Renal Immaturity, Comorbidities and Outcomes in Neonatal Acute Kidney Injury

The kidneys of newborns are morphologically and physiologically different from those of children and adults. Embryonic kidney development begins at the 3rd week after conception and ends at 32-35 weeks prenatally, while in premature infants it continues for some time after birth. Neonatal kidney function is “immature”, due to high vascular resistance and low renal blood flow. Therefore, neonatal kidneys are particularly vulnerable to the effects of hypoperfusion. Predisposing factors for the occurrence of acute kidney injury (AKI) in newborns are certain clinical conditions such as prematurity, respiratory distress, sepsis, asphyxia, meconium aspiration, and congenital heart disease. Timely treatment of associated comorbidities reduces the risk of kidney injury in newborns. Diagnosing AKI in newborns is accompanied by certain difficulties due to the lack of blood samples for analysis, especially in premature babies, and variable glomerular filtration due to immaturity of renal function. Early detection of kidney injury provides an opportunity for timely and appropriate treatment, which leads to a better outcome and prognosis of the disease. Renal markers, especially NGAL, enable early diagnosis of AKI even in the first hours of its occurrence, when the disease is not clinically manifested. Due to the possibility of developing chronic kidney disease, monitoring of children at risk is necessary. Extremely premature babies and those with oliguric AKI are susceptible to neurocognitive disorders, anxiety and depression. Therefore, long-term multidisciplinary follow-up of children who manifested acute kidney injury in the neonatal period is warranted.