Introduction: Haematopoietic stem cells (HSCs) can migrate to injured kidney and aid in tissue repair. However, clinical success remains poor and can be attributed to limited HSC recruitment. Understanding adhesive mechanisms governing HSC recruitment may allow the development of strategies that enhance their homing, thus improving the efficacy of HSC-based therapies. This study therefore determined the adhesive mechanisms critical for renal HSC recruitment, whether pre-treating HSCs with chemokines enhanced recruitment and the mechanisms by which this occurred and what vasculoprotective effects were being conferred by recruited HSCs. Methods: Numbers of HSCs, neutrophils and platelet microthrombi in renal peritubular capillaries of sham and ischemia-reperfusion (IR) injured mice (ketamine/xylazine; i.p.) were visualised using dyes that fluoresce different colours. Some HSCs were pre-treated with function-blocking antibodies to surface adhesion molecules (CD49d, CD44, CD18) or chemokines (SDF-1α, KC). Changes in surface expression and clustering of HSC adhesion molecules was determined using flow cytometry and confocally. HSC adhesion to endothelial counterligands (VCAM-1, hyaluronan) was determined using static adhesion assays in vitro. Results: HSC adhesion was significantly (p<0.001) increased in IR kidney when compared to sham controls. This resulted in a significant (p<0.01) reduction in adherent neutrophils and platelet microthrombi at 6 hours post-reperfusion when compared to mice receiving no HSCs. Recruitment was dependent on CD49d and CD44, but not CD18. Both SDF-1α and KC pre-treatments significantly (p<0.01) enhanced HSC adhesion within IR kidney. Neither pre-treatment strategy increased adhesion molecule expression. However, SDF-1α (p<0.01) and KC (p<0.05) did increase numbers of CD49d and CD44 surface clusters on HSCs respectively. This likely explained their increased adhesion to VCAM-1 (p<0.05) and hyaluronan (p<0.001). SDF-1α also significantly (p<0.01) increased HSC deformability as demonstrated using a micropipette aspiration method. This resulted in increased (p<0.01) numbers of free-flowing HSCs being continuously observed in the renal microcirculation. Conclusion: Chemokine pre-treatment increased HSC adhesion within injured renal microvessels. Interestingly, it also increased the pool of circulating transplanted HSCs available for renal recruitment. This was possibly due to the increased deformability preventing their entrapment within non-injured tissue (eg. lungs). Our data also demonstrates for the first time that HSCs exhibit marked anti-inflammatory and anti-platelet effects. Ongoing studies will determine whether enhancing their local presence with chemokine pre-treatment confers faster and more efficient vasculoprotective effects.