The incidence of ACUTE REJECTION of the kidney allograft in the world has been around 15% during the period between 2001 and 2003. It is clinically defined as an elevation in the level of serum creatinine by more than 0.3 mg/dL and is diagnosed by kidney biopsy. On pathologic examination, the interstitium of the allograft is diffusely edematous and infiltrated by CD4 and CD8 lymphocytes. Tubulitis occurs when the lymphocytes and monocytes extend into the walls and lumina of the tubules. Presence of leukocytes determines infection or antibody-mediated REJECTION. Typically C4d staining is negative. Other causes of ACUTE allograft dysfunction included prerenal factors, interstitial nephritis, infection, ACUTE tubular necrosis, toxicity by drugs, and obstruction in the urinary tract.The primary diagnostic assessments include history, especially adherence to immunosuppressive therapy, physical examination, blood and urine laboratory tests, measurement of the serum levels of the drugs, and ultrasonography. Diagnosis of ACUTE cellular REJECTION depends on biopsy, CD20 staining for refractory cases, negative C4d staining, presence of markers of activating lymphocyte, and proteomic study. Treatment of ACUTE cellular REJECTION in kidney transplant recipients include pulse steroid for the first REJECTION episode. It can be repeated for recurrent or resistant REJECTION. Thymoglobulin and OKT3 are used as the second line of treatment if graft function is deteriorating. Changing the protocol from cyclosporine to tacrolimus or adding mycophenolate mofetil or sirolimus might be effective. Prognosis depends on number of REJECTION episodes, the use of potent drugs, time of REJECTION from transplantation, and response to treatment.

Background: ACUTE cellular REJECTION (ACR) has a reversible effect on graft and its survival.Objective: To evaluate the relation between ACR and clinical factors in recipients of liver transplant allografts.Methods: 47 consecutive liver recipients were retrospectively studied. Their data were extracted from records and analyzed.Results: 38 (81%) of the 47 recipients experienced ACR during a 24-month follow-up. The rate of REJECTION was associated with none of the studied factors—recipient’s blood group, sex, age, familial history of disease, drugs and blood products received, type of donor, and Child score and class.Conclusion: During a limited follow-up period, we did not find any association between ACR and suspected risk factors.

Background: Monitoring of chemokines, CXCL9 and CXCL10, in serum may present a non-invasive detection method for REJECTION. Objective: To investigate the relationship between urinary levels of CXCL9 and CXCL10 and graft function following renal transplantation. Methods: 75 living-related donor renal transplant recipients were studied. Urinary levels of chemokines were collected pre-operatively, on post-operative 1st day, 7th day, 1st month, 3rd month, and at the time of REJECTION. Chemokines levels were assayed using and enzyme-linked immunosorbent assay. Results: Clinical variables were monitored. 10 (15%) patients had biopsy-proven REJECTION during the follow-up period. The urinary CXCL9 level in those with REJECTION was significantly higher than that in those with non-REJECTION group at the 1st day (p<0. 001), 7th day (p<0. 001), and at the time of REJECTION (p=0. 002). The urinary CXCL10 level was also significantly higher in those with REJECTION compared with non-REJECTION group at 1st day (p<0. 001), 7th day (p<0. 001), and at the time of REJECTION (p=0. 001). Serum creatinine level was strongly correlated with the urinary CXCL9 and CXCL10 levels at the time of REJECTION (r=0. 615, p=0. 002; and r=0. 519, p=0. 022, respectively). Among those with T cell-mediated REJECTIONs the mean urinary CXCL10 level increased to as high as 258. 12 ng/mL. Conclusion: Urinary CXCL9 and CXCL10 levels might have a predictive value for T cell-mediated REJECTION in early post-transplantation period. Measurement of urinary CXCL9 and CXCL10 levels could provide an additional tool for the diagnosis of REJECTION.

Background: ACUTE REJECTION is the main problem in liver transplantation that occurs in the first days or months of transplantation. It includes histological and cellular REJECTION. ACUTE histological REJECTION is confirmed by biopsy. Glutathione S-transferase family is the most important genes in phase II detoxification working in xenobiotic and drug metabolism. GSTO2 is one of the members of this family. GSTO2 (N142D) polymorphism may influence metabolism of immunosuppressive drugs.Objective: To determine if GSTO2 polymorphism has association with ACUTE liver REJECTION.Methods: The present study included 120 patients with histological-proven ACUTE liver REJECTION and 182 patients without ACUTE REJECTION. Both groups were matched for sex and age. To determine variants of GSTO2, we used polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).Results: There was a significant association between the GSTO2 genotype and ACUTE liver REJECTION (NN: OR: 3.642, 95% CI: 1.179–5.444) and (ND: OR: 2.533, 95% CI: 1.672–8.149) compared to those with DD geneotype.Conclusion: Recipients with either NN or ND genotype for GSTO2 are more likely to develop ACUTE liver REJECTION compared to those with DD genotype.

Implication for health policy/practice/research/medical education: ACUTE antibody-mediated endothelial damage and subsequent disseminated intravascular coagulation and thrombotic microangiopathy are life-threatening conditions that can affect not only graft but also the patient’s survival significantly. Please cite this paper as: Jahangiri D, Ardalan M, Mubarak M, Alimohammadi S, Jahantigh HR, Saeifar S. ACUTE antibody-mediated REJECTION of kidney allograft,mind the fibrin thrombi. J Renal Inj Prev. 2023,12(2): e32094. doi: 10. 34172/jrip. 2022. 32094.

Introduction. CD86 is a costimulatory molecule that participates in the regulation of T-cell lymphocytes activation. Thus, we examined a genetic marker on theCD86 gene in kidney transplant outcome.Materials and Methods. In our retrospective study, 168 kidney allograft recipients were genotyped by direct sequencing. Patients were classified into 2 groups of 29 human leukocyte antigen (HLA)-identical haplotype allograft recipients and 139 recipients showing one or more mismatches in the HLA haplotype. Forty-five patients (26.8%) developed at least 1 ACUTE REJECTION (AR) episode, 7 in the first and 38 in the second group.Results. ACUTE REJECTION was associated with the presence anti-HLA antibodies before transplantation (P=.03). The AA genotype and A allele at position+1057 in theCD86 gene were more frequent in patients without AR (9.75% and 28.5%, respectively) compared with those showing an AR (2.22% and 23.3%, respectively). This difference was statistically significant in the anti-HLA-positive recipients, as AA frequency was 31.3% in non-AR patients and zero in AR ones (P=.04) and A allele frequency was 46.9% and 20.8%, respectively (P=.04). Patients bearing AA genotype reached a higher graft survival time (9.84 years) than those carrying GA (8.21 years, P=.32) or GG (7.61 years, P=.72) genotypes.Conclusion. These results suggest that AA genotype and A allele ofCD86+1057G>A polymorphism may confer a protection against ACUTE kidney allograft REJECTION in Tunisian patients.