Chronic kidney disease features chronic inflammation and fibrosis, both of which contribute to and are exacerbated by arterial hypertension. The contribution of immune responses to renal sodium retention has received intense scrutiny. In this regard, the article by Furusho et al. details a mechanism wherein intrarenal TNFα augments salt-sensitive hypertension during CKD via activation of the WNK1-SPAKNCC phosphorylation cascade.
