The wait time for deceased-donor kidney transplantation has increased to 4-5 years in the Netherlands. Strategies to expand the donor pool include a living donor kidney exchange program. This makes it possible that patients who cannot directly receive a kidney from their intended living donor, due to ABO blood type incompatibility or a positive cross match, exchange donors in order to receive a compatible kidney. All Dutch kidney transplantation centers agreed on a common protocol. An independent organization is responsible for the allocation, cross matches are centrally performed and exchange takes place on an anonymous basis. Donors travel to the recipient centers. Surgical procedures are scheduled simultaneously. Sixty pairs participated within 1 year. For 9 of 29 ABO blood type incompatible and 17 of 31 cross match positive combinations, a compatible pair was found. Five times a cross match positive couple was matched to a blood type incompatible one, where the recipients were of blood type O. The living donor kidney exchange program is a successful approach that does not harm any of the candidates on the deceased donor kidney waitlist. For optimal results, both ABO blood type incompatible and cross match positive pairs should participate.

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Early graft failure was significantly more likely in recipients of kidneys from NHB donors. A prolonged WIT was strongly associated with this failure. Standard allocation procedures do not have a negative effect on outcome, and there is no reason to allocate NHB kidneys differently from HB kidneys.

A 71-yr-old male kidney transplant recipient suffered from delayed graft function. Eighty days after transplantation complete obstruction of the proximal ureter was observed, complicated by recurrent urinary tract infections. Two months later, the donor kidney was removed because of infectious complications and inadequate arterial perfusion. Histological examination of the removed graft showed signs of rejection as well as a low-grade papillary urothelial cell carcinoma of donor origin in the ureter. The remaining donor ureter was removed subsequently and showed no further signs of malignancy. Follow-up of the patient until 12 months after surgery did not reveal recurrence of the tumor. This case report is the first to describe accidental transfer of urothelial cell carcinoma in the ureter by transplantation, highlighting the possibility of malignancy when early stenosis is not related to the anastomosis. It again emphasizes the need for precise and cautious screening of organ donors, especially those of higher age.

A 52-year-old male presented with an asymptomatic palpable mass of the right testicle. Ultrasound confirmed the presence of a testicular tumour and a hemicastration was performed. None of the testis cancer-related tumour markers were elevated and histological findings revealed a neuroendocrine carcinoma, possibly a metastasis from another primary site. The radiological findings showed a lesion in the lung, and a positron emission tomography (PET)-scan was made. The PET scan revealed an increased fluorodeoxyglucose (FDG) uptake in the pulmonary lesion. It also showed lymphatic and hepatic metastases. The patient had no complaints besides a palpable testicular mass and was diagnosed with a cT1aN3M1b neuroendocrine carcinoma of the lower left field of the lung, stage IV. To our knowledge, the presentation of testicular metastasis of a neuroendocrine carcinoma of the lung has not been described in the literature. No curative options were available and the patient is being treated with salvage chemotherapy. IntroductionPrimary testicular cancer is the most common solid malignancy in men between the ages of 20 and 45; it is rare in patients under 15 and over 60. It constitutes 1% to 2% of all male cancers and 5% of all urological tumours, and is considered the most curable cancer. Most are germ cell tumours.1 Neuroendocrine (carcinoid) tumours (NETs) of the testes represent less than 1% of all testicular tumours. Case reportA 52-year-old vital, slender male presented to the outpatient clinic with a palpable mass in the right testicle, which he had noticed a couple of weeks before. His medical history included one session of prostate biopsies in 2009 because of an elevated PSA (prostate-specific antigen) level, all of which were benign. Other than the tender mass, he had no further complaints. Ultrasound showed a suspect, hypo-echogene, vascularized lesion, 2 cm, in the right testicle. The other testicle showed no pathology.A hemicastration was performed on the right side. Three tumour markers were measured preoperatively and none were elevated: lactate dehydrogenase (LDH) 247 U/L (normal <250 U/L), human chorionic gonadotropin (hCG) <2.0 U/L (normal range: 0-5 U/L) and alpha fetoprotein (aFP) 2.9 ug/L (normal <10 ug/L). A computed tomography (CT) scan of the thorax and abdomen was made to exclude metastases. It showed an unusual, possibly metastatic lesion in the lower field of the left lung; it was partially solid, partially cystic. Furthermore, it revealed multiple lesions in the liver, also suspect for metastases (Fig. 1).The pathologist showed the unusual histopathological findings during a multidisciplinary meeting. Immunohistochemical markers for malignant germ cell tumours (e.g., placental alkaline phosphatase [PLAP] and CD30) were negative, which ruled out (non)-seminoma and embryonal carcinoma. Four neuroendocrine markers (synaptophysin, chromogranin, CD56 and keratin) were all positive, suggesting it to be a NET (Fig. 2a, Fig. 2b, Fig. 2c, Fig. 2d). The thyroid transcription factor 1 (TTF-1) was po...