Our findings support the practice of living-donor kidney transplantation as a good means to meet the persisting organ shortage. Further effort must be put into minimizing donor and recipient complications. The specific demands of younger donors should be further elucidated. In addition to medical follow-up, living kidney donors should also be offered lifelong psychologic counseling.
Allocation of kidneys from donors older than 64 years to recipients older than 64 years was started in 1999 to improve use of older donor kidneys. Kidneys are allocated locally without HLA-matching to keep cold ischemia short.We compared survival and rejection rates in elderly patients allocated in the old-for-old program (ESP) to patients aged 60 years and older based on HLA-matching, expected ischemia and waiting time (ETKAS).The 69 ESP patients were older (67.9 ± ± 2.5 vs. 63.9 ± ± 2.9 years), had older donors (71.2 ± ± 3.9 vs. 44.6 ± ± 14.5 years) and more HLA-mismatches (4.2 ± ± 1.2 vs. 1.6 ± ± 1.7) than the 71 ETKAS patients, while ischemia was shorter (7.8 ± ± 3.4 vs. 14.2 ± ± 5.5 h). ESP and ETKAS had similar graft (1-year: 83.6% vs. 86.9%) and patient survival (85.2% vs. 89.5%). With the introduction of ESP, use of older recipients and donors rose from less than 2% to 16% and 11%, respectively. Incidence of acute rejections was significantly higher in the ESP group (1 year: 43.2% vs. 27.4%) and significantly correlated with the degree of HLA-matching.Introduction of old-for-old allocation allows successful expansion of the donor and recipient pool without affecting patient and graft survival. HLA-matching should not be ignored, as the risk of acute rejection in elderly patients is substantial.
Ga-PSMA PET/CT appears to be a promising method for detecting RCC metastases. However, no additional diagnostic value in assessing the primary tumour was found.
We studied 51 cervical carcinomas, among them 25 squamous-cell carcinomas (SCC) and 26 cervical adenocarcinomas (AdCa), and 40 vulvar SCC for the presence of HPV and mutant p53. HPV was detected by PCR, and p53 alterations by temperature-gradient gel electrophoresis/direct sequencing and immunohistochemistry. HPV, mostly type 16/18, was found in 80.4% of the cervical tumors (92.0% of the SCC and 69.2% of the AdCa), but in only 27.5% of vulvar carcinomas. In contrast, p53 mutations were found in 7.8% and 52.5% of cervical and vulvar tumors respectively. Mutant p53 occurred in pre-invasive vulvar lesions, indicating that this oncogenic factor is involved early in carcinogenesis. Further analysis of recurrent/metastatic lesions of 9 cervical and 14 vulvar tumors also showed remarkable differences: in cervical cancer, HPV was persistent, and p53 mutations absent, whereas in vulvar tumors, HPV was mostly absent or not persistent, and the p53 mutation rate was very high (78.6%). These observations suggest that HPV persistence is an important event for the evolution and maintenance of cervical cancer, whereas for vulvar cancers p53 mutation and not HPV activity is a central oncogenic event.
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