102) from January 2010 to December 2018, matched with non-obese recipients (BMI < 30 kg/m², n = 204). For comparison, for every obese patient we selected 2 nonobese patients with a similar age, sex, and period of transplantation. The comparative analysis included patient and graft survival as primary outcomes and graft function and postoperative complications as a secondary outcome.ResultsRecipient demographics were comparable in both groups except for diabetic nephropathy in obese patients (P = .0006). Obesity was strongly related to a poorer patient survival (risk ratio [RR] = 2.83 confidence interval [CI] 95% 1.14-7.04; P = .020) but there was no observed difference in graft survival (P = .6). While early graft function was inferior in the obese population (RR = 2.41; CI 95% 1.53-3.79; P = .00016), during late follow-up, no statistically significant differences were observed between both groups (P = .36). Obese recipients had a significantly higher risk of delayed graft function (RR = 1.93; CI 95% (1.19-3.1), P = .0077), heart infarction (RR = 7; CI 95% 1.68-29.26; P = .0042), wound infections (RR = 8; CI 95% 1.96-32.87; P = .0015), diabetes aggravation (RR = 3.13; CI 95% 1.29-7.6; P = .011), and surgical revision for eventration (RR = 8; CI 95% 1.22-52.82; P = .026) when compared with nonobese recipients.ConclusionsDespite the inferior early kidney graft function in obese recipients, there was no difference observed at the long-term follow-up. However, recipient obesity demonstrated a negative effect on patient survival and postoperative complications.     

Factor Analysis for Body Mass Index Changes in Kidney Transplant Recipients

BackgroundThe purpose of this study was to identify factors influencing changes in the body mass index (BMI) of kidney transplant (KT) patients and provide data for the management of the BMI of patients who have undergone KT.MethodThe participants were 106 patients who underwent KT at a single center from August 2014 to June 2017. BMIs were compared and analyzed for 6 months and 24 months after KT, and the survey details were collected through medical records. Analysis was performed between 2 groups, one with increased BMI and the other without. Multivariate logistic regression analysis was performed to identify the factors related to an increase in BMI.ResultsBMI increased from 22.60 ± 2.72 kg/m² at 6 months to 23.18 ± 3.06 kg/m² 2 years after KT. The group with increased BMI (n = 39) had more patients with higher low-density cholesterol levels at the time of KT (low-density cholesterol ≥100 mg/dL; 34 [54.0%] vs 10 [26.3]; P = .008) and without statin drug use than the other group (n = 67) (statin drug use, 48 [70.6%] vs 34 [87.2%], P = .044). Multiple logistic regression analysis showed that age >50 years (odds ratio [OR] = 2.942; 95% confidence interval [CI], 1.075-8.055; P = .036), low-density lipoprotein >100 mg/dL at KT (OR = 6.618; 95% CI, 2.225-19.682; P = 0.001), and no statin drugs (OR = 5.094; 95% CI, 1.449-17.911, P = .011) were the risk factors for an increased BMI after KT.ConclusionsAfter KT, to prevent an increase in the BMI, clinicians should strongly recommend the use of drugs to treat hyperlipidemia, especially in elderly patients with high low-density lipoprotein levels before KT.     

Early Postoperative Transaminase Activities Affecting Early and Late Liver Graft Survival

BackgroundThis study aimed to examine the effect of transaminases’ activities in the first posttransplant day on early (90-day) and late (5-year) graft survival.MethodsThis retrospective cohort study included 612 patients after liver transplantation (LT) in the period between 2015 and 2019. Patients with acute liver failure and with vascular complications after LT were excluded. The natural logarithms of alanine transaminase (ALT) and aspartate transaminase (AST) were used for analyses using the logistic regression and Cox proportional hazards regression models. The optimal cut-off point for transaminases was determined using receiver operating characteristic curves. The 5-year graft survival was calculated after previously excluding the patients with 90-day graft loss.ResultsThe ALT and AST were risk factors for 90-day graft loss (odds ratio 2.16; 95% CI 1.45-3.23; P < .001 and 2.23; 95% CI 1.55-3.19; P < .001, respectively). The optimal cut-off for ALT and AST in prediction of 90-day graft loss was ≥1030 and ≥3899 U/L; area under the curve 0.694 (95% CI 0.602-0.786; P < .001), with 11.3% and 97.1% positive predictive value (PPV) and negative predictive (NPV) value, and 0.673 (95% CI 0.575-0.772; P < .001), with 18.4% PPV and 95.6% NPV, respectively. The activities of AST and ALT on first posttransplant day were not identified as risk factors for late graft loss (P = .924 and P = .629, respectively).ConclusionsEarly post-transplant transaminase activities can be used to determine early liver graft loss; however, their utility is lost for assessing the late graft survival.     

Clinical Courses of Renal Transplant Recipients with High BK Viremia

Objective

We sought to investigate the clinical courses of renal transplant recipients with plasma BK viral loads >10⁴ copies/mL.

Methods

A single-center retrospective review was performed of 88 kidney transplant patients in whom high BK viremia (defined as plasma BKV load >10⁴ copies/mL) was detected more than once from January 1, 2004, to December 31, 2011.

Results

At the time of transplantation, the mean recipient and donor ages were 44.5 ± 11.1 and 43.9 ± 11.3 years, respectively, and 59 subjects (67.0%) were male. The median times to first BK positivity and high BK viremia after transplantation were 44 and 136 days, respectively. Within 3 months after transplantation, we detected, 56 cases of high BK viremia (63.6%). The mean duration of high BK viremia was 8.2 ± 7.7 months. When plasma BKV load was first >4 logs, the mean log BKV load was 5.50 ± 1.11 log copies/mL, which rose to a maximum of 5.82 ± 1.11. At these times, mean serum creatinine concentrations were 1.67 ± 0.79 and 2.64 ± 2.78 mg/dL, respectively. There were 31 cases (35%) of biopsy-proven BK nephropathy patients among 51 (58%) biopsies. Treatment modalities included discontinuation or dose reduction of mycophenolic acid drugs (n = 68) and switch from tacrolimus to cyclosporine (n = 9), cidofovir (n = 9), and leflunomide (n = 3). Based on the serum creatinine elevation after high BK viremia, patients were divided into group 1 (n = 27; 30.1%), whose maximal creatinine change was <0.5 mg/dL, and group 2, with a greater alteration. On multivariate logistic regression analysis, the maximal plasma BK viral load was significantly associated with a greater serum creatinine elevation (P < .001).

Conclusions

High BK viremia mostly occurred within 3 months after kidney transplantation. About 30% of renal allograft recipients with high BK viremia maintained stable renal function. Maximal plasma BK viral load was the only independent risk factor for high serum creatinine elevation.     

Correlation between CYP3A5 gene polymorphism and BK virus infection in kidney transplant recipients

BackgroundCytochrome P450 3A5 (CYP3A5) includes two active genotypes, namely CYP3A5*1/*1 or *1/*3 with the fast metabolic activity and CYP3A5*3/*3 with slow metabolic. We retrospectively analyzed the correlation between CYP3A5 gene polymorphism and the susceptibility to the BK virus (BKV) infection in renal transplant recipients.MethodsAccording to the inclusion/ exclusion criteria, we selected 134 recipients who received kidney transplantation at the Renmin Hospital of Wuhan University from January 2019 to December 2019. Based on the pre-operative CYP3A5 sequencing results, 134 recipients were divided into two groups: those expressing the fast metabolic CYP3A5*1/*1 or *1/*3 genotype; and, those expressing slow metabolic CYP3A5*3/*3 genotype. These two recipient groups were then analyzed for the BKV infection rate with different metabolic types to establish the potential relationship between CYP3A5 gene polymorphism and BKV infection.ResultsThe overall incidence of BKV viruria was 37.3%, whereas BKV viremia was 4.5% among all 134 recipients. The fast metabolism group had 9.1% incidence of BKV viremia and 49.1% incidence of BKV viruria. In contrast, the slow metabolism group had only 1.3%incidence of BKV viremia (P = 0.031) with only 29.1% BKV viruria (P = 0.011). The incidence of low levels of urinary BKV in the fast metabolism group was higher than that in the slow metabolism group (P = 0.005), while no significant statistical difference in the incidence of high levels of urinary BKV and high and low levels of blood BKV.ConclusionAfter kidney transplantation, CYP3A5 gene polymorphism of recipients present a certain relationship with the occurrence of BKV infection, which may be of value for the prediction and prevention of BKV infection.     

Ciprofloxacin for BK viremia prophylaxis in kidney transplant recipients: Results of a prospective,double‐blind,randomized, placebo‐controlled trial

In kidney transplantation, BK virus infection has historically resulted in high rates of graft dysfunction and graft loss. Unlike other opportunistic infections, no therapies have been shown to prevent BK. The purpose of the current study was to evaluate the safety and efficacy of ciprofloxacin for the prevention of BK viremia in kidney transplant recipients. Two hundred kidney transplant recipients were enrolled in a prospective, randomized, double‐blind, placebo‐controlled trial comparing a 3‐month course of ciprofloxacin (n = 133) vs placebo (n = 67) for the prevention of BK viremia. The primary endpoint of BK viremia at month 6 posttransplant occurred in 25 (18.8%) patients in the ciprofloxacin group and 5 (7.5%) in the placebo group (P = .03). Higher rates of BK viremia (23.3% vs 11.9%; P = .06) and BK nephropathy (5.8% vs 1.5%; P = .26) remained at 12 months in the ciprofloxacin group. Ciprofloxacin use was associated with a significantly higher rate of fluoroquinolone‐resistant gram‐negative infections (83.3% vs 50%; P = .04). A 3‐month course of ciprofloxacin was ineffective at preventing BK viremia in kidney transplant recipients and was associated with an increased risk of fluoroquinolone‐resistant infections. Clinical trial registration number: NCT01789203.     

Prevalence and Risk Factors of BK Viremia in Patients With Kidney Transplantation: A Single-Center Experience From Turkey

Background

BK virus is the cause of nephropathy, which can progress to graft loss after kidney transplantation. In this study, we aimed to investigate the prevalence and risk factors of BK viremia in patients with kidney transplantation at our center.

Endocrine Management and Hormone Replacement Therapy in Cardiac Donor Management: A Retrospective Observational Study

BackgroundPituitary dysfunction after brainstem death can cause various hormone deficiencies in potential heart donors. The aim of this study was to evaluate the relationship between hormone replacement therapy (HRT; including antidiuretic hormone analog, thyroid hormone, and methylprednisolone) in heart donors and the recipients’ outcomes after heart transplantation (HTx).MethodsWe retrospectively analyzed HTxs performed between January 2012 and October 2018. Donor and recipient characteristics were retrieved with a focus on endocrine parameters and HRT. The primary outcome was primary graft dysfunction (PGD). Secondary outcomes were the 30-day and 2-year mortality of the recipients. Univariate and multivariate Cox regression analyses were applied.ResultsThe study included 297 HTxs. PGD occurred in 56 recipients (18.9%). In the multivariable Cox analysis, methylprednisolone and thyroxine treatment in donors were associated with a lower odds for PGD (odds ratio [OR], 0.43; 95% CI, 0.19-1.01; P = .052; and OR,: 0.34; 95% CI, 0.15-0.76; P = .009, respectively). In multivariate analysis, thyroxine treatment in donors was associated with a lower odds of PGD (OR, 0.38; 95% CI, 0.17-0.86; P = .020). Donor thyroxine supplementation also had a beneficial effect on recipients’ 2-year survival (OR, 0.53; 95% CI, 0.29-0.96; P = .036).ConclusionsCombined thyroxine and methylprednisolone treatment could be a protective factor against PGD. Thyroxine administration was associated with better 2-year survival in recipients.     

Association of DNA Amplification With Progress of BK Polyomavirus Infection and Nephropathy in Renal Transplant Recipients

Purpose

BK polyomavirus-associated nephropathy (BKVAN) is an important cause of renal allograft loss. Immunosuppression therapy in renal transplant recipients can lead to the reactivation of latent BK polyomavirus (BKV) infection, leading to BK viruria and viremia. This single-center study aimed to clarify the association between quantitative measurement of BKV DNA and the progression of BKV infection, and secondly to identify the risk factors associated with the evolution of viruria to viremia.

Methods

We retrospectively analyzed 266 patients who underwent renal transplantation in our center from October 2006 to February 2013. We examined the viral loads of BKV in urine and plasma by quantitative real-time polymerase chain reaction assay after screening all of the recipients by urinary sediment examination. BKVAN was diagnosed by histological examination with immunohistochemistry of the large T antigen in biopsy specimens.

Results

Overall, 22 recipients showed BK viruria alone, whereas 22 progressed to BK viremia, of which 6 patients were diagnosed with BKVAN. Among BKVAN patients, 2 cases progressed to graft loss at 59 months and 31 months after diagnosis, respectively. In BKVAN group, the plasma viral loads were significantly higher than those in viremia without nephropathy (P < .001). Multivariate analysis revealed that the evolution of viruria to viremia was associated with recipient age over 55 years (odds ratio, 32.08; 95% confidence interval, 2.1–489.5) and tacrolimus exposure (odds ratio, 11.98; 95% confidence interval, 1.34–107.04).

Conclusions

The progression from viremia to BKVAN was strongly associated with increasing plasma viral loads for BKV DNA. The cutoff value of 1 × 10⁴ copies/mL for plasma viral loads could differentiate between BKVAN and viremia alone. Further, recipient age over 55 years and tacrolimus exposure were independently associated with the evolution of viruria to viremia.     

Increased CMV disease and “severe” BK viremia with belatacept vs. sirolimus three-drug maintenance immunosuppression

ObjectivesBelatacept may provide benefit in delayed graft function, but its association with infectious complications is understudied. We aim to assess the incidence of CMV and BK viremia in patients treated with sirolimus or belatacept as part of a three-drug immunosuppression regimen after kidney transplantation.Materials and methodsKidney transplant recipients from 01/01/2015 to 10/01/2021 were retrospectively reviewed. Maintenance immunosuppression was either tacrolimus, mycophenolate and sirolimus (B⁰) or tacrolimus, mycophenolate, and belatacept (5.0 mg/kg monthly) (B¹). Primary outcomes of interest were BK and CMV viremia which were followed until the end of the study period. Secondary outcomes included graft function (serum creatinine, eGFR) and acute rejection through 12 months.ResultsBelatacept was initiated in patients with a higher mean kidney donor profile index (B⁰:0.36 vs. B¹:0.44, p = .02) with more delayed graft function (B⁰:6.1% vs. B¹:26.1%, p < .001). Belatacept therapy was associated with more “severe” CMV viremia >25,000 copies/mL (B⁰:1.2% vs. B¹:5.9%, p = .016) and CMV disease (B⁰:0.41% vs. B¹:4.2%, p = .015). However, there was no difference in the overall incidence of CMV viremia >200 IU/mL (B⁰:9.4% vs. B¹:13.5%, p = .28). There was no difference in the incidence of BK viremia >200 IU/mL (B⁰:29.7% vs. B¹:31.1%, p = .78) or BK-associated nephropathy (B⁰:2.4% vs. B¹:1.7%, p = .58), but belatacept was associated with “severe” BK viremia, defined as >10,000 IU/mL (B⁰:13.0% vs. B¹:21.8%, p = .03). The mean serum Cr was significantly higher with belatacept therapy at 1-year follow up (B⁰:1.24 mg/dL vs. B¹:1.43 mg/dL, p = .003). Biopsy-proven acute rejection (B⁰:1.2% vs. B¹:2.6%, p = .35) and graft loss (B⁰:1.2% vs. B¹:0.84%, p = .81) were comparable at 12 months.ConclusionsBelatacept therapy was associated with an increased risk of CMV disease and “severe” CMV and BK viremia. However, this regimen did not increase the overall incidence of infection and facilitated comparable acute rejection and graft loss at 12-month follow up.     

No clinical benefit of rapid versus gradual tapering of immunosuppression to treat sustained BK virus viremia after kidney transplantation: a single‐center experience

Immunosuppressive drug tapering is currently the recommended treatment of BK virus (BKV) viremia after kidney transplantation; however, its exact modalities remain unclear. We retrospectively compared two consecutive strategies in 111 patients with sustained viremia: a gradual monitoring/tapering group (GT, n = 57) before 2012 and a rapid monitoring/tapering group (RT, n = 54) after 2012. At viremia diagnosis, the dose of mycophenolic acid (MPA) and tacrolimus levels (T₀) were similar among patient groups. However, following onset, the dose of MPA at 1 month (P = 0.002) and 3 months (P = 0.005) and Tac T₀ at 1 month (P = 0.030) and 3 months (P = 0.006) were lower in the RT group. This rapid minimization shortened BKV viremia (P < 0.001) and resulted in a better protection of graft function in patients with confirmed BKV‐associated nephropathy (P = 0.033) without impacting 5‐year graft survival. Survival without rejection was similar (P = 0.571), but the RT group had increased the development of de novo donor‐specific antibodies (dnDSAs; P < 0.001). Multivariate Cox analysis identified basiliximab versus Thymoglobulin^® induction [hazard ratio (HR), 3.090; P = 0.001] and the RT strategy (HR, 6.021; P = 0.002) as independently associated with dnDSAs. Compared to a gradual tapering, rapid immunosuppression tapering to treat sustained BKV viremia does not improve medium‐term clinical outcome but increases the risk of developing dnDSAs.     

Effect of Delayed Graft Function on the Outcome and Allograft Survival of Kidney Transplanted Patients from a Deceased Donor

BackgroundIn kidney transplantation (KT), delayed graft function (DGF) is a significant early complication observed in the first week. The study aimed to investigate the impact of DGF on the outcome, allograft, and patient survival after KT with organs from deceased donors.MethodsThis retrospective study was conducted using 304 KT patients who received an organ from deceased donors from 2008 to 2018. The patients were divided into 2 groups, DGF positive (DGF⁺) and DGF negative (DGF^–). The database containing the clinical, laboratory, and immunologic information of donors and recipients was statistically analyzed using the SSPS program.ResultsIn this study, 189 (62.17%) were DGF⁺ and 115 (37.83%) were DGF^–. Until 6 months after KT, the estimate glomerular filtration rate was better in group DGF^–, but it was similar between the groups during 10-year follow-up. Graft losses were higher in DGF⁺ group than in the DGF^– (P = .046). The serum creatinine level was persistently higher in DGF⁺ group until the sixth month (P ≤ .05). Allograft survival rates were better in patients who were DGF^– (P = .033). Those who had DGF for more than 15 days had a worse graft survival (P = .003), but in 10 year follow-up, patient survival rates were similar (P = .705).ConclusionDGF⁺ patients were associated with dialysis time before KT, ischemia time, and the donors’ clinical status, such as age, organ quality, and serum creatinine. All these factors had a great impact on graft survival but not on patient survival.     

Effect of Pre-Transplant Recipient Underweight on the Postoperative Outcome and Graft Survival in Primary Kidney Transplantation

BackgroundThe objective of this study was to evaluate the influence of recipient underweight on the short- and long-term outcomes of patients undergoing primary kidney transplantation (KT).Patients and methodsThree hundred thirty-three patients receiving primary KT in our department between 1993 and 2017 were included in the study. Patients were divided according to their body mass index (BMI) into underweight (BMI <18.5 kg/m²; N = 29) and normal weight (BMI 18.5-24.9 kg/m²; N = 304) groups. Clinicopathological characteristics, postoperative outcomes, and graft and patient survival were analyzed retrospectively.ResultsThe postoperative rate of surgical complications and renal function were comparable between the groups. One year and 3 years after KT, 70% and 92.9%, respectively, of the pre-transplant underweight patients reached a normal BMI (≥18.5 kg/m²). The mean death-censored graft survival was significantly lower in pre-transplant underweight patients than in pre-transplant normal-weight patients (11.5 ± 1.6 years vs 16.3 ± 0.6 years, respectively; P = .045). Especially KT recipients with a moderate or severe pre-transplant underweight (BMI <17 kg/m²; N = 8) showed an increased rate of graft loss (5- and 10-year graft survival: 21.4% each). No statistical difference could be observed between the 2 groups regarding causes of graft loss. In multivariate analysis, recipient underweight (P = .024) remained an independent prognostic factor for graft survival.ConclusionBeing underweight did not affect the early postoperative outcome after primary KT. However, underweight, and especially moderate and severe thinness, is associated with reduced long-term kidney graft survival, and therefore this group of patients should be monitored with special attention.     

Different risk factor profiles distinguish early‐onset from late‐onset BKV‐replication

Two of three reactivations of latent BKV‐infection occur within the first 6 months after renal transplantation. However, a clear differentiation between early‐onset and late‐onset BKV‐replication is lacking. Here, we studied all kidney transplant recipients (KTRs) at our single transplant center between 2004 and 2012. A total of 103 of 862 KTRs were diagnosed with BK viremia (11.9%), among which 24 KTRs (2.8%) showed progression to BKV‐associated nephropathy (BKVN). Sixty‐seven KTRs with early‐onset BKV‐replication (65%) and 36 KTRs with late‐onset BKV‐replication (35%) were identified. A control group of 598 KTRs without BKV‐replication was used for comparison. Lymphocyte‐depleting induction, CMV‐reactivation, and acute rejection increased the risk of early‐onset BKV‐replication (P < 0.05). Presensitized KTRs undergoing renal retransplantation were those at increased risk of late‐onset BKV‐replication (P < 0.05). Among KTRs with BK viremia, higher doses of mycophenolate increased the risk of progression to BKVN (P = 0.004). KTRs with progression to BKVN showed inferior allograft function (P < 0.05). KTRs with late‐onset BK viremia were more likely not to recover to baseline creatinine after BKV‐replication (P = 0.018). Our data suggest different risk factors in the pathogenesis of early‐onset and late‐onset BKV‐reactivation. While a more intensified immunosuppression is associated with early‐onset BKV‐replication, a chronic inflammatory state in presensitized KTRs may contribute to late‐onset BKV‐replication.     

Comparison of Outcomes in Patients Undergoing Renal Transplantation With Impaired vs Normal Left Ventricular Ejection Fraction

BackgroundRenal transplantation improves long-term outcomes in patients with end-stage renal disease (ESRD); however, patients with impaired left ventricular ejection fraction (LVEF) are less likely to be selected for renal transplantation. We sought to evaluate the effect of renal transplantation in this population.MethodsWe retrospectively evaluated 181 patients who underwent renal transplantation between 2011 and 2016. For patients with pretransplant LVEF <50% (cohort 1) and ≥50% (cohort 2), we evaluated the effect of renal transplantation on LVEF, graft failure, and mortality.ResultsCohort 1 comprised 24 patients (mean age, 47 years; pretransplant LVEF 38%). Cohort 2 comprised 157 patients (mean age, 53 years; pretransplant LVEF 64%). Forty-six percent of cohort 1 experienced significant improvement in LVEF posttransplant, with mean LVEF improvement from 38% to 66%. There was no significant association between pretransplant LVEF and graft failure (hazard ratio [HR] = 2.7; 95% confidence interval [CI], 0.6-11.4; P = .1) or mortality (HR = 1.02; 95% CI, 0.3-3.6; P = .9). Coronary artery disease predicted mortality (HR = 3.12; 95% CI, 1.2-8.4; P = .02). Older age trended toward higher mortality (HR = 1.04; 95% CI, 1.0-1.1; P = .05). Younger age predicted graft failure (HR = 0.96; 95% CI, 0.8-0.9; P = .02).ConclusionsIn patients with ESRD undergoing renal transplantation, there was no significant association between pretransplant LVEF and mortality or graft failure, suggesting that patients with ESRD with impaired LVEF can experience positive posttransplant outcomes.