Mutant mice provide new insight into the role of (mis-)glycation in IgA nephropathy and other glomerular diseases.

In the 24 October 2006 issue of PNAS, Alexander and colleagues[1] describe the results of a systematic search for thrombocytopenicmice generated by large-scale mutagenesis. Amongst 3523 mice,one pedigree indeed exhibited 50% reduction in platelet counts.Apart from thrombocytopenia, the only other notable featureof these mice was prominent renal disease (albuminuria/proteinuria,glomerulosclerosis and tubulointerstitial inflammatory infiltration)leading to uraemia and death at around 200 days after birth.This renal disease was not immune mediated, since it persistedin mutant mice crossed to