Respiratory distress syndrome (RDS) is the most common respiratory disorder of premature newborns and its incidence is directly proportional to the degree of prematurity (Monica et al., 2017).It is caused primarily by deficiency of pulmonary surfactant in an immature lung (Johansson and Curstedt, 2019).
Neonates with RDS are at increased risk of acute kidney injury (AKI) due to exposure to hypoxia, acidosis, hypovolemia, vasopressors and mechanical ventilation (Jetton et al., 2016).
AKIis a complex disorder with clinical manifestations ranging from mild dysfunction to anuric kidney failure. It is an important contributing factor to the morbidity and mortality of critically ill neonates(Macedo et al., 2018).The incidence of AKI ranges between 6 and 24% of the neonatal intensive care unit (NICU) admissions (Sethi et al., 2020).
The diagnosis of AKI is problematic, as current diagnosis depends on serum creatinine as a marker of estimated glomerular filtration rate and oliguria. Both are late consequences of injury and are not markers of the injury itself (Katariya et al, 2019).
The serum creatinine use in the neonatal period is associated with some limitations. During the first 48–72 h of life, neonatalserum creatinine still reflects maternal levels and these values may declineat varying rates over days, depending on gestational age. Moreover, serum creatinine concentrations may not change until 25–50%of the kidney function has already been lost and at lower GFR, serum creatinine will overestimaterenal function due to tubular secretion of serum creatinine. Serum creatinine varies by muscle mass, hydration state, age and gender (Zhang et al, 2019).
Early diagnosis of AKI helps in timely intervention to have favorable outcome. Given the importance of the early diagnosis and treatment of AKI, there has been much recent focus on the discovery of novel biomarkers.These novel biomarkers include serum cystatin C, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 and others(Cruzado et al., 2015).
Serum cystatin C (sCysC) which is a low molecular mass protein of the cystatin family is a protease inhibitor, produced at a constant rate in all nucleated cells, freely filtrated through the glomerular membrane, completely reabsorbed and degraded by the proximal tubule (Glogauer et al., 2018).
Serum cystatin does not appear to be affected by body muscle mass, age, gender, inflammatory state, or nutritional conditions and does not cross the placental barrier like creatinine (Treiber et al., 2014).
Serum cystatin C has all the theoretical properties needed to be an ideal marker of renal function. It can be used to determine renal function in sick Neonates.Serum cystatin C could detect AKI earlier than serum creatinine in premature neonates with RDS (Elmas et al., 2013).