Abstract
A BSTRACT Platelet-rich plasma (PRP) has emerged as a promising autologous biological product with potential regenerative applications in kidney transplantation. By concentrating platelets and their bioactive mediators, PRP delivers growth factors, cytokines, and chemokines that may influence tissue repair processes. In the context of kidney transplantation, ischemia–reperfusion injury (IRI) represents a critical determinant of early graft dysfunction and long-term outcomes, including interstitial fibrosis and tubular atrophy (IFTA). PRP has been proposed as a therapeutic strategy to mitigate these injuries by enhancing tubular epithelial repair, promoting angiogenesis, and modulating inflammatory responses. However, current evidence remains limited and largely derived from preclinical renal injury models rather than direct transplantation studies. Experimental findings are inconsistent, with some studies demonstrating improved renal function, reduced oxidative stress, and attenuated inflammation, whereas others report exacerbation of injury, possibly due to leukocyte-rich PRP formulations, microvascular thrombosis, or profibrotic signaling pathways. Mechanistically, PRP exhibits a dual role: It can support adaptive repair through pro-survival and pro-angiogenic effects, yet it may also promote maladaptive responses via transforming growth factor-β (TGF-β) and platelet-derived growth factor (PDGF)-mediated fibrosis. This complexity highlights the importance of PRP composition, timing, and delivery route in determining therapeutic outcomes. Furthermore, heterogeneity in preparation protocols remains a major barrier to clinical translation. Future research should focus on standardized PRP characterization, transplant-specific models, and controlled clinical trials to clarify its safety and efficacy in kidney allograft regeneration.