Ammonium alginate suppresses disease progression exacerbated by salt loading in mouse model of unilateral ureteral obstruction

Chronic kidney disease (CKD) particularly increases the risk of dialysis, cerebral infarction, cardiovascular disease, and renal fibrosis and poses a major challenge to patient quality of life and healthcare economics. Excessive salt intake increases the risk of developing various chronic diseases such as hypertension, stroke, and CKD. We recently showed that ammonium alginate (AAL) salt exhibits the “salt excretion effect” where it suppresses the increase in blood sodium concentration and promotes sodium excretion in the feces of healthy mice after salt overloading. In this study, we investigated the effect of AAL-induced salt excretion on renal fibrosis progression during salt overloading in mice model established through unilateral ureteral obstruction (UUO). We found that AAL administration significantly suppressed the increase in urinary salt concentration caused by salt loading. It also suppressed renal fibrosis and expression of renal inflammation- and fibrosis-related factors aggravated by salt loading. These findings suggest that AAL-mediated salt removal inhibits salt loading-exacerbated progression of inflammation and fibrosis in UUO mice. Therefore, as a natural polysaccharide with food and pharmaceutical applications, the use of AAL can be further explored to mitigate adverse effects of salt loading in patients with renal inflammation and fibrosis, such as those with CKD. • Ammonium alginate (AAL) suppresses the increase in urinary salt concentration. • AAL attenuates the renal fibrosis and renal-inflammation caused by salt loading. • AAL inhibits the progression of the renal fibrosis and renal-inflammation by salt loading.