US measurements of AVF at 2-4 months in patients undergoing hemodialysis are highly predictive of fistula maturation and adequacy for dialysis.

Routine preoperative vascular mapping results in a marked increase in placement of AV fistulas, as well as an improvement in the adequacy of forearm fistulas for dialysis. This approach resulted in a substantial increase in the proportion of patients dialyzing with a fistula in our patient population. Fistulas have a higher primary failure rate than grafts, but have a lower subsequent failure rate and require fewer procedures to maintain their long-term patency.

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Preoperative US mapping before hemodialysis access placement can result in a change in surgical management, with an increased number of AVFs placed and an improved likelihood of selecting the most functional vessels preoperatively. Further study is needed to determine longer term outcomes.

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Background Arteriovenous fistulas (AVF) for hemodialysis frequently fail to mature due to inadequate dilation or early stenosis. The pathogenesis of AVF non-maturation may be related to preexisting vascular pathology: medial fibrosis or micro-calcification may limit arterial dilation, and intimal hyperplasia may cause stenosis. Study design Observational study. Setting & Participants Chronic kidney disease patients (N=50) undergoing arteriovenous fistula (AVF) placement. Predictors Medial fibrosis, microcalcification, and intimal hyperplasia in arteries and veins obtained during AVF creation. Outcome and Measurements AVF non-maturation. Results AVF non-maturation occurred in 38% of patients despite attempted salvage procedures. Preoperative arterial diameter was associated with upper arm AVF maturation (p=0.007). Medial fibrosis was similar in patients with non-maturing and mature AVFs (60±14 vs 66±13%, p=0.2). AVF non-maturation was not associated with patient age or diabetes, even though both variables were significantly associated with severe medial fibrosis. Conversely, AVF non-maturation was higher in females than males, despite similar medial fibrosis in both sexes. Arterial micro-calcification (assessed semi-quantitatively) tended to be associated with AVF non-maturation (1.3±0.8 vs 0.9±0.8, p=0.08). None of the arteries or veins obtained at AVF creation had intimal hyperplasia. However, repeat venous samples obtained in 6 patients during surgical revision of an immature AVF exhibited venous neointimal hyperplasia. Limitations Single center study. Conclusion Medial fibrosis and micro-calcification are frequent in the arteries used to create AVFs, but do not explain AVF non-maturation. Unlike previous studies, intimal hyperplasia was not present at baseline, but developed de novo in non-maturing AVFs.

There is limited data pertaining to the risk of EndESRD rates for LKDs overall and for Black, White, male and female donors compared favorably to the ESRD incidence in the general population. The LKD ESRD rate was nearly five times higher for Blacks than for Whites and two times higher for males than females. However, these ethnic and gender-related differences were similar to those previously reported for ESRD in the general population. Our findings do not show an increase in the risk of ESRD for LKDs and support the current practice of living kidney donation. Further research is needed to determine if improved donor screening or follow-up will reduce the risk of postdonation ESRD.

Although ϳ1 million islets exist in the adult human pancreas, current pancreas preservation and islet isolation techniques recover <50%. Presently, cadaveric donors remain the sole source of pancreatic tissue for transplantation. Brain death is characterized by activation of proinflammatory cytokines and organ injury during preservation and reperfusion. In this study, we assessed the effects of brain death on islet isolation yields and functionality. Brain death was induced in male 250-to 350-g Lewis rats by inflation of a Fogarty catheter placed intracranially. The rats were mechanically ventilated for 2, 4, and 6 h before removal of the pancreas (n ‫؍‬ 6). In controls, the catheter was not inflated (n ‫؍‬ 6). Shortly after brain death induction, a significant increase in serum tumor necrosis factor-␣ (TNF-␣), interleukin (IL)-1␤, and IL-6 was demonstrated in a time-dependent manner. Upregulation of TNF-␣, IL-1␤, and IL-6 mRNA was noted in the pancreas. Brain death donors presented lower insulin release after glucose stimulation assessed by in situ perfusion of the pancreas. Islet recovery was reduced in brain death donors compared with controls (at 6 h 602.3 ؎ 233.4 vs. 1,792.5 ؎ 325.4 islet equivalents, respectively; P < 0.05). Islet viability assessed in dissociated islet cells and in intact cultured islets was reduced in islets recovered from brain death donors, an effect associated with higher nuclear activities of NF-B p50, c-Jun, and ATF-2. Islet functionality evaluated in vitro by static incubation and in vivo after intraportal transplantation in syngeneic streptozotocin-induced diabetic rats was significantly reduced in preparations obtained from brain death donors. In conclusion, brain death significantly reduced islet yields and functionality. These observations may lead to strategies to reduce the effects of brain death on pancreatic islets and improve the results in clinical transplantation.