Table 1.

Examples of changes in the overall pattern of DNA methylation or histone modifications during kidney disease.

Epigenetic modification	Overall levels in kidney	Reference
DNA methylation (-CH3):	Overall increase in: peripheral blood leukocytes from inflamed CKD G5 patients kidney in RASAL1 genes in mouse model of folic acid-induced fibrosis kidney in Klotho gene in mouse model of adenine-induced CKD	(Hunag et al., 2012; Ko et al., 2013; Zhao et al., 2017)
	Overall decrease in: kidney in experimental AKI induced by IRI kidney in tubules of CKD patients	(Stenvinkel et al., 2017; Bechtel et al., 2010; Zhang et al., 2017)
Histone methylation (Km, Rm, -CH3):	Overall increase in: kidney in experimental renal fibrosis induced by UUO kidney in diabetic nephropathy in uninephrectomy db/db mice	(Sayyed et al., 2010; Zhou et al., 2016; Hewitson et al., 2017)
	Overall decrease in: kidney in db/db mice kidney in uninephrectomy C57BL/6 mice	(Sayyed et al., 2010)
Histone acetylation (Kac, -CO-CH3):	Overall increase in: kidney in experimental AKI-CKD transition induced by IRI kidney in experimental renal fibrosis induced by UUO kidney in diabetic nephropathy in uninephrectomy db/db mice	(Sayyed et al., 2010; Zager et al., 2011; Hewitson et al., 2017)
	Overall decrease in: kidney: early decrease in severe IRI AKI, and recovery during reperfusion kidney in db/db mice	(Marumo et al., 2008; Sayyed et al., 2010)
Histone crotonylation (Kcr, -CO-CH=CH-CH3)	Overall increase in: kidney in experimental nephrotoxic AKI by folic acid Changes in specific histones peripheral blood mononuclear cells from IgA nephropathy patients: increased (HIST1H2AC, HIST1H4A, and decreased HIST1H1B)	(Ruiz-Andres et al., 2016; Lin et al., 2020)

In parenthesis, modified amino acid (K, lysine; R, arginine) and the residue added.

AKI, acute kidney injury; CKD, chronic kidney disease; Kcr, crotonylation; IRI, ischemia-reperfusion injury; UUO, unilateral ureteral obstruction.