| Models (Ref) | Strains | Defects | Phenotypic alterations | Kidney pathology |
| NOD mouse [10, 28–32]
| Inbred line derived from ICR (outbred line) | Autoimmune insulitis caused by polygenes including specific MHC class II alleles and many non-MHC loci | T1DM, hyperglycemia, albuminuria, autoimmune insulitis, and other autoimmune manifestations | Related reports are few, enlarged glomeruli, and mesangial sclerosis |
| Insulin-2 Akita mouse [10, 18, 33]
| C57BL/6, C3H | Autosomal dominant mutation in the Ins-2 gene causes misfolding of insulin protein | T1DM, hyperglycemia, and modest levels of albuminuria | Increased mesangial matrix, GBM thickening, and no mesangiolysis or widespread marked or nodular mesangial sclerosis |
| db/db mouse [10, 20, 33–37]
| C57BL/6, C57BLKS, DBA, FVB, CBA | G-to-T mutation in the gene coding the leptin receptor (db/db) | T2DM, hyperglycemia, obesity,and albuminuria | Glomerular hypertrophy, mesangial matrix expansion, GBM thickening, and no mesangiolysis or nodular mesangial sclerosis |
| OLETF rat [38–40] | Long-Evans | Poor pancreatic proliferation caused by multiple genes including several QTLs and the gene encoding CCKAR | T2DM, mild obesity, late-onset hyperglycemia, macroalbuminuria, hypertension, and dyslipidemia | Glomerular hypertrophy, GBM thickening, extracellular matrix expansion, nodular lesions, diffuse glomerulosclerosis, and severe tubulointerstitial fibrosis |
| GK rat [41–45] | Wistar | Pancreatic beta-cell deficit caused by polygenes | T2DM, hypertension, moderate hyperglycemia, albuminuria, nonobesity, nonhyperlipidemia | Glomerular hypertrophy and GBM thickening by 35 weeks; segmental glomerulosclerosis and tubulointerstitial fibrosis at 24 months of age |
| BTBR ob/ob mouse [46–48] | BTBR | ob/ob
mutation (a recessive mutation in the gene coding leptin) in BTBR strain | T2DM, severe hyperglycemia, pancreatic islet hypertrophy, macroalbuminuria, hypercholesterolemia, elevated triglycerides, obesity, and decreased GFR | Glomerular hypertrophy, mesangial matrix expansion, GBM thickening, loss of podocytes, diffuse mesangial sclerosis (focally approaching nodular glomerulosclerosis), focal mild interstitial fibrosis, focal arteriolar hyalinosis, and mesangiolysis |
| NZO mouse [10, 49] | NZO | Obesity/diabetes caused by polygenes including QTLs on chromosomes 1, 2, 4, 5, 6, 7, 11, 12, 13, 15, 17, and 18 | T2DM, obesity, hyperglycemia, albuminuria, low-titer IgM antibodies to the insulin receptor, and susceptibility to lupus nephritis | Glomerular proliferation, mesangial deposits, mild GBM thickening, glomerulosclerosis, eosinophilic nodules in some glomeruli, occasional hyalinization of the glomerular arterioles, and healing arteriolar inflammation |
| KK-Ay mouse [10, 50–53]
| KK, C57BL, C3H, FVB | Yellow/obese/diabetic phenotype caused by polygenes including dominant mutation in agouti yellow (Ay) gene | T2DM, hyperglycemia, obesity, albuminuria, hypertriglyceridemia, and obstructive uropathy | Glomerular hypertrophy, mild and moderated mesangial matrix expansion, and segmental proliferative glomerular nephritis |
| ZDF rat [54–62]
| Zuker | Missense mutation in the gene coding the leptin receptor (fa/fa) | T2DM, hyperglycemia, obesity, hyperlipidemia, hypertension, and macroalbuminuria | mesangial expansion, focal segmental glomerulosclerosis, macrophage infiltration, and interstitial fibrosis |
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