The global obesity epidemic has led to a 10-fold increase in the incidence of obesity-related chronic kidney disease, highlighting the need for improved understanding of its pathogenesis. Perirenal and pararenal fat capsules surround the kidneys and the thickness of these specific fat deposits is an independent predictor of chronic kidney disease in type-2 diabetes patients. Whilst visceral fat is well-known to promote inflammation in obesity, the role of pararenal and perirenal fat in renal inflammation is still unknown. Due to their close proximity to the kidneys, we hypothesize that pararenal and perirenal fat deposits directly cause renal inflammation and damage in obesity. Thus, we aimed to characterize perirenal, pararenal and renal inflammation in a diet-induced mouse model of obesity. Six-week-old male C57BL/6 mice were fed either normal chow (NC; n=12) or a high-fat diet (HFD; n=12) for 10 weeks. Compared with NC, the HFD resulted in greater bodyweight (38.4±1.1g vs. 29.4±0.6g), blood cholesterol (184±13mg/dL vs. 115±6mg/dL) and fasting blood glucose levels (12.3±0.6mmol/L vs. 9.7±0.3mmol/L) by the completion of the diet regimen (all P <0.05). Flow cytometry was used to enumerate immune cell populations in the blood, kidneys and surrounding (perirenal and pararenal) adipose. In HFD mice, the frequency of CD11b+ cells and inflammatory (Ly6CHi) monocytes was higher in the blood (34±2% vs. 26±2% and 15±1% vs. 8±1%), perirenal (37±5% vs. 19±5% and 8±1% vs. 4±1%) and pararenal fat (65±4% vs. 50±3% and 8±1% vs. 3±1%) than in NC mice (all P <0.05). This was associated with greater Ly6CHi monocyte infiltration in the kidneys from HFD mice ( P <0.05). Interestingly, renal neutrophils (Ly6G+) were more prevalent in HFD than NC mice (3.5±0.5% vs. 2.2±0.3%; P <0.05), but not in pararenal and perirenal adipose. Our data is the first to reveal similarities in the inflammatory cell profiles of blood, perirenal and pararenal adipose tissues and kidneys during obesity.