Relationships between study habits, burnout, and general surgery resident performance on the American Board of Surgery In-Training Examination.

BACKGROUND: The American Board of Surgery In-Training Examination (ABSITE) is used by programs to evaluate the knowledge and readiness of trainees to sit for the general surgery qualifying examination. It is often used as a tool for resident promotion and may be used by fellowship programs to evaluate candidates. Burnout has been associated with job performance and satisfaction; however, its presence and effects on surgical trainees' performance are not well studied. We sought to understand factors including burnout and study habits that may contribute to performance on the ABSITE examination. METHODS: Anonymous electronic surveys were distributed to all residents at 10 surgical residency programs (n = 326). Questions included demographics as well as study habits, career interests, residency characteristics, and burnout scores using the Oldenburg Burnout Inventory, which assesses burnout because of both exhaustion and disengagement. These surveys were then linked to the individual's 2016 ABSITE and United States Medical Licensing Examination (USMLE) step 1 and 2 scores provided by the programs to determine factors associated with successful ABSITE performance. RESULTS: In total, 48% (n = 157) of the residents completed the survey. Of those completing the survey, 48 (31%) scored in the highest ABSITE quartile (≥75th percentile) and 109 (69%) scored less than the 75th percentile. In univariate analyses, those in the highest ABSITE quartile had significantly higher USMLE step 1 and step 2 scores (P < 0.001), significantly lower burnout scores (disengagement, P < 0.01; exhaustion, P < 0.04), and held opinions that the ABSITE was important for improving their surgical knowledge (P < 0.01). They also read more frequently to prepare for the ABSITE (P < 0.001), had more disciplined study habits (P < 0.001), were more likely to study at the hospital or other public settings (e.g., library, coffee shop compared with at home; P < 0.04), and used active rather than passive study strategies (P < 0.04). Gender, marital status, having children, and debt burden had no correlation with examination success. Backward stepwise multiple regression analysis identified the following independent predictors of ABSITE scores: study location (P < 0.0001), frequency of reading (P = 0.0001), Oldenburg Burnout Inventory exhaustion (P = 0.02), and USMLE step 1 and 2 scores (P = 0.007 and 0.0001, respectively). CONCLUSIONS: Residents who perform higher on the ABSITE have a regular study schedule throughout the year, report less burnout because of exhaustion, study away from home, and have shown success in prior standardized tests. Further study is needed to determine the effects of burnout on clinical duties, career advancement, and satisfaction.

Chromosome substitution modulates resistance to ischemia reperfusion injury in Brown Norway rats.

Brown Norway rats (BN, BN/NHsdMcwi) are profoundly resistant to developing acute kidney injury (AKI) following ischemia reperfusion. To help define the genetic basis for this resistance, we used consomic rats, in which individual chromosomes from BN rats were placed into the genetic background of Dahl SS rats (SS, SS/JrHsdMcwi) to determine which chromosomes contain alleles contributing to protection from AKI. The parental strains had dramatically different sensitivity to ischemia reperfusion with plasma creatinine levels following 45 min of ischemia and 24 h reperfusion of 4.1 and 1.3 mg/dl in SS and BN, respectively. No consomic strain showed protection similar to the parental BN strain. Nine consomic strains (SS-7(BN), SS-X(BN), SS-8(BN), SS-4(BN), SS-15(BN), SS-3(BN), SS-10(BN), SS-6(BN), and SS-5(BN)) showed partial protection (plasma creatinine about 2.5-3.0 mg/dl), suggesting that multiple alleles contribute to the severity of AKI. In silico analysis was performed using disease ontology database terms and renal function quantitative trait loci from the Rat Genome Database on the BN chromosomes giving partial protection from AKI. This tactic identified at least 36 candidate genes, with several previously linked to the pathophysiology of AKI. Thus, natural variants of these alleles or yet-to-be identified alleles on these chromosomes provide protection against AKI. These alleles may be potential modulators of AKI in susceptible patient populations.

Protective effect of Lifor solution in experimental renal ischemia-reperfusion injury.

BACKGROUND: Improved kidney preservation methods are needed to reduce ischemia-reperfusion (IR) injury in kidney allografts. Lifor is an artificial preservation solution comprised of nutrients, growth factors, and a non-protein oxygen and nutrient carrier. The current study compared the effectiveness of Lifor to University of Wisconsin solution (UW) in protecting rat kidneys from warm IR and cold storage injury. MATERIALS AND METHODS: In a warm IR model, rat kidneys were perfused in situ with either saline, UW, or Lifor for 45 min. Renal function and histology were assessed 24 h later. In a cold IR model, kidney slices were cold-stored in saline, UW, or Lifor at 4°C. Kidney injury was assessed by the release of lactate dehydrogenase (LDH) and immunoblot analysis for cleaved caspase-3. RESULTS: Lifor perfusion significantly mitigated renal dysfunction and tubular injury at 24 h compared with saline or UW. Lifor and UW prevented LDH release in hypoxic kidney slices in vitro, however activation of caspase-3 following hypoxia-reoxygenation was attenuated only with Lifor. Cold storage with Lifor or UW significantly decreased LDH release from kidney slices or normal rat kidney cells in comparison to storage in saline or culture media. After 24 h of cold storage there was a significant decrease in cleaved caspase-3 in Lifor stored slices compared that seen following cold storage in saline or UW solution. CONCLUSIONS: Lifor solution mitigates both warm and cold renal IR and appears to provide greater protection from apoptosis compared with UW solution.

Burnout and its relationship with perceived stress, self-efficacy, depression, social support, and programmatic factors in general surgery residents.

BACKGROUND: Burnout affects surgical residents' well-being. OBJECTIVE: We sought to identify factors associated with burnout among surgery residents. METHODS: An electronic/anonymous survey was sent to surgical residents at 18 programs, consisting of demographic/programmatic questions and validated scales for burnout, depression, perceived stress, self-efficacy, and social support. Residents were grouped into quartiles based off burnout, and predictors were assessed using univariate and multivariate analyses. RESULTS: 42% of residents surveyed completed it. Burnout was associated with depression, higher perceived stress/debt, fewer weekends off, less programmatic social events, and residents were less likely to reconsider surgery if given the chance. Low burnout was associated with lower depression/stress, higher social support/self-efficacy, more weekends off per month, program mentorship, lower debt, and residents being more likely to choose surgery again if given the chance. On multivariate analysis, higher depression/perceived stress were associated with burnout, and lower burnout scores were associated with lower stress/higher self-efficacy. CONCLUSIONS: Burnout in surgery residents is associated with higher levels of depression and perceived stress. The addition of programmatic social events, limiting weekend work, and formal mentoring programs may decrease burnout.

Protective effect of 20-HETE analogues in experimental renal ischemia reperfusion injury.

While it is known that the arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to ischemic injury in the heart and brain, its role in kidney injury is unclear. Here we determined the effects on ischemia-reperfusion injury of the 20-HETE analogues, 20-hydroxyeicosa-5(Z), 14(Z)-dienoic acid (5,14-20-HEDE), and N-[20-hydroxyeicosa-5(Z),14(Z)-dienoyl]glycine (5,14-20-HEDGE), and of the inhibitor of 20-HETE synthesis N-hydroxy-N-(4-butyl-2 methylphenyl) formamidine (HET0016). Using Sprague-Dawley rats we found that while treatment with the inhibitor exacerbated renal injury, infusion of both 5,14-20-HEDE and 5,14-20-HEDGE significantly attenuated injury when compared to vehicle or inhibitor-treated rats. Medullary blood flow, measured by laser-Doppler flowmetry, decreased to half of the baseline one hour after reperfusion in the control rats, but 5,14-20-HEDGE completely prevented this. Treatment of control animals with 5,14-20-HEDGE increased urine output and sodium excretion without altering their mean arterial pressure or glomerular filtration rate. Our results suggest that 20-HETE analogues protect the kidney from ischemia-reperfusion injury by inhibiting renal tubular sodium transport and preventing the post-ischemic fall in medullary blood flow. Analogues of 20-HETE may be useful in the treatment of acute ischemic kidney injury.

Oxidant-mediated apoptosis in proximal tubular epithelial cells following ATP depletion and recovery.

Oxidant-mediated apoptosis has been implicated in renal injury due to ischemia reperfusion (IR); however, the apoptotic signaling pathways following IR have been incompletely defined. The purpose of this study was to examine the role of oxidants on cell death in a model of in vitro simulated IR injury in renal proximal tubular epithelial cells by analyzing the effects of a cell-permeable superoxide dismutase mimetic, manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride (MnTmPyP). Renal proximal tubular epithelial cells were ATP depleted for 2, 4, or 6 h, followed by 2 h of recovery. We found that MnTmPyP was effective in attenuating cytotoxicity (P<0.001) and decreasing steady-state oxidant levels (P<0.001) and apoptotic cell death (P<0.001) following ATP depletion-recovery. MnTmPyP treatment prevented the early cytosolic release of cytochrome c and increased Bcl-2 protein levels following short durations of ATP depletion-recovery. After longer periods of ATP depletion-recovery, we observed a significant increase in TNF-alpha protein levels (P<0.001) and caspase-8 activation (P<0.001), both of which were decreased (P<0.001) by treatment with MnTmPyP. Our results suggest that oxidant mediated apoptosis via the mitochondrial pathway during the early phase of ATP depletion and by activation of the receptor-mediated apoptotic pathway following longer durations of injury.

Gamified Twitter Microblogging to Support Resident Preparation for the American Board of Surgery In-Service Training Examination.

OBJECTIVE: We sought to determine if a daily gamified microblogging project improves American Board of Surgery In-Service Training Examination (ABSITE) scores for participants. DESIGN: In July 2016, we instituted a gamified microblogging project using Twitter as the platform and modified questions from one of several available question banks. A question of the day was posted at 7-o׳clock each morning, Monday through Friday. Respondents were awarded points for speed, accuracy, and contribution to discussion topics. The moderator challenged respondents by asking additional questions and prompted them to find evidence for their claims to fuel further discussion. Since 4 months into the microblogging program, a survey was administered to all residents. Responses were collected and analyzed. After 6 months of tweeting, residents took the ABSITE examination. We compared participating residents׳ ABSITE percentile rank to those of their nonparticipating peers. We also compared residents׳ percentile rank from 2016 to those in 2017 after their participation in the microblogging project. SETTING: The University of Connecticut general surgery residency is an integrated program that is decentralized across 5 hospitals in the central Connecticut region, including Saint Francis Hospital and Medical Center, located in Hartford. PARTICIPANTS: We advertised our account to the University of Connecticut general surgery residents. Out of 45 residents, 11 participated in Twitter microblogging (24.4%) and 17 responded to the questionnaire (37.8%). RESULTS: In all, 100% of the residents who were participating in Twitter reported that daily microblogging prompted them to engage in academic reading. Twitter participants significantly increased their ABSITE percentile rank from 2016 to 2017 by an average of 13.7% (±14.1%) while nonparticipants on average decreased their ABSITE percentile rank by 10.0% (±16.6) (p = 0.003). CONCLUSIONS: Microblogging via Twitter with gamification is a feasible strategy to facilitate improving performance on the ABSITE, especially in a geographically distributed residency.

IL-1 regulates in vivo C-X-C chemokine induction and neutrophil sequestration following endotoxemia.

The influx of neutrophils into tissues in response to inflammatory stimuli involves C-X-C chemokines. Interleukin-1 (IL-1) stimulates chemokine production in vitro, but its role in vivo on chemokine production is not as clearly understood. We hypothesized that IL-1 mediates in vivo tissue C-X-C chemokine production induced by systemic lipopolysaccharide (LPS). IL-1 activity was blocked by IL-1 receptor antagonist (IL-1Ra). Rats were injected with Salmonella typhi LPS (0.5 mg/kg) with and without prior administration of IL-1Ra. Cytokine-induced neutrophil chemoattractant-1 (CINC-1) and macrophage inflammatory protein-2 (MIP-2) protein and mRNA levels, tissue neutrophil accumulation, and indices of organ injury were measured. LPS administration resulted in increased plasma, lung, and liver IL-1beta that was decreased by Il-1Ra. LPS also induced an increase in plasma, lung, and liver CINC-1 and MIP-2 protein and mRNA. However, IL-1Ra had no effect on LPS-induced plasma or lung tissue CINC-1 levels. In contrast, IL-1Ra pretreatment did significantly decrease CINC-1 protein expression in the liver (45% decrease) and MIP-2 protein expression in plasma (100% decrease), lung (72% decrease) and liver (100% decrease) compared to LPS- treated controls. Steady-state mRNA levels by Northern blot analysis of both CINC-1 and MIP-2 in lung and liver were similar to the protein findings. Pretreatment with IL-1Ra also resulted in a 47% and 59% decrease in lung and liver neutrophil accumulation, respectively, following LPS. In addition, indices of both lung and liver injury were decreased in animals pretreated with IL-1Ra. In summary, LPS induces IL-1beta and MIP-2 expression in the lung and liver, both of which are IL-1 dependent. Although lung neutrophil accumulation in both lung and liver after LPS is also IL-1 mediated, lung CINC-1 levels were unaffected by IL-1Ra. These data suggest that IL-1 regulates tissue chemokine expression and neutrophil accumulation after LPS.

Ischemia alone is sufficient to induce TNF-alpha mRNA and peptide in the myocardium.

Over-production of tumor necrosis factor-alpha (TNF-alpha) following myocardial ischemia-reperfusion contributes to cardiac dysfunction, and anti-TNF-alpha has therapeutic potential for myocardial protection in cardiac surgery with obligatory ischemia. It remains unclear, however, whether myocardial TNF-alpha production occurs during ischemia and whether cardiac myocytes constitute a source of myocardial TNF-alpha. Ischemia alone has been shown to activate myocardial NF-kappaB. We hypothesized that ischemia alone is sufficient to induce myocardial TNF-alpha gene expression and peptide synthesis. We examined TNF-alpha production and NF-kappaB activation in the isolated rat heart subjected to global normothermic ischemia. Myocardial ischemia resulted in rapid IkappaB-alpha degradation and NF-kappaB activation. Immunofluorescence staining detected NF-KB intranuclear translocation primarily in myocardial interstitial cells. Ischemia alone induced a time-dependent increase in myocardial TNF-alpha. TNF-alpha peptide increased to 20.3+/-3.0 pg/mg after 25 min of ischemia (P < 0.05 vs 8.9+/-2.0 pg/mg in perfusion control). TNF-alpha was also localized to myocardial interstitial cells. Increased TNF-alpha peptide level correlated with TNF-alpha mRNA expression. We conclude that ischemia alone induces TNF-a gene expression and peptide synthesis in the myocardium that are associated with NF-kappaB activation. Non-myocytes constitute the main source of myocardial TNF-alpha following ischemia. The results suggest that therapeutic strategies attempting to decrease myocardial TNF-alpha production need to be applied before or in the early phase of ischemia.

Donation after cardiac death: the University of Wisconsin experience.

OBJECTIVES: The objective of this analysis was to compare the results of transplantation of livers, pancreases, kidneys, and lungs from donation after cardiac death (DCD) donors to organs transplanted from donation after brain death (DBD) donors. METHODS: From January 1984 through July 2000, outcomes of 382 DCD kidneys were compared to 1,089 kidneys (SPK) transplants and 36 liver transplants from DCD donors were compared to 455 SPK and 510 liver transplants from DBD donors. Likewise, 31 simultaneous pancreas-kidneys transplants from DBD donors. RESULTS: The rate of delayed graft function (DGF) was higher in kidneys transplanted from DCD donors (27.5% versus 21.3%, p=0.01). Likewise, discharge creatinines were higher in recipients of DCD kidneys (1.9 mg/dL versus 1.7 mg/dL, p=0.001). There was no difference in 10-year graft survival between DCD and DBD recipients (45.0% versus 48.0%, p=0.054). No difference in 5-year pancreatic and renal allograft survival was seen after SPK from DCD or DBD donors. After liver transplantation, biliary strictures were higher in recipients of DCD livers (13.9% versus 8.0%, p=0.03). Likewise, 3-year patient and graft survivals were lower for recipients of DCD livers (65.8% versus 84.9%, p=0.01; and 58.6% versus 76.9%, p=0.006). CONCLUSIONS: This large experience with transplantation from DCD donors demonstrates that similar patient and graft survivals can be expected when compared to recipients of organs from DBD donors.

Diagnostic accuracy of solid phase HLA antibody assays for prediction of crossmatch strength.

Solid phase antibody assays are increasingly used to provide quantitative measures of donor-specific HLA antibodies for assessment of pretransplant risk, although cell-based crossmatches continue to serve as gold standards for determination of donor HLA antibody strength. This study determined the ability of HLA antibody solid phase assays to predict the strength of cell-based flow cytometric (FC) and complement-dependent cytotoxicity (CDC) crossmatches. Eighty-two recipient/donors pairs were analyzed using receiver operating characteristic (ROC) curve analyses to determine the accuracy of donor-specific median fluorescence intensity values (Σ MFI) from single antigen bead assays for predicting strong FC and CDC crossmatches. Diagnostic sensitivity and specificity of optimal Σ MFI values were highest for predicting strong T cell FCs. Σ MFI values showed good sensitivity for predicting positive direct and AHG-augmented CDC crossmatches (91% and 94%, respectively), but with lower specificity (67% each). Specificity and sensitivity for predicting positive B cell CDC crossmatches were 73% and 84%. Σ MFI values derived from single antigen bead assays can predict strong flow and positive CDC crossmatches, but with tradeoffs between sensitivity and specificity. The results support the use of solid phase assays for quantitative virtual crossmatching and as a replacement for cell-based crossmatching.

Favorable balance of anti-oxidant/pro-oxidant systems and ablated oxidative stress in Brown Norway rats in renal ischemia-reperfusion injury.

Oxidative stress is important in the pathogenesis of renal ischemia-reperfusion (IR) injury; however whether imbalances in reactive oxygen production and disposal account for susceptibility to injury is unclear. The purpose of this study was to compare necrosis, apoptosis, and oxidative stress in IR-resistant Brown Norway rats vs. IR-susceptible Sprague-Dawley (SD) rats in an in vivo model of renal IR injury. As superoxide (O (2) (.-) ) interacts with nitric oxide (NO) to form peroxynitrite, inducible NO synthase (iNOS) and nitrotyrosine were also examined. Renal IR was induced in SD and BN rats by bilateral clamping of renal arteries for 45 min followed by reperfusion for 24 h (SD 24 and BN 24, respectively). BN rats were resistant to renal IR injury as evidenced by lower plasma creatinine and decreased acute tubular necrosis. TUNEL staining analysis demonstrated significantly decreased apoptosis in the BN rats vs. SD rats after IR. Following IR, O (2) (.-) levels were also significantly lower in renal tissue of BN rats vs. SD rats (P < 0.05) in conjunction with a preservation of the O (2) (.-) dismutating protein, CuZn superoxide dismutase (CuZn SOD) (P < 0.05). This was accompanied by an overall decrease in 4-hydroxynonenal adducts in the BN but not SD rats after IR. BN rats also displayed lower iNOS expression (P < 0.05) resulting in lower tissue NO levels and decreased nitrotyrosine formation (P < 0.01) following IR. Collectively these results show that the resistance of the BN rat to renal IR injury is associated with a favorable balance of oxidant production vs. oxidant removal.

Influence of kidney function to the impact of acute rejection on long-term kidney transplant survival.

In kidney transplantation, timing of an initial acute rejection (AR) is correlated with a variable risk of graft loss. However, it is unknown whether the increased risk for graft loss because of AR is conditioned by impaired graft function. A total of 730 cadaveric kidney transplant recipients were retrospectively evaluated from 1994 to 2001. When AR occurred, the risk ratio (RR) for graft loss was strongly time-dependent and increased, the later the rejection episode occurred. Compared with the reference group (no rejection) having an AR within 0-30, 31-365, or >365 days post-transplant conferred a 3.1-, 9.1- and 49.3-fold risk for subsequent graft loss (P < 0.001). By including serum creatinine as an indicator for graft function at the time of rejection RR decreased to 2.4-, 7.1- and 21.8-fold, but remained still significant (P = 0.023). In conclusion, the higher risk of graft loss after late AR is not fully explained by impaired graft function measured by serum creatinine.

Liver transplantation for HELLP syndrome.

Hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome is a rare complication of pregnancy that is associated with preeclampsia and may result in rupture of the liver. Although there have been case reports of liver transplantation for HELLP syndrome, the outcomes of transplantation for this rare indication have not been reported. Furthermore, the optimal management of complicated HELLP syndrome and indications for liver transplantation are unclear. Our objective was to review the national experience with liver transplantation for HELLP syndrome and to develop a comprehensive algorithm for the management of liver complications of HELLP syndrome, including indications for transplantation. A recent case from our institution is reported and the literature is reviewed. The results of liver transplantation for HELLP syndrome were analyzed from the United Network for Organ Sharing database. Between October 1987 and November 2003 there have been 8 deceased donor liver transplants performed for complications related to HELLP syndrome. As of the most recent follow-up, 6 of the 8 patients are alive, with both deaths occurring within 1 month of transplantation, and 2 patients have required retransplantation. This review supports that good results can be obtained with liver transplantation for patients with complicated HELLP syndrome that have either ongoing, uncontrolled hemorrhage or liver necrosis and failure. Patients with complicated HELLP syndrome are best managed at a center with expertise in liver transplantation.

Simultaneous pancreas-kidney transplantation from donation after cardiac death: successful long-term outcomes.

OBJECTIVE: The outcomes of simultaneous pancreas-kidney (SPK) transplantation with donor organs procured from donation after cardiac death (DCD) are compared with transplants performed with donor organs recovered from donation after brain death (DBD). SUMMARY BACKGROUND DATA: Concerns exist regarding the utilization of pancreata obtained from DCD donors. While it is known that DCD kidneys will have a higher rate of DGF, long-term functional graft survival data for DCD pancreata have not been reported. METHODS: A retrospective review of all DCD SPK transplants performed at a single center was undertaken. RESULTS: Patient, pancreas, and kidney survival at 5 years were similar between DCD and DBD organs. Pancreas function and outcomes were indistinguishable between the 2 modes of procurement. As expected, the DCD kidneys had an elevated rate of DGF, which had no significant long-term clinical impact. CONCLUSION: SPK transplantation using selected DCD donors is a safe and viable method to expand the organ pool for transplantation.

Donation after cardiac death: the University of Wisconsin experience with liver transplantation.

OBJECTIVE: To determine whether the outcomes of liver transplantation (LTx) from donation after cardiac death (DCD) donors are equivalent to those from donation after brain death (DBD) donors. SUMMARY BACKGROUND DATA: Because of the significant donor organ shortage, more transplant centers are using livers recovered from DCD donors. However, long-term, single-center outcomes of liver transplantation from DCD donors are limited. METHODS: From January 1, 1993, to July 31, 2002, 553 liver transplants were performed from DBD donors and 36 were performed from DCD donors. Differences in event rates between the groups were compared with Kaplan-Meier estimates and the log-rank test. Differences in proportion and differences of means between the groups were compared with Fisher exact test and the Wilcoxon rank sum test, respectively. RESULTS: Mean warm ischemic time at recovery in the DCD group was 17.8 +/- 10.6 minutes. The overall rate of biliary strictures was greater in the DCD group at 1 year (33% versus 10%) and 3 years (37% versus 12%; P = 0.0001). The incidence of hepatic artery thrombosis, portal vein stenosis/thrombosis, ischemic-type biliary stricture (ITBS), and primary nonfunction were similar between groups. However, the incidence of both hepatic artery stenosis (16.6% versus 5.4%; P = 0.001) and hepatic abscess and biloma formation (16.7% versus 8.3%; P = 0.04) were greater in the DCD group. Trends toward worse patient and graft survival and increased incidence of ITBS were seen in DCD donors greater than 40 years compared with DCD donors less than 40 years. Overall patient survival at 1 year (DCD, 80%; versus DBD, 91%) and 3 years (DCD, 68%; versus DBD, 84%) was significantly less in the DCD group (P = 0.002). Similarly, graft survival at 1 year (DCD, 67%; versus DBD, 86%) and 3 years (DCD, 56%; versus DBD, 80%) were significantly less in the DCD group (P = 0.0001). CONCLUSIONS: Despite similar rates of primary nonfunction, LTx after controlled DCD resulted in worse patient and graft survival compared with LTx after DBD and increased incidence of biliary complications and hepatic artery stenosis. However, overall results of LTx after controlled DCD are encouraging; and with careful donor and recipient selection, LTx after DCD may successfully increase the donor liver pool.

Human T-cell lymphotrophic virus infection in organ donors: a need to reassess policy?

Human T-cell lymphotrophic virus (HTLV)-I/II infection has been considered a contra-indication to organ donation due to the risk of transmission of infection and the subsequent development of either adult T-cell leukemia or HTLV-I-associated myelopathy. However, neither the incidence of HTLV-I/II infection in organ donors nor the risk of transmission of HTLV-I/II by solid organ transplantation has been defined. Further, it is not known if HTLV infection contributes to significant morbidity in solid organ recipients. The purpose of this study was to evaluate the incidence of HTLV-I/II infection in organ donors in USA and to determine if transplanting these organs resulted in HTLV-related morbidity or mortality. We utilized the UNOS database to: (i) identify organ donors that were positive for HTLV-I or II infection between 1988 and 2000, and (ii) evaluate outcomes in the recipients of these organs. There were 25 HTLV-I/II-positive organ donors reported to UNOS between 1988 and 2000. Based on organ donors with a known HTLV-I/II status, the prevalence of HTLV-I infection in organ donors is 0.027% and the prevalence of HTLV-II is 0.064%. Twenty-two organs were transplanted from these HTLV-positive donors. There have been no reports of HTLV-I/II-related disease in the recipients with a median follow-up of 11.9 months. At our center, over the last 1.5 years there have been four multiorgan donors with false-positive HTLV-I/II screening assays, which resulted in the decision not to use organs from these donors. Based on the minimal chance of HTLV-related disease following transplantation of HTLV-I/II organs in this series, we recommend that careful consideration be given to transplanting organs from HTLV-I/II-positive organ donors.

Surgical repair of transplant renal artery stenosis with preserved cadaveric iliac artery grafts.

OBJECTIVE: To review the authors' experience with ABO-matched, preserved, cadaveric, iliac artery grafts for treatment of transplant renal artery stenosis (TRAS). SUMMARY BACKGROUND DATA: TRAS is an important and treatable cause of hypertension and graft dysfunction in renal allograft recipients. Surgical treatment is reserved for lesions that are not amenable to percutaneous transluminal angioplasty (PTA) or for recurrence after PTA. Various surgical options for reconstruction of the transplant renal artery exist, although no single technique has been demonstrated to be superior. The authors have used preserved, blood type-matched, iliac artery grafts procured from cadaver organ donors to reconstruct transplant renal arteries in patients with specific lesions and following unsuccessful PTAs. METHODS: Between 1991 and 2001, 21 patients underwent reconstruction of allograft renal arteries using cadaveric iliac artery as conduit. Charts, operative notes, and imaging studies of all patients were reviewed. A successful intervention for TRAS was defined as technical success as well as a decrease in serum creatinine and/or blood pressure 6 weeks after the procedure. Development of a hemodynamically significant lesion following renal artery reconstruction was considered a recurrence. RESULTS: In patients treated with surgical reconstruction, hemodynamically significant TRAS occurred at or within 1 to 2 mm of the anastomosis in 13 patients, in the middle of the renal artery in 4, and secondary to a kink in 2 patients. Surgical treatment was undertaken in seven patients following unsuccessful PTA. Two patients had aneurysms of the iliac artery. Reconstruction using cadaveric iliac artery was successful in 19 of 21 (90%) patients, and only 1 these patients (4.8%) failed due to recurrence, with a median follow-up of 42 months. Graft loss secondary to TRAS occurred in two patients. The authors have not seen any long-term complications related to cadaveric iliac artery grafts, and the majority of the allografts continue to function well. CONCLUSIONS: Surgical reconstruction of the transplant renal artery with blood type-matched iliac artery grafts should be considered a viable option for patients with specific anatomic lesions, those who have had an unsuccessful PTA, and those with recurrence following PTA.