INTRODUCTION

Gentamicin (GM) is an antibiotic of aminoglycoside group. Aminoglycosides are broad-spectrum antibiotics. The aminoglycosides are particularly effective against aerobic Gram-negative bacteria. Most common side effects of GM are ototoxicity and nephrotoxicity. A rise in creatinine (Cr) level is the typical sign of GM -induced nephrotoxicity.
The proximal tubule is specifically targeted in GM-induced nephrotoxicity. After glomerular filtration, about 5% of the given dosage accumulates within the proximal tubules. Megalin, a multi-ligand receptor, has been shown to be the primary mechanism for this accumulation by endocytosis. GM is then distributed to the lysosomes, Golgi apparatus, and endoplasmic reticulum. It binds to phospholipids and suppresses phospholipase activity, which leads to phospholipidosis.
In the pathophysiology of GM-induced nephrotoxicity, oxidative stress is one of the important factors that plays a significant role. Oxidative stress leads to the production of toxic free radicals, increased cellular lipid peroxidation, decreased cellular antioxidants and finally tubular necrosis.
Platelet-rich plasma (PRP) is an autologous blood concentrate with a higher platelet concentration than whole blood, ranging from 200,000 to 1,000,000 platelets/μL in a 5 mL plasma. The α-granules found in platelets contain a variety of substances, such as proteins, cytokines, and growth factors, which help to control the healing process.
The α-granules also contain the transforming growth factor β1 (TGF-β1), the fibroblastic growth factor (FGF), the epidermal growth factor (EGF), the vascular endothelial growth factor (VEGF), the platelet-derived growth factor (PDGF) and the insulin-like growth factor (IGF).