The role of renal Na+/H+ exchange in the regulation of acid-base and sodium homeostasis in premature infants

Early clinical studies on renal acidifying processes and sodium reabsorption in premature infants were revisited in the context of Na+/H+ exchangers (NHEs) and their developmental regulation. Relevant literature was analyzed to highlight the physiological and clinical significance of NHEs in controlling Na+/H+ exchange during kidney maturation. The immature kidney's low NHE capacity may lead to transient H+ retention, metabolic acidosis, sodium depletion, and late hyponatremia in premature infants. Sodium depletion excessively activates the renin-angiotensin-aldosterone system (RAAS), which stimulates NHE, reduces sodium loss, and mitigates late metabolic acidosis. Interestingly, NaCl supplementation suppresses systemic RAS activity while also preventing late metabolic acidosis, potentially through renal RAS-mediated NHE upregulation. Circulating and renal RAS may have distinct roles in regulating NHE activation and in maturity-related changes in sodium and acid-base homeostasis in premature infants. Key words Renal immaturity " Na+/H+ exchange " Hormonal regulation.