Hypoxic–ischemic encephalopathy (HIE) is a critical neonatal condition for which therapeutic hypothermia (TH) remains the cornerstone of neuroprotective intervention. Clinical observations and prior studies note that electrolyte imbalances—particularly hyponatremia and hypokalemia—frequently emerge during TH. Therefore, this study explores how activation of the renin–angiotensin–aldosterone system (RAAS) may contribute to sodium (Na) and potassium (K) disturbances in asphyxiated neonates receiving TH. In this prospective study, 38 newborns with HIE treated with TH and 21 healthy term newborns were enrolled. Serum renin, aldosterone, Na, K, and urinary electrolyte levels were measured at 24, 48, and 72 hours postnatally. Receiver operating characteristic analyses assessed the diagnostic performance of renin and aldosterone. Renin and aldosterone levels were significantly elevated in the TH group compared with controls ( p < 0.05). Serum sodium levels were consistently lower at all time points ( p = 0.001), while potassium levels were significantly reduced at 24 and 72 hours ( p < 0.05). Fractional excretion of sodium was increased at 24 hours, and potassium excretion remained elevated throughout the TH period ( p < 0.05). Among the biomarkers, aldosterone demonstrated excellent diagnostic performance at 24 hours (AUC = 0.919). Activation of the RAAS is evident in asphyxiated neonates undergoing TH, with aldosterone playing a pivotal role in electrolyte disturbances. These results highlight the clinical importance of vigilant monitoring and timely correction of serum sodium and potassium levels during the hypothermia protocol.
Baştuğ et al. (Fri,) studied this question.