Sclerotic Lesions in the Glomeruli of Buffalo/Mna Rats

Abstract

Spontaneously developing focal and segmental glomerulosclerosis (FGS) in Buffalo/Mna rats was studied. There were no differences in the occurrence of the disease between male and female rats. Plasma macromolecules were detected in the urine samples of 2-month-old rats using sodium dodecyl sulphate polyacrylamide gel electrophoresis. All 4-month-old animals had proteinuria in excess of 30 mg/24 h. At the age of 4 months, sclerotic glomeruli were rarely observed. At the age of 6 months, all animals had a few sclerotic glomeruli in every kidney section examined. Animals which were 22 months old had sclerotic lesions in 37.8–52.1% of the glomeruli. Ultrastructural examination revealed that alterations in epithelial cells, such as effacement of foot processes, vacuolization, and a podocytic membrane-like structure, were found at the age of 2 months. The animals examined were neither uremic nor hypertensive. Our present study showed that female as well as male Buffalo/Mna rats had an earlier onset of the disease than the other strains of rats and that alterations in glomerular epithelial cells were first detected in the early stage of the disease.

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

“…At the age of 6 months, these animals had a few sclerotic glomeruli in all sections of kidney examined. At 22 months of age, about 37.8-52.1% of the glomeruli became sclerotic (82). These rats are suitable for use as animal models to investigate renal fibrosis in humans (23).…”

Recent advances of animal model of focal segmental glomerulosclerosis

“…Buffalo/Mna rats are a strain with a benign thymoma and the spontaneous development of proteinuria and nephrosclerosis [27]. The reason for the development of the FSGS-like lesions is not yet clear, but a circulating nephrotoxic factor in addition to aging and hypertension has been considered, because proteinuria had recurred after kidney transplantation from healthy Lewis rats.…”

Mapping genetic determinants of kidney damage in rat models

“…[19][20][21] Strain characteristics The normotensive 22 BUF rat strain develops spontaneous progressive proteinuria [23][24][25] in the nephrotic range, that is, 4150 mg per 24 h, 26 hypoproteinemia, 23 abnormal lipid metabolism, 23 structural renal lesions such as focal and segmental glomerulosclerosis (FSGS) and glomerular epithelial cell alterations with foot process effacement later in life. 22,23,25,[27][28][29] Both proteinuria and FSGS are not linked to the genetic susceptibility to develop spontaneous thymomas 21,25,27,30 …”