The purpose of the study was to review the characteristics of renal macrophages and dendritic cells during homeostasis and disease, with a particular focus on lupus nephritis.

Resident renal macrophages derive from embryonic sources and are long-lived and self-renewing; they are also replaced from the bone marrow with age. The unique characteristics of macrophages in each tissue are imposed by the microenvironment and reinforced by epigenetic modifications. In acute renal injury, inflammatory macrophages are rapidly recruited and then replaced by those with a wound healing/resolution phenotype. In lupus nephritis, dendritic cells infiltrate the kidneys and function to present antigen and organize tertiary lymphoid structures that amplify inflammation. In addition, both infiltrating and resident macrophages contribute to ongoing injury. These cells have a mixed inflammatory and alternatively activated phenotype that may reflect failed resolution, potentially leading to tissue fibrosis and irreversible damage.

A further understanding of the renal inflammatory cells that mediate tissue injury and fibrosis should lead to new therapies to help preserve renal function in patients with lupus nephritis.