The kidney has limited capacity to regenerate following injury and preferentially repairs chronic injury with secreted extracellular matrix proteins. This can be a progressive process with functioning kidney tissue being replaced detrimentally with fibrotic scar tissue, ultimately leading to kidney failure. Whilst the renal response to injury has been well described it has been examined at whole organ resolution and there has been very limited description of the contribution of individual cells to the kidney’s reparative ability. Using the reversible unilateral ureteric obstruction model, a model of reversable injury, we describe the transcriptomic changes that occur during obstructive renal injury and subsequent repair at a single cell resolution and describe the altered myeloid cell populations and kinetics likely involved in ongoing tissue repair. Overall design: 5 single cell libraries, (4*10x workflows and 1*smartseq2), 3 mice pooled per library, deep sequencing on Nextseq 550