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Abstract ARenal function impairment and morphological damage are both signs of CsA nephrotoxicity. Renal vasoconstriction, tubular epithelial cell alterations, tubulointerstitial fibrosis, and glomerular abnormalities all contribute to irreversible renal failure secondary to long term CsA treartment (Korolczuk et al., 2010). The stimulation of the renin-angiotensin-aldosterone system, upregulation of the transforming growth factor-beta (TGF-β), direct activation of apoptosis genes and enhanced apoptosis in tubular and interstitial cells, and oxidative stress are thought to be the underlying mechanisms of toxicity (AbuFarsakh et al., 2017). Marx et al., (1998) were the first to describe platelet-rich plasma (PRP). Itis an autologous growth factor-rich product made from a blood sample centrifuged to separate the platelet-rich supernatant. Many growth factors, such as epidermal growth factor (EGF), hepatocyte growth factor (HGF), platelet derived growth factor (PDGF), and vascular endothelial growth factor (VEGF), are released locally by PRP up to three weeks following administration |