Globally, acute kidney injury (AKI) and chronic kidney disease (CKD) cause an estimated 13 million and 700 million cases/year, and 1.7 million and 1.2 million deaths/year, respectively. Kidney disease is the result of many different insults. Kidney injury promotes the recruitment and proliferation of different leukocyte populations, including macrophages to the kidney that play a major role in disease pathogenesis. Recruitment of resolution and reparative macrophages induce anti-inflammatory responses and promote kidney repair, but the characteristics of these cell populations are not clearly defined. GATA6+ macrophages had been reported to facilitate tissue repair following injury in organs other than the kidney. However, whether GATA6+ macrophages are resolution and repair macrophages in the kidney is not known. Using immunofluorescence imaging, flow cytometry, and nCounter transcriptome techniques, we assessed GATA6+ cells in normal and diseased kidney of mouse and human while probing common tissue macrophage markers specifically CD206+ and CD163+ as a benchmark. We showed that both CD206+ and CD163+ macrophages were detectable in normal and diseased mouse and human kidney. In mouse, both CD206+ and CD163+ macrophages were upregulated in various kidney compartments especially during CKD. Whereas in human, CD206+ and CD163+ macrophages appeared to be resident in the kidney and upregulated in diseased states. Using the same technique, significant population of GATA6+ cells were identified in mouse and human kidney particularly during CKD. GATA6+ cells were mainly localized in the tubulointerstitial area of the kidney cortex. In mouse and human kidney, the majority of GATA6+ cells did not co-express common leukocyte/macrophage markers. Conversely, in mouse and human CKD, GATA6+ cells mostly co-expressed the stromal cell marker αSMA. Using nCounter transcriptome profile of mouse samples, GATA6+ cells represented a distinct non-immune cell population that expressed genes associated with stromal cell identity, inflammation regulation, angiogenesis and collagen biosynthesis. The role of GATA6+ cells in CKD will require further exploration to unravel specific pathological and/or repair mechanisms that may lead to improved management of kidney disease.