The incidence rate of Acute Kidney Injury (AKI) gets escalated each year. Kidney ischemia/reperfusion injury (IR injury) is the main cause of AKI after major cardiovascular surgery, trauma, or kidney transplantation. Reperfusion is considered essential for ischemic tissue. However, the evidence revealed that reperfusion itself has impact in cellular destruction. Vitamin D is not only known as calcium regulating hormone, but also as renoprotective agent. This study aimed to investigate the effect of vitamin D treatment on kidney IR injury in mice. Kidney IR injury was performed using 30 minutes of bilateral clamping of renal pedicles, then released in male Swiss Webster mice (3 months, 30-40 grams, n=20), which were divided into three groups: sham operation (SO) group, IR injury (IRI) group, and IR injury with 0.25 µg/ kg body weight of vitamin D treatment (IR7+VD). Mice were terminated at day 7 post operation, kidneys were harvested and used for paraffin making, immunostaining and RNA extraction. Tubular injury was quantified based on Periodic Acid-Schiff's (PAS) staining. Immunostaining was done for quantification of macrophage (CD68) and myofibroblast (α-SMA). Reverse Transcriptase PCR (RT-PCR) was done to examine Monocyte Chemoattractant Protein-1 (MCP-1) and Toll-like Receptor 4 (TLR4) mRNA expression. Kidney IR injury induced significant increase of tubular injury, which was associated with higher myofibroblast and macrophage number. Meanwhile, Vitamin D treatment significantly reduced tubular, myofibroblast and macrophage number. RTPCR revealed reduction of TLR4 and MCP-1 mRNA expressions after Vitamin D treatment (p<0.05 vs IR group). Vitamin D ameliorates kidney IR injury through reducing inflammation and myofibroblast formation.
Keywords: Inflammation; Kidney IR injury; Myofibroblast; Tubular injury; Vitamin D.