In a recent study by our group, targeted disruption of Cd40 in a model of salt-sensitive hypertension in rats (Dahl S) resulted in attenuated hypertensive renal dysfunction, characterized by decreased renal fibrosis, enhanced creatinine clearance, and reduced tubular injury, despite being just as hypertensive as the Dahl S wild-type [88]. Here, CD40 is linked to renal fibrosis.