Renal dysfunction in heart failure (HF) involves congestion-associated injury, tubular damage, and inflammatory remodeling. Although SGLT2 inhibitors improve renal outcomes in HF, associated renal structural changes in nondiabetic HF remain incompletely characterized. Kidney samples from a previously published cohort of nondiabetic male Wistar rats with myocardial infarction-induced HF treated with empagliflozin (10 mg/kg/day) or vehicle for 4 weeks were analyzed histologically and by immunohistochemistry. Congestion-associated histological changes, tubular atrophy, tubular morphometric changes, CD68+ macrophages, CD206+ macrophages, and CD3+ T lymphocytes were evaluated. HF animals exhibited increased congestion-associated histological scores and tubular atrophy compared with sham controls. Empagliflozin was associated with lower congestion-associated scores in HF animals (median 1 [1] vs. 3.5 [3, 4], p = 0.0401) and reduced tubular atrophy (median 1 [0-1] vs. 3 [1-3.75], p = 0.0150). Empagliflozin did not reduce total CD68+ macrophage counts in HF animals, but was associated with increased CD206+ macrophage representation (9.0 ± 1.9 vs. 5.5 ± 1.6 cells/field, p = 0.0058), reduced CD3+ T-cell infiltration (12.0 ± 3.5 vs. 21.0 ± 8.0 cells/field, p = 0.0051), and increased tubular large-lumen profiles. Empagliflozin was associated with attenuation of congestion-associated histological changes, reduced tubular atrophy, tubular morphometric remodeling, and altered renal immune cell composition in nondiabetic HF.