Effects of Platelet-Rich Plasma (PRP) on a Model of Renal Ischemia-Reperfusion in Rats

Abstract

Renal ischemia-reperfusion injury is a major cause of acute renal failure, causing renal cell death, a permanent decrease of renal blood flow, organ dysfunction and chronic kidney disease. Platelet-rich plasma (PRP) is an autologous product rich in growth factors, and therefore able to promote tissue regeneration and angiogenesis. This product has proven its efficacy in multiple studies, but has not yet been tested on kidney tissue. The aim of this work is to evaluate whether the application of PRP to rat kidneys undergoing ischemia-reperfusion reduces mid-term kidney damage. A total of 30 monorrenal Sprague-Dawley male rats underwent renal ischemia-reperfusion for 45 minutes. During ischemia, PRP (PRP Group, n = 15) or saline solution (SALINE Group, n = 15) was administered by subcapsular renal injection. Control kidneys were the contralateral organs removed immediately before the start of ischemia in the remaining kidneys. Survival, body weight, renal blood flow on Doppler ultrasound, kidney weight, kidney volume, blood biochemistry and histopathology were determined for all subjects and kidneys, as applicable. Correlations between these variables were searched for. The PRP Group showed significantly worse kidney blood flow (p = 0.045) and more histopathological damage (p<0.0001). Correlations were found between body weight, kidney volume, kidney weight, renal blood flow, histology, and serum levels of creatinine and urea. Our study provides the first evidence that treatment with PRP results in the deterioration of the kidney’s response to ischemia-reperfusion injury.

Controlled Delivery of Stem Cell-Derived Trophic Factors Accelerates Kidney Repair After Renal Ischemia-Reperfusion Injury in Rats

“…These results indicate positive effects of the PRP treatment on the renal functions. Conversely, Martin‐Sole et al recently reported opposite results, where PRP treatment worsened renal blood flow and caused more renal histologic damage in rats with I/R. The authors suggested early thrombus formation, high osmolality of PRP, and the role of inflammatory cytokines from PRP as possible causes.…”

“…The authors suggested early thrombus formation, high osmolality of PRP, and the role of inflammatory cytokines from PRP as possible causes. In their report [46], the authors injected 1 ml of PRP solution to a left kidney, whereas our study used 20 μl for the injections into two kidneys. It can be considered that the significant difference in the injection volume may be a critical reason for the discrepancy in the results.…”

Histological and immunohistochemical study of the potential healing effects of glucosamine and platelets rich plasma on experimentally induced oral mucositis in adult male rats

“…These factors stimulates cell proliferation, promote chemotaxis, differentiation and metabolism regulation, also mediate mitogenesis and the antiapoptotic effect through many receptors. Other authors [14,17] revealed that PRP products containing white blood cells, which capable to inhibit the growth of some bacteria and improve healing in soft tissue injuries associated with infection through release of bactericidal factors.…”

“…PRP is an autologous output of blood and it formed of a high platelet concentration in a small quantity of plasma. It has great advantage on clinical proposal as it is an cheap product, easy to obtain, and there is no risk of rejection or immune reaction and also had an antimicrobial action [12,14].…”

miR-191 secreted by platelet-derived microvesicles induced apoptosis of renal tubular epithelial cells and participated in renal ischemia-reperfusion injury via inhibiting CBS

“…Renal ischemia-reperfusion (IR) injury is a common cause for delayed function of renal transplantation, which is responsible for 20-30% primary graft dysfunction during renal transplantation [1]. There are two main features of IR injury at the renal level, namely apoptosis of tubular cells and interstitial inflammation [2]. H 2 S plays a protective role as a signaling molecule and antioxidant in kidney tubular epithelial cells that could resist IR-induced lipid peroxidation, reduce cell damage in the kidney tissue, and improve renal function [3].…”