Withdrawn as duplicate: Expanding the phenotypic spectrum of Kenny-Caffey syndrome: a case series and systematic literature review.

This article has been withdrawn due to a publisher error that caused it to be duplicated. The definitive version of this article is published under https://doi.org/10.

SLC41A1 knockout mice display normal magnesium homeostasis.

Transcellular Mg reabsorption in the distal convoluted tubule (DCT) of the kidneys plays an important role in maintaining systemic Mg homeostasis. SLC41A1 is a Na/Mg exchanger that mediates Mg efflux from cells and is hypothesized to facilitate basolateral extrusion of Mg in the DCT. In this study, we generated a SLC41A1 knockout mouse model to examine the role of SLC41A1 in Mg homeostasis.

FAM111A is dispensable for electrolyte homeostasis in mice.

Autosomal dominant mutations in FAM111A are causative for Kenny-Caffey syndrome type 2. Patients with Kenny-Caffey syndrome suffer from severe growth retardation, skeletal dysplasia, hypoparathyroidism, hypocalcaemia, hyperphosphataemia and hypomagnesaemia. While recent studies have reported FAM111A to function in antiviral response and DNA replication, its role in regulating electrolyte homeostasis remains unknown.

Circadian Potassium Excretion is Unaffected Following Furosemide Induced Increase in Sodium Delivery to the Distal Nephron.

The mineralocorticoid aldosterone is widely accepted as a key regulator of K+ balance as well as urinary K+excretion. However, recent evidence suggests that the circadian control of K+ excretion is independent of aldosterone. Thedelivery of Na+ to the distal nephron is known to be an important determinant of aldosterone mediated secretion of K+ in thissegment of the nephron.