Introduction: Kidney transplantation restores many of the disorders accompanying endstage renal disease (ESRD). However, hypophosphatemia is common complication after renal transplantation. High levels of fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) are two suspected factors determining the hypophosphatemia after kidney transplantation. Objectives: This observational prospective study was carried out to clarify the role of mentioned factors in hypophosphatemia after kidney transplantation. Patients and Methods: Living donor kidney transplant recipients which admitted to the ward of the renal transplantation, enrolled to the study. Parameters of bone and mineral metabolism including FGF23 and intact PTH levels were assessed. Results: High FGF23 level before transplantation was related to lower phosphate levels at 3rd month after transplantation. PTH levels showed no relationship with hypophosphatemia after kidney transplantation. Conclusion: High levels of FGF23 in ESRD patients undergoing kidney transplantation is an important determinant of hypophosphatemia in long-term follow up.

Introduction: The FOXP3 protein is an immune regulatory protein that specifically maintains the function and differentiation of regulatory T cells (Tregs) and prevents autoimmunity. Variations in FOXP3 gene may alter its function and also the immune response. Objectives: The present study was conducted to investigate the association of the FOXP3 gene polymorphisms -3499 A/G and -3279 A/C with renal allograft function and survival in kidney transplant recipients. Patients and Methods: In this cross-sectional study, 150 eligible kidney transplant recipients were evaluated. Kidney function was evaluated at three- and five-year post-transplant using serum creatinine level and glomerular filtration rate as indicators. Genotyping of the study participants was performed using the PCR– restriction fragment length polymorphism method. Results: The frequencies of AA, AG, and GG genotypes of the -3499 A/G polymorphism were 62.42%, 29.53%, and 8.05%, respectively. For the -3279 A/C polymorphism, the frequencies of the AA, AC, and CC genotypes were 21.33%, 32%, and 46.67%, respectively. The mean ± SD of serum creatinine level, three and five years after transplantation were 1.70 ± 1.58 and 1.87 ± 1.94, respectively. Serum creatinine level and kidney function did not show any significant association with these polymorphisms. Conclusion: In the present study, only 10% of participants experienced episodes of severe kidney dysfunction and we did not find any significant association between kidney function and the subjects’ genotypes. Further epidemiologic studies with greater sample sizes may be needed to clarify this association.

Introduction: Kidney transplantation gives us the opportunity to study kidney vascular anatomical variations and their probable effect on allograft survival. Objectives: The aim of this study was to evaluate the renal arteries’ branching patterns of the engrafted kidneys and their impact on transplant outcomes. Patients and Methods: Three hundred patients who received kidney transplantation between 2014 -2017 were included. Peri-hilar and hilar branching patterns of the engrafted kidney were studied by reviewing the archived CT angiographies of donors and then they categorized based on the existing knowledge in this field. Clinical data were also gathered from medical records and recipients’ latest clinical and laboratory evaluations. Results: Based on peri-hilar and their corresponding hilar branching patterns, our morphology findings were classified into 17 groups. From different peri-hilar branching patterns, the fork pattern was more common which is detected in 95% (242) while the ladder pattern was observed in 5% (13) of kidney grafts. In a later branching sub-categorization, among the fork pattern, 65.2% (158) were duplicated and 34.7% (84) had triplicated hilar branching patterns. There was not a statistically significant correlation between each of those patterns and allograft function (P > 0.05). Conclusion: Peri-hilar and hilar branching patterns of the kidney allografts’ renal artery were different, but they follow certain patterns. Although it may not influence the allograft survival, it provides us precise knowledge about renal vasculature patterns and outcome of probable vascular events meanwhile; it could be useful in the field of transplantation.

A plasma protease, ADAMTS13, cleaves the von Willebrand factor (VWF) and its deficiency is associated with the pathogenesis of thrombotic thrombocytopenic purpura (TTP). According to the Human Gene Mutation Database (HGMD), about 150 mutations have been identified in the ADAMTS13 gene. A 23-year-old man, with hematuria and gingival bleeding was admitted to our University Hospital. Four years ago he was diagnosed with a TTP history. During these years, he was under intermittent plasma exchange. A blood sample was taken for genetic study. He effectively responded to one session of fresh frozen plasma replacement and plasma exchange. Genetic study indicated that this case carries two heterozygous mutations in ADAMTS13 gene; a novel splicing variant (c.2610+5G>A) and a nonsense p.Arg910X mutation that previously is reported to relate to TTP. The novel variant predicted to result in an aberrant ADAMTS13 transcript processing.