Spontaneous and age-related amyloidosis has been reported in C57BL/6J mice; however, the biochemical characteristics of age-related amyloidosis remain unclear. Therefore, we herein investigated the age-related prevalence of amyloidosis, the types of amyloid fibril proteins, and the effects of amyloid deposition on renal function in C57BL/6J mice. The results obtained revealed a high incidence of amyloidosis in C57BL/6J mice originating from the Jackson laboratory as well as the deposition of large amounts of amyloid in the glomeruli of aged mice. We identified the amyloid fibril protein in C57BL/6J mice as wild-type apolipoprotein A-II. We induced renal amyloid deposition in 40-week-old mice, equivalent to that of spontaneous development in 80-week-old mice, to rule out the effects of aging, and revealed subsequent damage to kidney function by amyloid deposits. Furthermore, amyloid deposition in the mesangial region decreased podocyte density, compromised foot processes, and led to the accumulation of fibroblast growth factor 2 (FGF2) in glomeruli. Collectively, these results suggest that AApoAII deposition is a general pathology in aged C57BL/6J mice and is dependent on supplier colonies. Therefore, the effects of age-related amyloid deposition need to be considered in research on aging in mice.