Changes of Renal Lesion-Related Parameters in FGS/Nga and the Parental Mouse Strains, CBA/N and RFM/Nga

• Published in: Experimental Animals Vol. 53; no. 2; pp. 97 - 102
• Main Authors: KIM, Eun-Hee, CHOI, Kwang-Soo, LEE, Kang-Wook, SUH, Jun-Gyo, CHOI, Yang-Kyu, HYUN, Byung-Hwa, ISHIKAWA, Akira, NAMIKAWA, Takao, LEE, Chul-Ho
• Format: Journal Article
• Language: English
• Published: Japan Japanese Association for Laboratory Animal Science 01-04-2004
• Subjects: animal model; Animals; Blood Pressure; Blood Proteins - metabolism; Blood Urea Nitrogen; Body Weight; Creatine - blood; Disease Models, Animal; focal glomerular sclerosis (FGS); Glomerulosclerosis, Focal Segmental - genetics; Glomerulosclerosis, Focal Segmental - metabolism; Glomerulosclerosis, Focal Segmental - pathology; Kidney Glomerulus - pathology; Mice; Mice, Mutant Strains; mouse; proteinuria; Proteinuria - metabolism; Serum Albumin
• ISSN: 1341-1357; 1881-7122
• DOI: 10.1538/expanim.53.97

The FGS/Nga mouse strain, established from an outcross between CBA/N and RFM/Nga mice strains, has previously been reported as a spontaneous mouse model for focal glomerular sclerosis (FGS) and is considered to have two pairs of autosomal recessive genes associated with FGS. In this study, we examined the changes of seven renal lesion-related parameters, blood urea nitrogen (BUN), creatinine, albumin and total protein in plasma, urinary protein, systolic blood pressure, and a glomerulosclerosis index on histological observation, in 20-week-old FGS/Nga mice and their age-matched two parental strains, CBA/N and RFM/Nga. The levels of plasma BUN and creatinine, urinary protein and systolic blood pressure were significantly increased in FGS/Nga, compared with those of the parental strains. RFM/Nga mice showed slightly elevated levels of all biochemical makers. In histological analysis, a higher glomerulosclerosis index was observed in FGS/Nga than the two parental strains. RFM/Nga mice appeared to have slight sclerotic lesions of glomeruli, but no renal failure was observed in CBA/N mice. These results suggest that at least one mutant gene that causes the progression of renal lesion in FGS/Nga mice is derived from RFM/Nga.