Kidney transplantation remains the treatment of choice for end-stage renal failure. When the immune system of the recipient recognizes the transplanted kidney as a foreign object, graft rejection occurs. As part of the host immune defense mechanism, human leukocyte antigen (HLA) is a major challenge for graft rejection in transplantation therapy. The impact of HLA mismatches between the donor and the potential recipient prolongs the time for renal transplantation therapy, tethered to dialysis, latter reduces graft survival, and increases mortality. The formation of pretransplant alloantibodies against HLA class Iand II molecules can be sensitized through exposures to blood transfusions, prior transplants, and pregnancy. These preformed HLA antibodies are associated with rejection in kidney transplantation. On the other hand, the development of de novo antibodies may increase the risk for acute and chronic rejections. Allograft rejection results from a complex interplay involving both the innate and the adaptive immune systems. Thus, further insights into the mechanisms of tissue rejection and the risk of HLA sensitization is crucial in developing new therapies that may blunt the immune system against transplanted organs. Therefore, the purpose of this review is to highlight facts about HLA and its sensitization, various mechanisms of allograft rejection, the current immunosuppressive approaches, and the directions for future therapy

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Kidney Transplantation: The Challenge of Human Leukocyte Antigen and Its Therapeutic Strategies

BACKGROUND Chronic renal insufficiency (CRI) is a global public health problem with a high incidence in the Romanian population. In this study, we aimed to investigate genomic HLA polymorphisms in Romanian patients with CRI waiting for kidney transplantation. To determine the existence of a potential strong link between certain HLA polymorphisms and CRI, we also looked at HLA specificity combinations within the same locus or even different loci, referring to randomly inherited allelic combinations rather than potential haplotypes. METHODS A total of 2199 patients with CRI on the kidney transplantation waiting list were included. A total of 2786 healthy individuals were included as controls. Both patients and controls were assessed for both HLA I and class II genes. HLA genes were typed using the low-resolution method polymerase chain reaction sequence-specific primer. RESULTS Certain class I and class II HLA allele groups, genotypes and haplotypes were significantly more frequent in patients with CRI than in the control individuals (eg B* 40 (p ≤ .001, pc ≤ .001), C* 12 (p ≤ .001, pc ≤ .001), DRB1*14 (p = .0022, pc = .04), C*12,- (p < .001, pc < .001), A*01-C*15 (p = .0003, pc = .03) and A*02-C*12 (p = .0005, pc = .0486)). CONCLUSIONS HLA gene polymorphisms could be clinically relevant CRI-associated genetic profiles in Romanian patients with CRI.

Relevance of HLA gene polymorphisms in Romanian patients with chronic renal insufficiency undergoing renal transplantation.

Multiple works have studied possible associations between human leukocyte antigen (HLA) alleles and end stage renal disease (ESRD) showing, however, contradictory and inconsistent results. Here, we revisit the association between ESRD and HLA antigens, comparing HLA polymorphism (at HLA-A, -B, -C, -DRB1, -DQB1 and DQA1 loci) in ESRD patients (n = 497) and controls (n = 672). Our data identified several HLA alleles that displayed a significant positive or negative association with ESRD. We also determined whether heterozygosity or homozygosity of the ESRD-associated HLA alleles at different loci could modify the prevalence of the disease. Few HLA allele combinations displayed significant associations with ESRD, among which A*3_26 combination showed the highest strength of association (OR = 4.488, P≤ 0.05) with ESRD. Interestingly, the age of ESRD onset was not affected by HLA allele combinations at different loci. We also performed an extensive literature analysis to determine whether the association of HLA to ESRD can be similar across different ethnic groups. Our analysis showed that at least certain HLA alleles, HLA-A*11, HLA-DRB1*11, and HLA-DRB1*4, display a significant association with ESRD in different ethnic groups. The findings of our study will help in determining possible protective or susceptible roles of various HLA alleles in ESRD.

/pdf/revisiting-the-association-between-human-leukocyte-antigen-4tm0wx0txt.pdf

Revisiting the association between human leukocyte antigen and end-stage renal disease.

Multiple works have studied possible associations between human leukocyte antigen (HLA) alleles and end stage renal disease (ESRD). However, there are several contradictions in these previous works and no consistent HLA associations with ESRD itself have been identified. Most of these works have several limitations, for instance, the population size was too small, or only limited HLA loci were studied. The presented work aims to revisit the association between ESRD and HLA antigens while taking in to account the previously overlooked limitations. Here, we compared the HLA polymorphism (at HLA-A, -B, -C, -DRB1, -DQB1 and DQA1 loci) in ESRD patients (n=497) and controls (n=672). Our data identified several HLA alleles that displayed a significant positive or negative association with ESRD. We also determined whether heterozygosity or homozygosity of the ESRD-associated HLA alleles at different loci could modify the prevalence of the disease. Few HLA allele combinations displayed significant associations with ESRD among which HLA-A*3 -HLA-A*26 combination showed the highest strength of association (OR= 4.488, P[≤] 0.05) with ESRD. However, the age of ESRD onset was not affected by HLA allele combinations at different loci. Most of the previous works have studied the association of HLA with ESRD in homogeneous ethnic groups and have interpreted their data accordingly. Here, we also performed an extensive literature analysis to determine whether the association of HLA to ESRD can be similar across different ethnic groups. This analysis showed that at least for certain alleles, the association of HLA to ESRD can be similar in different ethnic groups. For instance, HLA-A*11, HLA-DRB1*11, and HLA-DRB1*4 all showed significant positive associations with ESRD in different ethnic groups. The findings of our study will help in determining possible protective or susceptible roles of various HLA alleles in ESRD.

/pdf/revisiting-the-association-between-human-leukocyte-antigen-kbj1mg8os9.pdf

Revisiting the Association between Human Leukocyte Antigen and End-Stage Renal Disease

Objectives We recently studied the association between various human leukocyte antigen (HLA) alleles and end-stage renal disease (ESRD). According to our analysis, HLA-B*50 and HLA-DQA1*3 alleles were positively associated with ESRD, while B*40, DRB1*12, DRB1*13, and DQA1*6 alleles were negatively associated with ESRD. However, a single case-control study does not have enough statistical power to evaluate the possible impact of genetic polymorphism on any disease. Hence, the main objective of this meta-analysis is to determine the association between these abovementioned HLA alleles and ESRD. Design MEDLINE/PubMed, EMBASE, Web of Science, and Cochrane databases were searched through December 2020 for case-control studies on the associations between HLA polymorphisms and ESRD. Independent reviewers screened the texts of potentially eligible studies and assessed the risk of bias. The meta-analysis was conducted based on the checklists and guidelines based on PRISMA. Results We identified 26 case-control studies comprising 1,312 ESRD and 3,842 healthy subjects. A non-significant positive association was observed between HLA-B*50 (OR = 1.02, 95% CI [0.90, 1.24]), HLA-B*40 (OR = 1.75, 95% CI [0.98, 3.2]), HLA-DQA1*3, (OR = 1.17, 95% CI [0.74, 1.84]), DRB1*12 (OR = 1.05, 95% CI [0.94, 1.18]) alleles and ESRD. In addition, a non-significant negative association was observed between HLA-DRB1*13 (OR = 0.90, CI [0.81, 1.01]), HLA-DQB1*6 (OR = 0.79, 95% CI [0.58, 1.07]) alleles and ESRD. Conclusions Our meta-analysis indicates no significant association between HLA-B*50, HLA-DQA1*3, B*40, DRB1*12, DRB1*13, and DQA1*6 alleles and ESRD. Further studies with larger sample sizes and adjustments for confounders are required to confirm these conclusions.

Association between human leukocyte antigen (HLA) and end-stage renal disease (ESRD): a meta-analysis

Introduction The prevalence of chronic kidney failure is significantly increasing in Vietnam, causing a burden for health care. This study assessed the relationship of HLA-A, -B, and –DRB1 alleles with end-stage renal disease (ESRD). Method A retrospective, cross-sectional study and a comparative study using secondary data analysis were conducted on 196 ESRD patients and 187 controls from 2009 to 2017. The patient and donor profiles were collected from medical records, including age, sex, etiology of renal failure, and HLA phenotypes. HLA-A*, -B*, and -DRB1* typing were done by polymerase chain reaction-sequence specific primers. Result The most frequent HLA alleles in Vietnamese patients with ESRD were HLA-A*02, -A*11, -B*15, -B*46, -DRB1*04, -DRB1*09, and -DRB1*12. The haplotypes HLA-A*0233 (odds ratio [OR] = 0.40, 95% CI: 0.15–0.98) had a negative association for ESRD. The haplotypes HLA-B*1515 (OR = 4.14, 95% CI: 1.52–11.26) and HLA-DRB1*1212 (OR = 2.01, 95% CI: 1.06–3.81) had a positive association for ESRD. The haplotypes HLA-B*1515 (OR = 4.69, 95% CI: 1.69–13.03) and -DRB1*1212 (OR = 2.15, 95% CI: 1.10–4.21) had a positive association for ESRD related to glomerulonephritis. The HLA-B*1557 (OR = 17.34, 95% CI: 2.70–11.49) had a positive association for ESRD related to hypertension. Conclusion The haplotypes of HLA class I and II had significant relationships with ESRD. The results of our study should be confirmed in further investigations.

Association of Human Leukocyte Antigen Haplotypes With End-Stage Renal Disease in Vietnamese Patients Prior to First Transplantation.

Objective: To determine the incidence of urinary tract infections in kidney transplant patients in our hospital, to identify the microbial pathogens, risk factors for urinary tract infection. Subject and method: Primary kidney transplant patients at 108 Military Central Hospital with full follow-up records in the first year were included in the study. Age, sex, cause of kidney failure, pre-transplantation treatment measures, post-transplantation immunosuppressive regimen were collected. Patient was followed and midstream urine was cultured monthly. Result: There were 94 kidney transplant patients included in our study. Seventy patients (74.5%) were male and 24 (25.5%) were female. One hundred and two episodes of urinary tract infections in 37 patients (39.4%) were reported. Sex (female) (p=0.003; 95% CI: 1.716-14.021), urologic complications (p=0.006, 95% CI: 0.001-0.320) were found as risk factors for UTI in the first year of transplantation. Escherichia coli and Klebsiella pneumoniae were the most frequently isolated pathogens. UTI had no negative impact on short-term graft survival. Conclusion: The results of our study showed a high incidence of UTI in kidney transplant recipients. Infection control methods should be used regularly during post-transplant therapy.

Incidence and risk factors for urinary tract infection in the first year after kidney transplantation at 108 Military Central Hospital, Vietnam

Background: Polyomavirus BK and JC are the most common viral infection after renal transplantation. The current evidence shows that both virus infection has a greater risk on kidney graft function, leading the management of viral infection is becoming a major challenge. Methods: We included 89 patients including 70 males and 19 females (follow up of 104 patients, mean follow-up 16.66 months) who were transplanted at 108 Military Central Hospital between December 2016 and December 2021. BK and JC polyomavirus screening was performed every 3 months within the first year after kidney transplantation, and every 6 months after year-1, or when any clinical infection symptoms were recognised by the physician. Multivariable Cox-regression analysis was performed to evaluate risk factors for the onset of BK, JC infection. Results: 317 episodes of BK and JC infections were detected in 71 patients (52.8%) included Polyomavirus BK (26.0%), JC (21.8%), and BK and JC co-infection (5,0%). The mean time until onset of BK (15.39±20.06 months) was significantly earlier than JC (21.74±19.75 months), p<0.01. Risk factors for BK infection were hypertention (p<0.05, HR 1.79), and eGFR (p<0.05, HR 1.02). For sole JC infection, Systolic blood pressure (p<0.01, HR 1.06), Mycophenolate mofetil dose (p<0.001, HR 1.003). For the occurrence of co-infection, BMI (p<0.01, HR 1.25) and HDL-C (p<0.05, HR 1.25) were revealed as the most relevant factors. Male (p<0.05, HR 0.07) and eGFR (p<0.01, HR 0.94) were identified to reduce the risk of co-infection. Conclusion: Our results showed hypertension and eGFR were independent risk factors for BK infection, while high Systolic blood pressure and high dose of mycophenolate mofetil for JC infection. BK and JC co-infection was associated with gender, BMI, HDL-C and eGFR. The result provided initial evidence for appropriate control and the prevention of Polyomavirus infection. 

P8.115: Polyomavirus Infection in the Urine for Follow-up of Renal Transplant Patient: A Single Center Study

P8.147: Predictors of Metabolic Syndrome Following One-Year Post Kidney Transplantation Among Vietnamese Patients

Background The interaction of viral infection may be associated with increased morbidity after renal transplantation. This study aimed to identify the incidence and risk factors of viruria infections in renal transplant recipients. Material/Methods In this longitudinal study, 502 episodes recorded in 81 kidney transplant patients from 1/2019 to 12/2021 in a hospital in Vietnam were included. BK, JC polyomaviruses, CMV, EBV, and HSV were detected. Multivariable Cox regression analysis was performed to evaluate risk factors for the viruria infection. Results Fifty-six patients (69.1%) had viruria co-infection. The incidence of JC, CMV, and BK infection was the most common viruria, with 67.9%, 61.7%, and 56.8%, respectively. Cox regression revealed that the risk factors for JC were single infection, dose of MMF (HR 1.002), corticoid (HR 1.02), hypertension (HR 1.65), and hematuria (HR 2.03); risk factors for CMV infection were male sex (HR 1.92) and eGFR (HR 0.98); risk factors for BK single infection were hypertension (HR 1.67), proteinuria (HR 3.80), higher tacrolimus trough level (HR 1.17), and dose of MMF (HR 1.002). Hypertension (HR 1.68), fasting plasma glucose (HR 1.13), proteinuria (HR 6.01), tacrolimus trough level (HR 1.12), and dose of MMF (HR 1.004) were independent risk factors for the viruria co-infection. Conclusions Kidney function was associated with the incidence of viruria. Higher tacrolimus trough level and dose of MMF were associated with higher risk of BK, JC, and co-infection.

Risk Factors for Polyomavirus, Cytomegalovirus, and Viruria Co-Infection for Follow-Up of Renal Transplant Patients

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