Table 2.

Pathogenesis of dyslipidemia due to immunosuppressive agents.

Immunosuppressive agents	Pathogenesis of dyslipidemia	Pattern of dyslipidemia
Steroids	Increases FFA synthetase	Increases plasma total cholesterol Increases plasma triglyceride Increases plasma VLDL Reduces plasma HDL
	Reduces LDL receptor
	Reduces lipoprotein lipase activity
Calcineurin inhibitors: TAC/ CsA	CsA inhibits mitochondrial 27-hydroxylase and increases HMGR activity	Increases plasma total cholesterol Increases VLDL Increases LDL Increases plasma TG
	CsA binds LDL receptor
	Increases hepatic lipase and reduces lipoprotein lipase
Sirolimus/ everolimus	Reduces hepatic lipase but increases lipase enzyme in adipocytesDownregulates peroxisome proliferator-activated receptor-γ 2 (PPAR-γ 2)	Increase total plasma total cholesterol Increases plasma TG Increases plasma LDL Increases ApoB-100

CsA, cyclosporine; FFA, free fatty acid; HDL, high-density lipoprotein; HMGR, 3 hydroxy - 3-methyl-glutaryl-CoA reductase; LDL, low-density lipoprotein; TAC, tacrolimus; TC, total cholesterol; TG, triglyceride; VLDL, very low-density lipoprotein.