Comparison of Clinical Outcomes Among Deceased Donor Kidney Transplant Recipients Before and After Utilizing Estimated Posttransplant Survival Score for Kidneys Allocation in Malaysia

Background. The Malaysian Kidney Allocation System implemented in 2020 includes only kidney transplant candidates with estimated posttransplant survival (EPTS) score of ≤20%, in replacement of Malaysian Organs Sharing System, which was based solely on dialysis vintage. We aim to compare the clinical outcomes of deceased-donor kidney transplant recipients (DDKTRs) with EPTS ≤20% to those with EPTS >20%.Methods. All DDKTRs between January 1, 2015, and December 29, 2020, were included and categorized into 2 groups: EPTS ≤20% and EPTS >20%. Cox regression was performed to evaluate the association of EPTS score and patient survival. The rate of postoperative complications, graft failure and patient survival were compared between 2 groups. Data were analyzed with SPSS v26 and R v4.0.4. The study complies with the Helsinki Congress and the Istanbul Declaration.Results. We included 159 DDKTRs, with a median follow-up of 25 months (range, 10-60 months). The mean age of those with EPTS ≤20% was 32.2 ± 3.4 years and those with EPTS >20% was 46.0 ± 6.7 years, and the median EPTS score were 16% (range, 12%-18%) and 38% (range, 27%-56.5%), respectively. EPTS score was associated with patient survival (hazard ratio, 1.031; 95% CI 1.010-1.052; P = .003), and the cutoff points of 30% and above were associated with worse survival. It showed good discrimination (C-index, 0.729; 95% CI 0.579-0.878; P = .003) and the optimal cutoff value was 38% (65.5% sensitivity, 68.8% specificity, 17.8% positive predictive value, and 95.8% negative predictive value). Both groups had similar rate of surgical complications (P = .191), graft failure (P = .503), and patient survival (P = .654), but those with EPTS >20% had higher incidence of urinary tract infection (9.3% vs 27.6%, P = .016).Conclusions. There was no difference in clinical outcomes using an EPTS cutoff point of 20% but worse patient survival if higher cutoff point was used.     

miR-483-5p通过下调CDK15促进肾上腺皮质癌增殖和侵袭

目的探讨miR-483-5p在肾上腺皮质癌中的作用及其可能的作用机制。方法荧光定量PCR法检测miR-483-5p和CDK15在肾上腺皮质癌组织和细胞系中的表达,CCK-8增殖试验测定miR-483-5p对细胞增殖的影响,Transwell法检测ACC细胞侵袭性的变化。荧光素酶试验和挽救实验验证miR-483-5p与CDK15相关的分子机制。结果miR-483-5p在肾上腺皮质癌组织中高表达(2.36±1.02 vs 1.09±0.43),CDK15在肾上腺皮质癌组织中低表达(0.57±0.26 vs 1.06±0.32)。荧光素酶检测证实CDK15是miR-483-5p的直接靶点。过表达miR-483-5p可通过下调CDK15的表达促进ACC细胞的增殖(24 h:0.26±0.03 vs 0.23±0.04,48 h:0.56±0.05 vs 0.41±0.03,72 h:0.73±0.04 vs 0.59±0.03)和侵袭能力(95.78±4.66 vs 23.89±2.52)。结论miR-483-5p可通过下调CDK15的表达促进肾上腺皮质癌的发生发展,其可作为肾上腺皮质癌的潜在生物标志物及治疗肾上腺皮质癌的新的作用靶点。     

Anti-PF4/heparin antibodies are associated with arteriovenous fistula thrombosis in non-diabetic hemodialysis patients

Aim  

Anti-platelet factor 4/heparin complex antibodies (anti-PF4/heparin Ab) have been found to cause heparin-induced thrombocytopenia (HIT), a clinical syndrome thrombocytopenia and thrombosis. There is still controversy as to whether the presence of anti-PF4/heparin antibodies in hemodialysis patients augments clot formation in access fistula thrombosis, peripheral artery disease (PAD), and coronary heart disease (CHD).