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We aimed to evaluate the influence of urological complications occurring within the first year after kidney transplantation on long‐term patient and graft outcomes, and sought to examine the impact of the management approach of ureteral strictures on long‐term graft function. We collected data on urological complications occurring within the first year posttransplant. Graft survivals, patient survival, and rejection rates were compared between recipients with and without urological complications. Male gender of the recipient, delayed graft function, and donor age were found to be significant risk factors for urological complications after kidney transplantation (P< .05). Death censored graft survival analysis showed that only ureteral strictures had a negative impact on long‐term graft survival (P= .0009) compared to other complications. Death censored graft survival was significantly shorter in kidney recipients managed initially with minimally invasive approach when compared to the recipients with no stricture (P= .001). However, graft survival was not statistically different in patients managed initially with open surgery (P= .47). Ureteral strictures following kidney transplantation appear to be strongly negatively correlated with long‐term graft survival. Our analysis suggests that kidney recipients with ureteral stricture should be managed initially with open surgery, with better long‐term graft survival. Retrospective analyses show that ureteral strictures following kidney transplantation are negatively correlated with long‐term graft survival and that open surgical management seems to be a better approach to treat these strictures.

For donation after circulatory death (DCD), many centers allow 1 h after treatment withdrawal to donor death for kidneys. Our center has consistently allowed 2 h. We hypothesized that waiting longer would be associated with worse outcome. A single‐center, retrospective analysis of DCDkidneys transplanted between 2008 and 2013 as well as a nationwide survey of organ procurement organization DCDpractices were conducted. We identified 296 DCDkidneys, of which 247 (83.4%) were transplanted and 49 (16.6%) were discarded. Of the 247 recipients, 225 (group 1; 91.1%) received kidneys with a time to death (TTD) of 0–1 h; 22 (group 2; 8.9%) received grafts with a TTDof 1–2 h. Five‐year patient survival was 88.8% for group 1, and 83.9% for group 2 (p = 0.667); Graft survival was also similar, with 5‐year survival of 74.1% for group 1, and 83.9% for group 2 (p = 0.507). The delayed graft function rate was the same in both groups (50.2% vs. 50.0%, p = 0.984). TTDwas not predictive of graft failure. Nationally, the average maximum wait‐time for DCDkidneys was 77.2 min. By waiting 2 h for DCDkidneys, we performed 9.8% more transplants without worse outcomes. Nationally, this practice would allow for hundreds of additional kidney transplants, annually. Hundreds more kidney transplants could be performed in the United States each year if centers were willing to wait up to 2 hours for kidneys procured after circulatory death, with no decrease in outcome.

Although several primate cell types have been reported to support replication of hepatitis A virus, optimal conditions for the isolation and production of quantities of virus have not been defined. We therefore examined seven different primate cell types for their ability to support replication of primate-passaged and wild-type virus as reflected by intracytoplasmic accumulation of viral antigen (direct immunofluorescence and radioimmunoassay) and propagation of cell culture-adapted virus. Of the cells tested, low-passage African green monkey kidney (AGMK) cells were most sensitive for initial isolation. Viral replication was documented after inoculation of AGMK cells with seven of nine hepatitis A virus antigen-positive fecal specimens (from seven epidemiologically distinct sources). With six inocula, virus was successfully passed in serial cultures. AGMK-adapted virus was readily propagated in continuous AGMK (BS-C-1) cells. The optimal temperature for the growth of virus in BS-C-1 cells was 35 degrees C. Viral release into supernatant fluids was documented in the absence of any cytopathic effect, and infectivity titers in supernatant fluids 21 days after inoculation (50% tissue culture infective does [TCID50], 10(6.0)/ml) equalled or exceeded those in the cell fraction (TCID50, 10(5.5)/ml). Cells maintained in serum-free media readily supported viral growth, with yields of virus (TCID50, 10(6.5)/ml) equal to or greater than those obtained with cells maintained in 2% fetal bovine serum.

Serum samples from 27 patients infected with human T-cell lymphotropic virus type III (14 with acquired immune deficiency syndrome [AIDS] and 13 with AIDS-related complex) were examined for antibodies to viral proteins by the Western blot method and with four different commercial solid-phase enzyme-linked immunosorbent assays (ELISAs). Virus-specific bands on blots at molecular masses of 64, 55, 53, 41, 31, 24, and 17 kilodaltons were observed. Rank correlation matrices were calculated to relate the intensity of viral bands, stage of illness, and ELISA kit optical densities (ODs). Groups of bands tended to covary in intensity: p17, p24, and p55 (gag gene products); p53 and p64 (pol gene products); and p31 (pol/endonuclease gene product) and p41 (env gene product). Blots of sera from AIDS-related complex patients usually showed strong activity against all viral proteins, while those of sera from AIDS patients characteristically showed strong reactivity only at the pol/endonuclease and env bands. For one ELISA kit (Abbott Laboratories, North Chicago, Ill.), ODs correlated well with the env and pol band intensity scores, while ELISA ODs with other kits (from Litton Industries, Sunnyvale, Calif.; Electro-Nucleonics, Inc., Fairfield, N.J.; and E.I. du Pont de Nemours & Co., Inc., Wilmington, Del.) correlated closely with gag band intensity scores. We conclude that human T-cell lymphotropic virus type III Western blot patterns are determined by (i) viral protein processing pathways and (ii) the stage of illness of the patient and may reflect (iii) the ELISA method used for serum screening.

Hepatitis B hospitalization rates for US Army enlisted personnel were determined by occupation and geographic area for 1980. The only group in the US Army currently recommended to receive hepatitis B vaccine is medical personnel regularly exposed to blood. Other groups of Army personnel, specifically those working in areas of high hepatitis B endemicity, have been thought to be at higher risk. Therefore, this work was undertaken to document hospitalization rates for all personnel using occupational blood exposure criteria as well as geographic area of assignment as risk factors for hepatitis B. The hospitalization rates underestimate true rates of hepatitis B incidence by a wide margin, and therefore were not used to calculate specific costs and specific benefits for a new vaccination strategy. In spite of this limitation, these data were useful for calculating relative risk, attributable risk, and amount of vaccine preventable disease. The risk of hospitalization for blood-exposed employees was consistently higher than that for non-blood-exposed personnel. The magnitude of the relative risk for blood exposure may be as high as 3.8 times or as low as 1.2 times, depending on which occupational comparison group is used. The relative risk of hospitalization in South Korea vs. the United States was 3.1 (p less than 0.0001), that for Europe vs. the United States, 2.1 (p less than 0.0001). Of all occupational and geographic risk comparisons, assignment to South Korea carried the highest attributable risk: 225 per 100,000. The amount of vaccine preventable disease in personnel assigned to South Korea was similar to that in occupationally blood-exposed employees (5.5 vs. 5.2 hospitalized cases per 1,000 vaccinees) after prorating exposure to risk based on average number of days of exposure to risk over three years. These data support the argument that geographic factors are as important as occupational blood exposure in defining risk of hepatitis B hospitalization among the US Army enlisted personnel.

Hepatitis A virus infection is often described as mild or asymptomatic, particularly in children. The failure of most adults who are found to be immune to remember symptoms of an illness suggestive of hepatitis A virus supports this belief. In 1982, two large outbreaks occurred in well documented populations of military personnel. These outbreaks were each extensively studied epidemiologically and serologically. It was found that 28/29 (96.6%) hepatitis A infections recognized prior to immune serum globulin in Outbreak A and 35/46 (76.1%) infections in Outbreak A were symptomatic. Symptomatic cases failed to occur beyond eight days of immune serum globulin administration to these predominantly susceptible groups. Between 40 and 70% of patients were icteric. Apparent contrasts in symptoms associated with hepatitis A infection in adults and children suggest a basic age-dependent difference in immune response to such infection.