Table 2.
Advantages and disadvantages of experimental CKD mice models
Pathology | Models | Advantages | Disadvantages | Reference |
---|---|---|---|---|
Renal mass reduction | 5/6 nephrectomy (rats) | Mimics the progressive renal failure; after loss of renal mass in human | Highly influenced by back ground strains; surgery requires | Ergur et al., 2015; He et al., 2012; Kim et al., 2009 |
Hypertension | SHR rats+UNX; angiotensin II infusion models | Highly relevant to hypertension nephropathy; useful to study AngII effect over kidney | Surgery requires; high cost; slow progression | Guo et al., 2015; Lankhorst et al., 2015; Zhong et al., 2016 |
Diabetic nephropathy | Streptozotocin mice/rats; NOD mice BB-DP rat; ob/ob mice db/db mice; DBA/2J mice; STZ-eNOS-/-; db/db-eNOS/ mice | Gene modified; commercially available; available on multiple strains | No ideal model to mimics; diabetic nephropathy; expensive; some strains are infertile | Betz & Conway, 2014; Graham & Schuurman, 2015; Kitada et al., 2016; Ostergaard et al., 2017 |
Primary glomerular nephropathy; focal segmental glomerulosclerosis | Adriamycin (rat, mice) models; Puromycin (rat) models | Widely used; induce podocyte injury | Highly depends on species and strains; toxic for most other cells | De Mik et al., 2013; Hakroush et al., 2014; Lee & Harris, 2011; Wada et al., 2016 |
Crescentic glomerulonephritis | Nephrotoxic nephritis model; anti-GBM nephritis model | Similar to human Crescentic glomerulonephritis | Single symptom; difficult to induce | Borza & Hudson, 2002; Cheungpasitporn et al., 2016 |
Membranous nephropathy | heymann nephritis rats; Cationic BSA mouse model | Widely used; identical pathology; marked proteinuria | Antigen (megalin) not found in human MN; limited experience | Cybulsky, 2011; Jefferson et al., 2010; Motiram Kakalij et al., 2016 |
IgA nephropathy | ddY mouse, HIGA mice Uteroglobin-deficient mice CD89-transgenic mouse |
Reproduces human pathology; multiple models available | Mild disease development usually without progression towards end-stage renal disease | Eitner et al., 2010; Papista et al., 2015; Suzuki et al., 2014 |
Secondary nephrotic syndrome; Amyloid A (AA) amyloidosis | Injection of chemical or biological compounds models | Widely used; reproduce features of human diseases | Rarely develop renal failure | Kisilevsky & Young, 1994; Teng et al., 2014 |
Systemic lupus erythematosus | NZB/NZW F1 mice MRL and CD95 mutants model |
Widely used; marked proteinuria | Incomplete features of SLE | Fagone et al., 2014; Nickerson et al., 2013; Otani et al., 2015 |
Hereditary nephritis; polycystic kidney disease; Alport syndrome | pkd1 or pkd2 gene engineered mouse; COL4A43 gene knockout mouse | Widely used and useful to study PKD; major model; develop proteinuria and renal failure | Kashtan & Segal, 2011; Ko & Park, 2013; Korstanje et al., 2014; Ryu et al., 2012 |