BACKGROUND AND AIMS: Glomerular diseases are the third leading cause of kidney 
failure worldwide, behind only diabetes and hypertension. The molecular 
mechanisms underlying the cause of glomerular diseases are still largely 
unknown. The identification and characterization of new molecules associated 
with glomerular function should provide new insights into understanding the 
diverse group of glomerular diseases. The Chd2 protein belongs to a family of 
enzymes involved in ATP-dependent chromatin remodeling, suggesting that it 
likely functions as an epigenetic regulator of gene expression via the 
modification of chromatin structure.
METHODS: In this study, we present a detailed histomorphologic characterization 
of mice containing a mutation in the chromodomain helicase DNA-binding protein 2 
(Chd2).
RESULTS: We show that Chd2-mutant mice present with glomerulopathy, proteinuria, 
and significantly impaired kidney function. Additionally, serum analysis 
revealed decreased hemoglobin and hematocrit levels in Chd2-mutant mice, 
suggesting that the glomerulopathy observed in these mice is associated with 
anemia.
CONCLUSION: Collectively, the data suggest a role for the Chd2 protein in the 
maintenance of kidney function.