Urinary acidification in extremely low birth weight infants

Fluid and electrolyte balance in extremely preterm infants <24 weeks of gestation in the first week of life

“…One of the causative factors of metabolic acidosis in EPI is high HCO 3 − excretion rate in urine and the excessive total HCO 3 − excretion 16 . But said event was rapidly neutralized with postnatal days in the present study, although NH4 + excretion in urine has been demonstrated to remain at a low level until postnatal week 1 17 . In other words, impairment of HCO 3 − reabsorption was probably initially induced in the affected EPI between postnatal days 0 and 2, followed by metabolic acidosis, in which the major effect of excreting the endogenously generated acid as NH 4 + was incomplete 17 …”

“…Differences in fluid/electrolyte balance of EPI under highly humidified management were noted between appropriate‐for‐dates (AFD) and light‐for‐dates infants. Moreover, metabolic acidosis is easily induced in EPI due to their immature and thus underdeveloped renal functionality 3,5,16,17 …”

Parenteral Amino Acid and Metabolic Acidosis in Premature Infants

“…Sato and colleagues (13) showed that low birth weight infants have a higher urinary pH, higher fractional excretion of bicarbonate, and most importantly lower urinary ammonium excretion rate persisting even on days 4-6 after birth. They suggested that insufficiency of ammonium excretion was the main cause of metabolic acidosis in the early neonatal period (13). The reported pH in their study on day 4-6 (∼7.32), was significantly higher than that observed in the present study (∼7.24).…”

Effects of sodium bicarbonate correction of metabolic acidosis on regional tissue oxygenation in very low birth weight neonates

“…[1][2][3][4][5] NaHCO 3 infusions are occasionally used to address acid-base imbalances resulting from suspected renal bicarbonate wasting, a known consequence of renal tubular immaturity in preterm neonates. [6][7][8] Distinguishing this relatively benign pathophysiologic etiology of metabolic acidosis from other more serious causative mechanisms, including oxygen delivery/consumption imbalance, inherited metabolic diseases and/or possible iatrogenic causes is a central tenet of the clinical management of acid-base disturbances. Whether correction of renal acid-base imbalance confers measurable clinical benefits remains an area of active inquiry.…”

“…Whether correction of renal acid-base imbalance confers measurable clinical benefits remains an area of active inquiry. 2,3,5,[8][9][10] During the early neonatal period, metabolic acidosis in VLBW neonates may result in empiric clinical interventions such as volume expansion, packed red blood cell transfusion and/or vasopressor infusion prior to the firm establishment of a given pathophysiologic mechanism. [11][12][13] Should a diagnosis of renal tubular immaturity be clearly elucidated, these treatments would likely not represent best practices in this vulnerable patient population.…”