Dietary sodium modulates nephropathy in Nedd4-2-deficient mice.

ABSTRACT: Salt homeostasis is maintained by tight control of Na⁺ filtration and reabsorption. In the distal part of the nephron the ubiquitin protein ligase Nedd4-2 regulates membrane abundance and thus activity of the epithelial Na⁺ channel (ENaC), which is rate-limiting for Na⁺ reabsorption. Nedd4-2 deficiency in mouse results in elevated ENaC and nephropathy, however the contribution of dietary salt to this has not been characterized. In this study we show that high dietary Na⁺ exacerbated kidney injury in Nedd4-2-deficient mice, significantly perturbing normal postnatal nephrogenesis and resulting in multifocal areas of renal dysplasia, increased markers of kidney injury and a decline in renal function. In control mice, high dietary Na⁺ resu

SUBMITTER: Manning JA 

PROVIDER: S-EPMC7244563 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature