Open Management of the Renal Vein Is a Safe Modification in Right-Sided Laparoscopic Living Donor Nephrectomy to Maximize Graft Vein Length.

BACKGROUND: The primary objective in living donor kidney transplantation is donor safety. In laparoscopic living donor nephrectomy, most centers prefer the left kidney for donation given the shorter renal vein, higher rate of thromboses, and more difficult surgical procedure for right kidney retrieval. The goal of this study was to demonstrate the feasibility of a hybrid technique using a Satinsky clamp in right-sided living donor nephrectomy to obtain maximal renal vein and to compare the outcome with standard left-sided laparoscopic donor nephrectomies. MATERIAL AND METHODS: Between 2005 and 2013, 77 patients underwent a left (group L) and 54 a right (group R) living donor nephrectomy. In group R, after laparoscopic dissection and mobilization of the right kidney, two 12-mm trocar incisions in the right upper quadrant were connected in a 5-7 cm subcostal incision. The caval vein was partially clamped under direct vision prior to dissection of the renal vein. The venotomy was then closed with a running 4-0 Prolene suture. The two groups were compared with regard to surgical complications, graft function, and graft survival. RESULTS: Using this technique, no significant difference with regard to complications or graft function was observed. Serum creatinine at discharge in donor group L was 1.23 (±0.43) mg/dL and in donor group R 1.21 (±0.37) mg/dL (P = .71). Graft survival at one year was 100% in both groups. CONCLUSION: Open management of the renal vein is a safe alternative in laparoscopic right-sided donor nephrectomy and ensures maximal length of the vein.

Exogenous Lipocalin 2 Ameliorates Acute Rejection in a Mouse Model of Renal Transplantation.

Lipocalin 2 (Lcn2) is rapidly produced by damaged nephron epithelia and is one of the most promising new markers of renal injury, delayed graft function and acute allograft rejection (AR); however, the functional importance of Lcn2 in renal transplantation is largely unknown. To understand the role of Lcn2 in renal AR, kidneys from Balb/c mice were transplanted into C57Bl/6 mice and vice versa and analyzed for morphological and physiological outcomes of AR at posttransplantation days 3, 5, and 7. The allografts showed a steady increase in intensity of interstitial infiltration, tubulitis and periarterial aggregation of lymphocytes associated with a substantial elevation in serum levels of creatinine, urea and Lcn2. Perioperative administration of recombinant Lcn2:siderophore:Fe complex (rLcn2) to recipients resulted in functional and morphological amelioration of the allograft at day 7 almost as efficiently as daily immunosuppression with cyclosporine A (CsA). No significant differences were observed in various donor-recipient combinations (C57Bl/6 wild-type and Lcn2(-/-) , Balb/c donors and recipients). Histochemical analyses of the allografts showed reduced cell death in recipients treated with rLcn2 or CsA. These results demonstrate that Lcn2 plays an important role in reducing the extent of kidney AR and indicate the therapeutic potential of Lcn2 in transplantation.

Pancreatic graft survival despite partial vascular graft thrombosis due to splenocephalic anastomoses.

Thrombotic complications following pancreas transplantation are still the most common cause of nonimmunologic graft loss. The aim of this study was to analyze pancreatic graft function after partial arterial graft thrombosis and the investigation of the pancreatic arterial anatomy with regard to intraparenchymal anastomoses. We retrospectively analyzed the data for 175 consecutive pancreas transplants performed between January 2002 and October 2007. Selective Y-graft angiography was performed in 10 and rubber-milk injection in 5 fresh pancreas specimens. Thrombosis of one leg of the Y-graft was diagnosed in 18 (10.3%) patients. Only one of these patients with thrombosis of the splenic artery required exogenous insulin. Sufficient graft perfusion was demonstrated in all of the remaining grafts. One graft was lost due to acute rejection. In all specimens angiography showed an excellent perfusion of the pancreaticoduodenal arcade, even after selective cannulation of the splenic artery. Arterial collaterals between the gastroduodenal, splenic artery and the superior mesenteric artery were demonstrated. Our results demonstrate that global perfusion of the pancreatic graft and sufficient graft function is sustained after the thrombotic occlusion of one branch of the Y-graft by a complex system of intraparenchymal anastomoses. These anatomical findings may have consequences for resection strategies in pancreas surgery.

Lipocalin-2 regulates the inflammatory response during ischemia and reperfusion of the transplanted heart.

Ischemia and reperfusion (IR) are known to negatively affect early allograft function following solid organ transplantation. Lipocalin-2 (Lcn-2) has been described as a marker and potential positive modulator of acute inflammation during these processes. Using a heterotopic murine heart transplant model we previously found that IR resulted in a pronounced upregulation of Lcn-2 mRNA in the heart at 12 (22.7-fold increase) and 24 h (9.8-fold increase) of reperfusion. We now confirm this increase at the protein level and provide evidence for infiltrating polymorphonuclear cells as the primary source of Lcn-2 protein. Lcn-2 levels are increased 6.6-fold at 12 h, 11.4-fold at 24 h and 6.4 fold at 48 h after reperfusion. In Lcn-2(-/-) grafts the number of infiltrating granulocytes is reduced by 54% (p < 0.05) at 2 h, 79% (p < 0.01) at 12 h, 72% (p < 0.01) at 24 h and 52% (p < 0.01) at 48 h after reperfusion compared to Lcn-2(+/+) grafts, without any differences in cardiomyocyte apoptosis. These data suggest a function of Lcn-2 in the initiation of the inflammatory response. Moreover, an increase in Lcn-2 is not only restricted to the transplanted heart, but is also observed in the kidney, hinting at a possible involvement of Lcn-2 in the systemic response to IR.