Laparoscopic donor nephrectomy in unusual venous anatomy - donor and recepient implications

ABSTRACT Objectives Laparoscopic donor nephrectomy is now a commonly performed procedure in most of renal transplantation centers. However, the suitability of laparoscopy for donors with abnormal venous anatomy is still a subject of debate. Materials and methods Between August 2007 and August 2014, 243 laparoscopic donor nephrectomies were performed in our institution. All donors were evaluated with preoperative three-dimensional spiral computed tomography (CT) angiography Thirteen (5.35%) donors had a left renal vein anomaly. A retrospective analysis was performed to collect donor and recipient demographics and perioperative data. Results Four donors had a type I retroaortic vein, seven had type II retroaortic vein and a circumaortic vein was seen in three donors. The mean operative time was 114±11 minutes and mean warm ischemia time was 202±12 seconds. The mean blood loss was 52.7±18.4mL and no donor required blood transfusion. Mean recipient creatinine at the time of discharge was 1.15±0.18mg/dL, and creatinine at six months and one year follow-up was 1.12±0.13mg/dL and 1.2±0.14mg/dL, respectively. There were no significant differences in operative time, blood loss, warm ischemia time, donor hospital stay or recipient creatinine at 6 months follow-up, following laparoscopic donor nephrectomy in patients with or without left renal vein anomalies. Conclusion Preoperative delineation of venous anatomy using CT angiography is as important as arterial anatomy. Laparoscopic donor nephrectomy is safe and feasible in patients with retroaortic or circumaortic renal vein with good recipient outcome.

Dysregulation of interleukin 5 expression in familial eosinophilia.

BACKGROUND: Familial eosinophilia (FE) is a rare autosomal dominant inherited disorder characterized by the presence of lifelong peripheral eosinophilia (>1500/µL). Mapped to chromosome 5q31-q33, the genetic cause of FE is unknown, and prior studies have failed to demonstrate a primary abnormality in the eosinophil lineage. OBJECTIVE: The aim of this study was to identify the cells driving the eosinophilia in FE. METHODS: Microarray analysis and real-time PCR were used to examine transcriptional differences in peripheral blood mononuclear cells (PBMC), and in purified cell subsets from affected and unaffected family members belonging to a single large kindred. Cytokine levels in serum and PBMC culture supernatants were assessed by suspension array multiplexed immunoassays. RESULTS: Whereas IL-5 mRNA expression was significantly increased in freshly isolated PBMC from affected family members, this was not accompanied by increased mRNA expression of other Th2 cytokines (IL-4 or IL-13). Serum levels of IL-5 and IL-5 receptor α, but not IgE, were similarly increased in affected family members. Of note, IL-5 mRNA expression was significantly increased in purified CD3+ CD4+, CD14+, CD19+, and ILC2 cells from affected family members, as were IL-5 protein levels in supernatants from both stimulated PBMC and ILC2 cultures. CONCLUSIONS: These data are consistent with the hypothesis that the eosinophilia in FE is secondary to dysregulation of IL-5 production in PBMC (and their component subsets).