Background: Opportunistic infections remain a significant cause of morbidity and mortality after kidney transplantation. This retrospective cohort study aimed to assess the incidence and predictors of post-transplant DNA virus infections (CMV, EBV, BKV and JCV infections) in kidney transplant recipients (KTR) at a single tertiary centre and evaluate their impact on graft outcomes. Methods: KTR transplanted between 2000 and 2021 were evaluated. Multivariate logistic regression analysis and Cox proportional hazard analyses were used to identify factors associated with DNA virus infections and their impact on allograft outcomes respectively. A sub-analysis of individual viral infections was also conducted to describe the pattern, timing, interventions, and outcomes of individual infections. Results: Data from 962 recipients were evaluated (Mean age 47.3 ± 15 years, 62% male, 81% white). 30% of recipients (288/962) had infection(s) by one or more of the DNA viruses. Individually, CMV, EBV, BKV and JCV viruses were diagnosed in 13.8%. 11.3%, 8.9% and 4.4% of recipients respectively. Factors associated with increased risk of post-transplant DNA virus infection included recipient female gender, higher number of HLA mismatch, lower baseline estimated glomerular filtration rate (eGFR), CMV seropositive donor, maintenance with cyclosporin (rather than tacrolimus) and higher number of maintenance immunosuppressive medications. The slope of eGFR decline was steeper in recipients with a history of DNA virus infection irrespective of the virus type. Further, GFR declined faster with an increasing number of different viral infections. Death-censored graft loss adjusted for age, gender, total HLA mismatch, baseline eGFR and acute rejection was significantly higher in recipients with a history of DNA virus infection than those without infection (adjusted hazard ratio (aHR, 1.74, 95% CI, 1.08–2.80)). In contrast, dialysis-free survival did not differ between the two groups of recipients (aHR, 1.13, 95% CI, 0.88–1.47). Conclusion: Post-transplant DNA viral infection is associated with a higher risk of allograft loss. Careful management of immunosuppression and close surveillance of at-risk recipients may improve graft outcomes.
Background and Aims Internal jugular vein tunneled catheters are important vascular access for haemodialysis (HD). In our practice, Left-sided internal jugular (LIJ) catheter insertion is performed in radiology under direct X-ray screening. Most right-side internal jugular (RIJ) catheters are inserted under ultrasound guidance in dedicated renal procedure rooms. Vascular access can become challenging with the potential for venous stenosis and thrombosis with catheter use. The aims of this study are to evaluate our practices and outcomes of non-radiologically inserted RIJ tunneled HD catheters and to investigate the predictors of procedure failure. Method 200 successive RIJ tunnel HD catheters inserted from June 2016 under ultrasound guidance at our centre were included in this analysis. Data including demographics, co-morbidities, first or higher order insertion, outcome (success or failed attempt), and immediate complications were collated from electronic patient records. Binary logistic regression analysis was conducted to investigate the predictor for failure in catheter insertion. Results Of the 200 patients, 152 (76%) were first-time insertions and 48 (24%) were second or higher-order insertions. The median age of our cohort was 58 years, with a predominance of males (68%) and white ethnicity (82%). 36.5% were diabetic, with 37.5% having a history of cardiovascular disease. Nearly 30% of patients were on an antiplatelet agent, and 8% were on anticoagulants, which were appropriately managed before line insertion. Pre-operative median haemoglobin was 93 g/dl, with clotting screen and platelet counts in the target range. There was a statistically significant difference in the success of insertion, depending on the insertion being first or subsequent (96.1% vs 81.2%; p = 0.001). The reason for failure in insertion included on-table observation of a small calibre vein on ultrasound or failure to thread wire/dilator due to possible stenosis or thromboses. All line rewire (12/48) procedures were performed successfully. Immediate complication (<1 week) was recorded in 9% of patients, predominantly tunnel bleeding (n = 7) and malposition (deep or high; n = 7) (Table 1). Second or higher-order RIJ catheter insertion showed a higher risk for failure in a multivariable binary logistic regression analysis. (OR: 6.4; CI: 2.1-20.5; P = 0.002) (Figure 1). Of the higher-order insertions, the longer duration between the first and subsequent catheters showed a higher risk for failure (OR:1.19; CI-1.04-1.4; p = 0.010). Conclusion Second or higher-order catheter insertions with a longer duration between the first and the subsequent insertion carry a significant risk of failure due to vein stenosis and thrombosis. Therefore, a careful case-to-case triaging of patients based on previous access history is warranted before listing patients for routine ultrasound-guided insertion.
Calcific uraemic arteriolopathy (CUA), also known as calciphylaxis, is a rare and often fatal condition, frequently diagnosed in end-stage renal disease (ESRD) patients. Although exact pathogenesis remains unclear, iron supplementation is suggested as a potential risk factor. Iron and erythropoietin are the main stay of treatment for anaemia in ESRD patients. Few observational studies support the role of iron in the pathogenesis of calciphylaxis although data from the pivotal trial was not strongly supportive of this argument, i.e., no difference in incidence of calciphylaxis between the low-dose and high-dose iron treatment arms. Elevated levels of vascular cell adhesion molecules in association with iron excess were postulated to the pathogenesis of CUA by causing inflammation and calcification within the microvasculature. In-addition, oxidative stress generated because of iron deposition in cases of systemic inflammation, such as those seen in ESRD, may play a role in vascular calcification. Despite these arguments, a direct correlation between cumulative iron exposure with CUA incidence is not clearly demonstrated in the literature. Consequently, we do not have evidence to recommend iron reduction or cessation in ESRD patients that develop CUA.
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