Rehmana Waris

1 Introduction Aldosterone, a mineralocorticoid hormone, primarily controls electrolyte balance and intravascular volume by influencing the distal nephron. It increases sodium reabsorption and promotes potassium excretion in urine by indirectly enhancing the activity of the epithelial sodium channel and sodium-potassium ATPase. When there is a deficiency of aldosterone, these regulatory processes are disrupted, leading to hyponatremia, hypovolemia, and hyperkalemia [1].

CONFLICT OF INTEREST STATEMENT The authors declare no conflicts of interest. REFERENCES 1, . Review: pathogenesis of cholestatic liver diseases. World J Hepatol. 2020; 12(8): 423-435. 2, , , et al. Recessive mutations in KIF12 cause high gamma-glutamyltransferase cholestasis. Hepatol Commun. 2019; 3(4): 471-477. 3, , , et al. KIF12 variants and disturbed hepatocyte polarity in children with a phenotypic spectrum of cholestatic liver disease. J Pediatr. 2022; 240: 284-291. 4, , , et al.