Hyperoxaluria results from either inherited disorders of glyoxylate metabolism leading to hepatic oxalate overproduction (primary hyperoxaluria), or increased intestinal oxalate absorption (secondary hyperoxaluria). Hyperoxaluria may lead to urinary supersaturation of calcium oxalate and crystal formation, contributing to urolithiasis and deposition of calcium oxalate crystals in the kidney parenchyma, leading to oxalate nephropathy.

Establishment of oxalate diet induced oxalate nephropathy mouse model

Experimental animal: C57BL/6, 6-8 weeks old, male

Oxalate diet induced oxalate nephropathy

Fig.1 Serum urea nitrogen (UREA) and creatinine (CREA) were measured on  Day 7,14 and 21. Values represent as  means ± SEM, n=6, **P ＜0.01 and ***P ＜0.001 vs. Control group.

Fig.2 Representative pictures of HE, Masson, CD3, F4/80 and α-SMA staining showing increased crystal formation, inflammatory cell infiltration and interstitial fibrosis of Oxalate group. Scale bar: 100 μm.

5/6 nephrectomy produced high perfusion and filtration pressure to the remaining nephrons of mice. The residual nephrons were further destroyed, thus leading to chronic kidney disease characterized by sclerosis and hypertrophy of glomeruli.

Establishment of 5/6 nephrectomy-induced  chronic kidney disease

5/6 nephrectomy-induced  chronic kidney disease in Balb/c mice

Fig.3 5/6 nephrectomy produced chronic kidney injury in mice. Mice received 5/6 nephrectomy or sham surgery 1 week before experiment. Blood was collected at week 5, 8 and 12. At the end of experiment, kidney tissues were collected for Masson staining. 5/6 nephrectomy produced a significant increase in creatinine (A) and urea (B) in serum. Pathology of Masson staining (C) showed that there were glomerular hypertrophy, sclerosis, and obvious fibrosis in the kidney of 5/6 Nephrectomy mice.

5/6 nephrectomy-induced  chronic kidney disease in C57BL/6 mice

Fig.4 5/6 nephrectomy produced chronic kidney injury in mice. Mice received 5/6 nephrectomy or sham surgery 1 week before experiment. Blood was collected on week 0, 2, 4, 6 and 8. At the end of experiment, kidney tissues were collected for Masson staining. 5/6 nephrectomy produced an significant increase in creatinine (A) and urea (B) contention. Pathology of Masson staining (C) showed that there were glomerular hypertrophy, sclerosis, and obvious fibrosis in the kidney of 5/6 Nephrectomy mice.