Phosphate metabolism in red blood cells of critically ill neonates

Abstract

Very few data exist on phosphate metabolism in critically ill neonates. Therefore we studied the incidence of hypophosphataemia, the intracellular metabolism of phosphate by measuring adenosine 5'-triphosphate (ATP) and 2,3-diphosphoglycerate (2,3-DPG) in red blood cells, and excretion of phosphate in urine. The aims of the study were early detection of changes in phosphate metabolism as possible diagnostic markers of sepsis and defining the cause of hypophosphataemia. Neonates, treated in multidisciplinary paediatric intensive care unit (PICU), included in the study, were less than three days of age. Eighteen of them had respiratory distress syndrome (RDS) and 16 had microbiologically confirmed or clinical sepsis. The overall incidence of hypophosphataemia in critically ill neonates was over 80%, and was more common (88%) and more profound in those with sepsis than in those with RDS (79%). Therefore the septic neonates needed significantly larger amounts of phosphate to maintain normophosphataemia. In septic neonates ATP concentration in red blood cells was significantly lower than in neonates with RDS and controls, while the 2,3-DPG concentration was increased as a result of compensation. In septic neonates urinary losses of inorganic phosphate (Pi) were significantly higher than in neonates with RDS. Hypophosphataemia in critically ill neonates is at least partly due to higher urinary losses of phosphate.

Changes in red cell phosphate metabolism of preterm and fullterm infants with perinatal problems during their first month of life

“…Thereafter they appear to catch up with the controls both for ATP and 2,3-DPG up to the first month of life. Concerning the ATP levels, Kalan et al [12] reported them to be lower in their patients, which is in agreement with our results. In our study this occurred during the first days of life when the problem was in progress.…”

“…The renal tubular reabsorption of phosphate (TRP) was slightly lower in the preterms with problems in the second half of the month which explains the lower PlPi during the same period. It has been reported that in critically ill neonates hypophosphatemia is partly due to higher urinary losses of phosphate [12]. However, the hypophosphatemia and urinary phosphate excretion in the RDS neonates, according to the same authors, was milder than in the neonates with sepsis.…”

Hypophosphatemia in meningococcal sepsis

“…In the study of Kalan et al [8], however, the neonates included were less than 3 days of age [mean age (€SD) 21 (€18) h]. At this very young age, inappropriate phosphate intake is less likely to account for the hypophosphatemia.…”

“…Internal redistribution seems more likely than renal loss or inadequate intake of phosphate, since hypophosphatemia, with the exception of neonates, resolves quickly and with no phosphate supplementation in the majority of cases. However, in view of previous reports [8], further studies are needed to elucidate the role of the kidneys, if any, in the regulation of serum phosphate levels during acute infection.…”

“…Kalan et al [8] reported increased urinary loss of phosphate in septic neonates. An increased parathyroid hormone secretion was found in critically ill adult patients, some with septicemia, but was not associated with hypophosphatemia or changes in urinary calcium excretion [9].…”