Effect of Platelet Rich Plasma on an Experimental Rat Model of Adriamycin Induced Chronic Kidney Disease

Abstract
Background: Chronic kidney disease (CKD) is a world-wide health problem with increased mortality and morbidity. Currently, there is no effective protective therapy against CKD- induced renal damage with its sequel of end stage renal disease. Platelet-rich plasma (PRP) has a progressively gained consideration in wound healing, repair/regeneration of damaged tissues and conservation of organ function.
Aim of Study: This current study was planned to evaluate the possible protective effect of PRP treatment on a rat model of Adriamycin (ADR)-induced CKD.
Material and Methods: Sixty male albino rats were in-cluded; 30 were used for PRP preparation and the other 30, were randomly categorized into three equal groups of ten rat each: Normal control group, ADR group and PRP treated ADR group. At the end of experimental regimen (6 weeks), 24h urine samples were collected for measuring 24h urinary protein excretion and creatinine clearance (Cr Cl), then rats were decapitated and blood samples were collected for meas-uring serum albumin, triglycerides and cholesterol along with serum creatinine and blood urea nitrogen (BUN). Renal tissue samples were harvested and used for determination of renal level and mRNA expression of nephrin along with levels of hepatocyte growth factor (HGF), malondialdehyde (MDA), super oxide dismutase (SOD) activity, tumor necrosis factor alpha (TNF-a), interleukin 1-b  (IL-1b), and transforming growth factor 1b  (TGF 1b) in renal homogenates.
Results: Platelet rich plasma treatment improved ADR induced proteinuria, hyperlipidemia and renal dysfunction, which was accompanied by parallel upregulation of renal nephrin and inhanced levels of HGF and SOD activity, whereas the increased levels of TNF-a, IL-1b  and TGF 1b  were attenuated.
Conclusion: Platelet rich plasma could potentially protect against ADR induced CKD by alleviating its associated proteinuria, hyperlipidemia and the altered oxidative stress, inflammatory and fibrogenic responses.