CLCNKB and Hyponatremia: In this study, we identified four patients who had compound heterozygous variants or homozygous variants of the CLCNKB gene, including a novel nonsense variant c.239G > A (p.(Trp80*)), two splice site variants (c.1053-1G > A and c.1228-2A > G), a whole gene deletion and a novel synonymous variant c.228A > C. The clinical features present in our four patients are generally consistent with the pathophysiology found in Bartter syndrome, including hyponatremia, hypokalemia, hypochloremia, repeated vomiting and growth retardation.