Skip to main content
editorial
. 2019 Jun 21;30(7):1139–1141. doi: 10.1681/ASN.2019040373

Table 1.

Mouse models with an IgA nephropathy–like disease manifestation

Model Glomerular IgA Deposits (Species) Total IgA Levels in Blood GFR Proteinuria Hematuria Glomerular Pathology
Present study1
 AID wild-type mice ++ (Human) ↑ about fivefold Normal None None Mild mesangial expansion and C3 deposition
 AID-deficient mice +++ (Human) ↑ about 50-fold Reduced None None Mesangial expansion and C3 deposition
Mice expressing human IgA1 and CD89 +++ (Human) ↑ >100-fold Mildly reduced + ++ Mesangial expansion and C3 deposition
High-IgA mice +++ (Mouse) ↑ up to fourfold Reduced + None Mesangial expansion and C3 deposition
β-1,4-galactosyl-transferase–deficient mice ++ (Mouse) ↑ up to tenfold No data ++ + Mesangial expansion and C3 deposition
CD37-deficient mice +++ (Mouse) ↑ up to 15-fold Normal None None Mesangial expansion and hypercellularity; no data on C3
BAFF transgenic mice +++ (Mouse) ↑ up to 50-fold ESRD at 17 mo ++ +++ Mesangial matrix expansion; no data on C3; little C4
Uteroglobin-deficient mice +++ (Mouse) No data No data No data +++ Mesangial matrix expansion and C3 deposition
LIGHT transgenic mice +++ (Mouse) ↑ 30- to 40-fold No data ++ + Mesangial matrix expansion and C3 deposition
MBP20 peptide fusion protein +++ (Mouse) No data No data (+) ++ Mesangial matrix expansion and proliferation and C3 deposition
Monoclonal IgA from Peyer patch hybridomas of vomitoxin-exposed mice ++ (Mouse) ↑ two- to four-fold No data No data + Normal mesangium, C3 deposition

AID, activation-induced cytidine deaminase. Modified from ref. 9, with permission.