Protective response in renal transplantation: no clinical or molecular differences between open and laparoscopic donor nephrectomy

Abstract

OBJECTIVE:Prolonged warm ischemia time and increased intra-abdominal pressure caused by pneumoperitoneum during a laparoscopic donor nephrectomy could enhance renal ischemia reperfusion injury. For this reason, laparoscopic donor nephrectomy may be associated with a slower graft function recovery. However, an adequate protective response may balance the ischemia reperfusion damage. This study investigated whether laparoscopic donor nephrectomy modified the protective response of renal tissue during kidney transplantation.METHODS:Patients undergoing live renal transplantation were prospectively analyzed and divided into two groups based on the donor nephrectomy approach used: 1) the control group, recipients of open donor nephrectomy (n = 29), and 2) the study group, recipients of laparoscopic donor nephrectomy (n = 26). Graft biopsies were obtained at two time points: T-1 = after warm ischemia time and T+1 = 45 minutes after kidney reperfusion. The samples were analyzed by immunohistochemistry for the Bcl-2 and HO-1 proteins and by real-time polymerase chain reaction for the mRNA expression of Bcl-2, HO-1 and vascular endothelial growth factor. RESULTS:The area under the curve for creatinine and delayed graft function were similar in both the laparoscopic and open groups. There was no difference in the protective gene expression between the laparoscopic donor nephrectomy and open donor nephrectomy groups. The protein expression of HO-1 and Bcl-2 were similar between the open and laparoscopic groups. Furthermore, the gene expression of B-cell lymphoma 2 correlated with the warm ischemia time in the open group (p = 0.047) and that of vascular endothelial growth factor with the area under the curve for creatinine in the laparoscopic group (p = 0.01).CONCLUSION:The postoperative renal function and protective factor expression were similar between laparoscopic donor nephrectomy and open donor nephrectomy. These findings ensure laparoscopic donor nephrectomy utilization in renal transplantation.

Effects of Low Versus Standard Pressure Pneumoperitoneum on Renal Syndecan-1 Shedding and VEGF Receptor-2 Expression in Living-donor Nephrectomy: A Randomized Controlled Study

“…These injuries indicate that pneumoperitoneum and surgical manipulation causes acute tubular necrosis accompanied by peritubular capillary congestion. 42 Although the duration of pneumoperitoneum was relatively short, this study results showed the presence of endothelial and renal tubular markers to the inflammation were higher, especially when standard or high pressure pneumoperitoneum was used. The use of low pressure pneumoperitoneum may have attenuated these systemic and vascular inflammatory responses (Figure 7).…”

“…39,40 There is an increase in VGEF-mRNA expression at laparoscopic sites as a response to the injured tissue. [40][41][42] When inflammation occurs, IL-6 and activated syndecan-1 stimulate the synthesis of VEGF-A molecules and its binding to its regulator VEGFR-2 on the glomerular and peritubular capillaries endothelial cells, as well as tubular epithelial cells. 39,40 Increasing plasma sVEGFR-2 level and VEGFR-2 expression on tubular epithelial cells to the adjacent endothelial cells depends on the extent of inflammation that results in an increased endothelial permeability.…”

“…39,40 Increasing plasma sVEGFR-2 level and VEGFR-2 expression on tubular epithelial cells to the adjacent endothelial cells depends on the extent of inflammation that results in an increased endothelial permeability. 37,[41][42][43] The electron microscopy examination showed the low pressure group had intact tubular cell membranes with clear cell boundaries and attached brush borders. These morphologies were healthier when compared to the standard pressure group, which showed greater injury, tenuous tubular cell membranes, brush borders detached from the cell body, and more vacuolizations.…”

Effects of Low Versus Standard Pressure Pneumoperitoneum on Renal Syndecan-1 Shedding and VEGF Receptor-2 Expression in Living-donor Nephrectomy: A Randomized Controlled Study

“…39 There is an increase in VGEF-mRNA expression at laparoscopic sites as a response to the injured tissue. [40][41][42] In a normal human kidney, VEGFR-2 is expressed on glomerular and peritubular capillaries endothelial cells, as well as tubular epithelial cells at a low degree. 39,40 When inflammation occurs, IL-6 and activated syndecan-1 in the endothelial cells shedding and the release of VEGFR-2 are believed to have renal-protective roles.…”

“…In humans, acute tubular necrosis was observed in 44% of open nephrectomy and 45% of laparoscopic patients, and 54% of renal biopsy specimens taken from laparoscopic nephrectomy showed subcapsular cortical injury. These injuries indicate that pneumoperitoneum and laparoscopic surgical manipulation causes acute tubular necrosis accompanied by peritubular capillary congestion 42. Despite the absence of syndecan-1 from the glomerular and peritubular endothelial glycocalyx, it was found in the membrane of the proximal and distal tubules and was important for renal tubular cell survival during inflammation.…”