Neonatal Kidney Research Articles

Association between inequalities in human resources for health and all cause and cause specific mortality in 172 countries and territories, 1990-2019: observational study

ObjectiveTo explore inequalities in human resources for health (HRH) in relation to all cause and cause specific mortality globally in 1990-2019.DesignObservational study.Setting172 countries and territories.Data sourcesDatabases of the Global Burden...

Acute kidney injury decreases pulmonary vascular growth and alveolarization in neonatal rat pups.

Acute kidney injury (AKI) is common in sick neonates and associated with poor pulmonary outcomes, however, the mechanisms responsible remain unknown. We present two novel neonatal rodent models of AKI to investigate the pulmonary effects of AKI. In rat pups, AKI was induced surgically via bilateral ischemia-reperfusion injury (bIRI) or pharmacologically using aristolochic acid (AA). AKI was confirmed with plasma blood urea nitrogen and creatinine measurements and kidney injury molecule-1 staining on renal immunohistochemistry. Lung morphometrics were quantified with radial alveolar count and mean linear intercept, and angiogenesis investigated by pulmonary vessel density (PVD) and vascular endothelial growth factor (VEGF) protein expression. For the surgical model, bIRI, sham, and non-surgical pups were compared. For the pharmacologic model, AA pups were compared to vehicle controls. AKI occurred in bIRI and AA pups, and they demonstrated decreased alveolarization, PVD, and VEGF protein expression compared controls. Sham pups did not experience AKI, however, demonstrated decreased alveolarization, PVD, and VEGF protein expression compared to controls. Pharmacologic AKI and surgery in neonatal rat pups, with or without AKI, decreased alveolarization and angiogenesis, producing a bronchopulmonary dysplasia phenotype. These models provide a framework for elucidating the relationship between AKI and adverse pulmonary outcomes. There are no published neonatal rodent models investigating the pulmonary effects after neonatal acute kidney injury, despite known clinical associations. We present two novel neonatal rodent models of acute kidney injury to study the impact of acute kidney injury on the developing lung. We demonstrate the pulmonary effects of both ischemia-reperfusion injury and nephrotoxin-induced AKI on the developing lung, with decreased alveolarization and angiogenesis, mimicking the lung phenotype of bronchopulmonary dysplasia. Neonatal rodent models of acute kidney injury provide opportunities to study mechanisms of kidney-lung crosstalk and novel therapeutics in the context of acute kidney injury in a premature infant.

Neonatal nephrotoxic medication exposure and early acute kidney injury: results from the AWAKEN study.

We aimed to describe nephrotoxic medication exposure and investigate associations between exposure and acute kidney injury (AKI) in the neonatal intensive care unit during the first postnatal week. Secondary analysis of the AWAKEN cohort. We evaluated nephrotoxic medication exposure during the first postnatal week and associations with AKI using time-varying Cox proportional hazard regressions models.Nephrotoxic medication exposure categories were defined as: no nephrotoxic medication, nephrotoxic medications excluding aminoglycosides, aminoglycoside alone, and aminoglycoside and another nephrotoxic medication. Of 2162 neonates, 1616 (74.7%) received ≥1 nephrotoxic medication. Aminoglycoside receipt was most common (72%). AKI developed in 211(9.8%) neonates and was associated with a nephrotoxic medication exposure (p < 0.01). Nephrotoxic medicationexposures including a nephrotoxic medication excluding aminoglycoside (aHR 3.14, 95% CI 1.31-7.55) and aminoglycoside and another nephrotoxic medication (aHR 4.79, 95% CI 2.19-10.50) were independently associated with AKI and severe AKI (stage 2/3), respectively. Nephrotoxic medication exposure in critically ill infants is common during the first postnatal week. Specific nephrotoxic medication exposure, principally aminoglycosides with another nephrotoxic medication, are independently associated with early AKI.

Neonatal acute kidney injury during indomethacin therapy: does it predict ductal closure?

Preterm newborns are at risk for patent ductus arteriosus, and non-steroidal anti-inflammatory drugs are often used to facilitate patent ductus arteriosus closure. Acute kidney injury is common in critically ill neonates and may be caused by non-steroidal anti-inflammatory drugs. We sought to describe the incidence of acute kidney injury among preterm infants receiving indomethacin and determine whether acute kidney injury during indomethacin therapy is associated with subsequent patent ductus arteriosus closure. Retrospective cohort including neonates < 33weeks gestational age, admitted to two level IIIb neonatal intensive care units between November 2016 and November 2019, who received indomethacin in the first 2 weeks of life. Acute kidney injury in the 7-day period after treatment was defined by neonatal modified Kidney Disease Improving Global Outcomes (KDIGO) criteria. Patent ductus arteriosus closure was defined clinically and/or via echocardiogram. Clinical characteristics were extracted from medical records. Association between acute kidney injury during treatment and successful closure of patent ductus arteriosus was evaluated using chi-square tests and logistic regression. One hundred fifty preterm infants were included; acute kidney injury occurred in 8% (all KDIGO Stage 1). Patent ductus arteriosus closed in 52.9% of the non-acute kidney injury group and 66.7% of the acute kidney injury group (p = 0.55). Serum creatinine was checked a mean of 3.1 times in the acute kidney injury group and 2.2 times in the non-acute kidney injury group. There was no difference in survival. We found no association between acute kidney injury during indomethacin therapy and patent ductus arteriosus closure. Paucity of serum creatinine values likely underdiagnosed acute kidney injury. Surveillance of kidney function during indomethacin therapy using more sensitive renal biomarkers may better identify infants who develop acute kidney injury in the context of non-steroidal anti-inflammatory drug use.

Editorial introduction

Editorial introduction

Gut microbiota and neonatal acute kidney injury biomarkers.

One of the most frequent issues in newborns is acute kidney injury (AKI), which can lengthen their hospital stay or potentially raise their chance of dying. The gut-kidney axis establishes a bidirectional interplay between gut microbiota and kidney illness, particularly AKI, and demonstrates the importance of gut microbiota to host health. Since the ability to predict neonatal AKI using blood creatinine and urine output as evaluation parameters is somewhat constrained, a number of interesting biomarkers have been developed. There are few in-depth studies on the relationships between these neonatal AKI indicators and gut microbiota. In order to gain fresh insights into the gut-kidney axis of neonatal AKI, this review is based on the gut-kidney axis and describes relationships between gut microbiota and neonatal AKI biomarkers.

Association of intrauterine growth restriction and low birth weight with acute kidney injury in preterm neonates.

Preterm birth alters nephrogenesis and reduces the total nephron number. Intrauterine growth restriction (IUGR) seems to worsen nephron loss, but only a few studies have investigated its role in neonatal kidney impairment. We investigated whether IUGR, defined as reduced estimated fetal growth and/or placental flow alterations and low birth weight z-score, increases the risk of developing acute kidney injury (AKI) in very preterm infants. We performed a retrospective study including infants born with a birth weight (BW) ≤ 1500g and/or gestational age (GA) ≤ 32weeks admitted to our center between January 2016 and December 2021. Neonatal AKI was defined according to the neonatal KDIGO classification based on the decline of urine output and/or creatinine elevation. We used multivariable linear regressions to verify the association between AKI and GA, BW z-score, IUGR definition, and hemodynamically significant patent ductus arteriosus (PDA). We included 282 infants in the analysis, with a median (IQR) GA = 29.4 (27.4, 31.3) weeks, BW = 1150 (870, 1360) g, and BW z-score = - 0.57 (- 1.64, 0.25). AKI was diagnosed in 36 (13%) patients, and 58 (21%) had PDA. AKI was significantly associated with BW z-score (beta (std. error) = - 0.08 (0.03), p = 0.008) and severe IUGR (beta (std. error) = 0.21 (0.08), p = 0.009), after adjusting for GA and PDA. Our data suggest that low BW z-score and IUGR could represent adjunctive risk factors for kidney impairment in preterm babies. A higher resolution version of the Graphical abstract is available as Supplementary information.

Current and potential methods to assess kidney structure and morphology in term and preterm neonates.

After birth, the kidney structure in neonates adapt to the functional demands of extrauterine life. Nephrogenesis is complete in the third trimester, but glomeruli, tubuli, and vasculature mature with the rapidly increasing renal blood flow and glomerular filtration. In preterm infants, nephrogenesis remains incomplete and maturation is slower and may be aberrant. This structural and functional deficit has life-long consequences: preterm born individuals are at higher risk for chronic kidney disease and arterial hypertension later in life. This review assembles the literature on existing and potential methods to visualize neonatal kidney structure and morphology and explore their potential to longitudinally document the developmental deviation after preterm birth. X-rays with and without contrast, fluoroscopy and computed tomography (CT) involve relevant ionizing radiation exposure and, apart from CT, do not provide sufficient structural details. Ultrasound has evolved into a safe and noninvasive high-resolution imaging method which is excellent for longitudinal observations. Doppler ultrasound modes can characterize and quantify blood flow to and through the kidneys. Microvascular flow imaging has opened new possibilities of visualizing previously unseen vascular structures. Recent advances in magnetic resonance imaging display renal structure and function in unprecedented detail, but are offset by the logistical challenges of the imaging procedure and limited experience with the new techniques in neonates. Kidney biopsies visualize structure histologically, but are too invasive and remain anecdotal in newborns. All the explored methods have predominantly been examined in term newborns and require further research on longitudinal structural observation in the kidneys of preterm infants.

463 - Recurrent neonatal acute kidney injury: Incidence, predictors, and outcomes in the neonatal intensive care unit

463 - Recurrent neonatal acute kidney injury: Incidence, predictors, and outcomes in the neonatal intensive care unit

Food Insecurity Is Associated With an Increased Risk of Neonatal Acute Kidney Injury and Abnormal Kidney Function

Background: Prenatal food insecurity (FI) negatively affects both maternal and infant health. These effects may be even more notable in infants as 1) prematurity and neonatal intensive care unit (NICU) admission increase the risk of kidney disease, 2) maternal malnutrition leads to decreased kidney mass, and 3) FI accelerates the progression of kidney disease.Our aim was to determine the association between FI and kidney health.&#x0D; Methods: Single-site prospective cohort study.Parents of infants admitted to the NICU at Riley Children’s Health at Indiana University, Indianapolis, IN were interviewed. We collected demographic characteristics and FI status using the Hunger Vital Signs (a validated two-question screening tool). Maternal and infant data were abstracted from medical records and kidney outcomes were compared by FI status.&#x0D; Results: A total of 45 infants were enrolled in this study. In the cohort, the mean gestational age was 32 weeks and the average birthweight was 1.8kg. 26 (60%) reported a household income &gt;$50,000 per year and 21 (47%) held an Associate’s degree or higher. Of the cohort, 22% (10/45) lived in FI households. Infants from FI households were more likely to have AKI than those from food secure households (60% vs 17%, p=0.007) and were more likely to have an abnormal serum creatinine at two weeks of age (70% vs 31%, p=0.028). While not statistically significant, infants from FI households had a trend towards higher likelihood of IUGR (30% v 14%).&#x0D; Conclusion: Food insecurity was common among families with infants admitted to the NICU. Infants born into FI households were more likely to have AKI and delayed maturation of kidney function than those born in food secure households. This emphasizes the importance of FI screening as part of prenatal care along with the need for resources such as food pantries for families admitted to the NICU.

RNA sequencing and bioinformatics analysis of circular RNAs in asphyxial newborns with acute kidney injury.

As one kind of novel noncoding RNA, circular RNAs (circRNAs) are involved in different biological processes. Although growing evidences have supported the important role of circRNAs in renal diseases, the mechanism remains unclear in neonatal acute kidney injury (AKI). High-throughput sequencing analysis was used to investigate the expression of circRNAs between hypoxia-induced AKI neonates and controls. Bioinformatics analysis was conducted to predict the function of differentially expressed circRNAs. Finally, the differentially expressed circRNAs were screened and determined by quantitative real-time PCR (qPCR). (1) A total of 296 differentially expressed circRNAs were identified (Fold change >2 and p < 0.05). Of them, 184 circRNAs were markedly upregulated, and 112 were significantly downregulated in the AKI group. (2) The pathway analysis showed that ubiquitin-mediated proteolysis, renal cell carcinoma, Jak-STAT, and HIF-1 signaling pathways participated in AKI. (3) Top five upregulated and five downregulated circRNAs with higher fold changes were selected for qPCR validation. Hsa_circ_0008898 (Fold Change=5.48, p=0.0376) and hsa_circ_0005519 (Fold Change=4.65, p=0.0071) were significantly upregulated, while hsa_circ_0132279 (Fold Change=-4.47, p=0.0008), hsa_circ_0112327 (Fold Change=-4.26, p=0.0048), and hsa_circ_0017647 (Fold Change=-4.15, p=0.0313) were significantly downregulated in asphyxia-induced AKI group compared with the control group. This study could contribute to future research on neonatal AKI and facilitate the identification of novel therapeutic targets.

Single-center outcome analysis of 46 fetuses with megacystis after intrauterine vesico-amniotic shunting with the Somatex®intrauterine shunt

ObjectivesTo assess the spectrum of underlying pathologies, the intrauterine course and postnatal outcome of 46 fetuses with megacystis that underwent intrauterine vesico-amniotic shunting (VAS) with the Somatex® shunt in a single center.MethodsRetrospective analysis of 46 fetuses with megacystis that underwent VAS either up to 14 + 0 weeks (early VAS), between 14 + 1 and 17 + 0 weeks (intermediate VAS) or after 17 + 0 weeks of gestation (late VAS) in a single tertiary referral center. Intrauterine course, underlying pathology and postnatal outcome were assessed and correlated with the underlying pathology and gestational age at first VAS.Results46 fetuses underwent VAS, 41 (89%) were male and 5 (11%) were female. 28 (61%) fetuses had isolated and 18 (39%) had complex megacystis with either aneuploidy (n = 1), anorectal malformations (n = 6), cloacal malformations (n = 3), congenital anomalies overlapping with VACTER association (n = 6) or Megacystis–Microcolon Intestinal–Hypoperistalsis Syndrome (MMIHS) (n = 2). The sonographic ‘keyhole sign’ significantly predicted isolated megacystis (p < 0.001). 7 pregnancies were terminated, 4 babies died in the neonatal period, 1 baby died at the age of 2.5 months and 34 (74%) infants survived until last follow-up. After exclusion of the terminated pregnancies, intention-to-treat survival rate was 87%. Mean follow-up period was 24 months (range 1–72). The underlying pathology was highly variable and included posterior urethral valve (46%), hypoplastic or atretic urethra (35%), MMIHS or prune belly syndrome (10%) and primary vesico-ureteral reflux (2%). In 7% no pathology could be detected postnatally. No sonographic marker was identified to predict the underlying pathology prenatally. 14 fetuses underwent early, 24 intermediate and 8 late VAS. In the early VAS subgroup, amnion infusion prior to VAS was significantly less often necessary (7%), shunt complications were significantly less common (29%) and immediate kidney replacement therapy postnatally became less often necessary (0%). In contrast, preterm delivery ≤ 32 + 0 weeks was more common (30%) and survival rate was lower (70%) after early VAS compared to intermediate or late VAS. Overall, 90% of liveborn babies had sufficient kidney function without need for kidney replacement therapy until last follow-up, and 95% had sufficient pulmonary function without need for mechanical respiratory support. 18% of babies with complex megacystis suffered from additional health restrictions due to their major concomitant malformations.ConclusionsOur data suggest that VAS is feasible from the first trimester onward. Early intervention has the potential to preserve neonatal kidney function in the majority of cases and enables neonatal survival in up to 87% of cases. Despite successful fetal intervention, parents should be aware of the potential of mid- or long-term kidney failure and of additional health impairments due to concomitant extra-renal anomalies that cannot be excluded at time of intervention.

No matter the hemisphere or language, neonatal acute kidney injury is common and is associated with poor outcomes

No matter the hemisphere or language, neonatal acute kidney injury is common and is associated with poor outcomes

Validation of the STARZ neonatal acute kidney injury risk stratification score in an independent prospective cohort.

A rapid AKI risk assessment score would allow for improving management and outcomes. STARZ (Sethi, Tibrewal, Agrawal, Raina, waZir) score was developed for acute kidney injury (AKI) risk stratification of critically ill neonates. This is the first independent validation for the novel score outside the original enrolled centres. 750 neonates were included in the study. The STARZ score was calculated after 12 hours of admission. Neonates admitted in NICU and receiving IV fluids for at least 48 hours were included. A total of 8.8% neonates had AKI in the first 7 days post admission. The duration of hospital stay was significantly higher among neonates with AKI [10.5 (7-19) vs. 7 (5-10) days; p < 0.001]. Mortality risk was 6.4 times higher among those with AKI [8 (12.1%) vs. 13 (1.9%); p < 0.001; RR (95% CI): 6.38 (2.74-14.83)]. In this study, the STARZ neonatal scoring model showed a sensitivity of 89.4% in detecting AKI with a 90.9% specificity and a high negative predictive value of 98.9%. The area under ROC was 0.958 (0.934-0981) - a high discriminative power. The STARZ score allows for AKI risk stratification, providing opportunity for therapeutic interventions which may improve outcomes in critically ill neonates.

Whole-body analysis of TRPML3 (MCOLN3) expression using a GFP-reporter mouse model reveals widespread expression in secretory cells and endocrine glands.

TRPML3 (mucolipin 3, MCOLN3) is an endolysosomal cation channel belonging to the TRPML subfamily of transient receptor potential channels. Gain-of-function mutations in the Trpml3 gene cause deafness, circling behavior and coat color dilution in mice due to cell death of TRPML3-expressing hair cells of the inner ear or skin melanocytes, respectively. Furthermore, TRPML3 was found to play a role in the long term survival of cochlear hair cells (its absence contributing to presbycusis), in specialized giant lysosomes that neonatal (birth to weaning) enterocytes used for the uptake and digestion of maternal milk nutrients, and in the expulsion of exosome-encased bacteria such as uropathogenic E. coli, infecting bladder epithelial cells. Recently, TRPML3 was found to be expressed at high levels in alveolar macrophages and loss of TRPML3 results in a lung emphysema phenotype, confirmed in two independently engineered Trpml3 knockout lines. TRPML3 is not ubiquitously expressed like its relative TRPML1 and thus cellular expression of TRPML3 on a whole-tissue level remains, with the exceptions mentioned above, largely elusive. To overcome this problem, we generated a τGFP reporter mouse model for TRPML3 and compared expression data obtained from this model by immunofluorescence on tissue sections with immunohistochemistry using TRPML3 antibodies and in situ hybridization. We thus uncovered expression in several organs and distinct cell types. We confirmed TRPML3 expression in both neonatal and adult alveolar macrophages, in melanocytes of hair follicles and glabrous skin, in principle cells of the collecting duct of the neonatal and adult kidney, and in olfactory sensory neurons of the olfactory epithelium, including its fibres protruding to the glomeruli of the olfactory bulb. Additionally, we localized TRPML3 in several glands including parathyroid, thyroid, salivary, adrenal, and pituitary gland, testes and ovaries, suggestive of potential roles for the channel in secretion or uptake of different hormones.

Neonatal Acute Kidney Injury Association With Mortality—Culprit, Innocent Bystander, or Canary in the Coal Mine?

Neonatal Acute Kidney Injury Association With Mortality—Culprit, Innocent Bystander, or Canary in the Coal Mine?

De novo SIX2 activation in human kidneys treated with neonatal kidney stem/progenitor cells

During development, nephron structures are derived from a SIX2+ stem cell population. After 36 weeks of gestation, these cells are exhausted, and no new nephrons are formed. We have previously described a non-invasive strategy to isolate and expand the native SIX2+ kidney stem cells from the urine of preterm neonates, named neonatal kidney stem/progenitor cells (nKSPC). Here, we investigated the safety and feasibility of administering nKSPC into human kidneys discarded for transplantation during normothermic machine perfusion (NMP) and evaluated the regenerative and immunomodulatory potential of nKSPC treatment. We found that nKSPC administration during NMP is safe and feasible. Interestingly, nKSPC induced the de novo expression of SIX2 in proximal tubular cells of the donor kidneys and upregulated regenerative markers such as SOX9 and VEGF. This is the first time that SIX2 re-expression is observed in adult human kidneys. Moreover, nKSPC administration significantly lowered levels of kidney injury biomarkers and reduced inflammatory cytokine levels via the tryptophan-IDO-kynurenine pathway. In conclusion, nKSPC is a novel cell type to be applied in kidney-targeted cell therapy, with the potential to induce an endogenous regenerative process and immunomodulation.

Characteristics and Outcome of Babies with Antenatal Renal Pelvis Dilatation (RPD)

Background: Antenatal renal pelvis dilatation (RPD) is the most common congenital renal anomaly detected on antenatal ul-trasound. The present study was planned to determine the characteristics and outcome of neonates with antenatal renal pel-vis dilatation. Patients and Methods: A prospective, observational, non-interventional study was conducted in Fatima Memorial Hospital over a period of 12 months from April 2021 to March 2022. This study included 130 kidneys of 91 neonates &gt;28 weeks of gestation with antenatally diagnosed isolated renal pelvis dilatation. Postnatal ultrasound was performed at 24-72 hours of life. Cases those resolved spontaneously were labelled as Physiological RPD (Transient RPD) , while all others were labelled as Pathological RPD (Persistent RPD).Descriptive statistics and tests of significance were calculated for all variables. Univariate analysis was performed to compare all possible risk factors for postnatal transient vs. persistent RPD of any grade. Correla-tion coefficients were calculated between risk factors with pathological RPD. Results: Every 4th neonate of antenatally diagnosed RPD had persistent RPD (p&lt;0.05). Only 5% of neonates showed a se-vere variety of persistent RPD. Statistically significant risk factors associated with pathological RPD were maternal anemia, oligohydramnios, diabetes mellitus, gestation age &lt; 37 weeks, birth weight &lt;3 kg, antibiotics administration, admission in in-tensive care unit, urinary tract infections, oliguria, high BUN and creatinine, posterior urethral valve, vesicoureteral reflux, neurogenic bladder and other urinary tract malformations (P&lt;0.05). Persistent RPD had a strong positive direct correlation with the severity of antenatally diagnosed RPD, a moderate positive correlation of persistent RPD was seen with maternal anemia, oligohydramnios, high serum creatinine, PUV, and PUJ. Hence the study will help us in formulating management and follow up plan of our newborns with antenatal RPD. Conclusion: About 71% of neonates with antenatally diagnosed RPD undergo spontaneous resolution. Severe antenatally diagnosed RPD persisted in neonatal life and persistent RPD has a strong correlation with the severity of renal pelvis dilata-tion. Keywords: Ultrasonography, Renal Pelvis Dilatation (RPD), Antenatal, Postnatal, PUJ, Urinary tract malformation, neonatal kidney.

Optimal stage of initiating continuous renal replacement therapy in the treatment of neonatal acute kidney injury.

To explore the optimal stage of initiating continuous renal replacement therapy (CRRT) in the treatment of neonatal acute kidney injury (AKI), a total of 25 AKI neonates treated with CRRT were hospitalized at the Department of Neonatology of Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University (Shanghai, China) from November 2016 to June 2021. According to the renal function, the AKI neonates prior to CRRT were divided into two groups as follows: AKI stage 0-1 and AKI stage 2-3. The changes noted in specific indicators including renal function, electrolyte concentration, and acid-base balance index were analyzed at 0, 12, 24 and 48 h, and at the end of the CRRT treatment. Among the 25 neonates with AKI, serum potassium, urea nitrogen and creatinine levels were significantly decreased following 12 h of CRRT treatment and reached the normal range following 24 h of CRRT treatment with a significant increase in the volume of urine. The serum creatinine levels of the neonates in the AKI stage 0-1 group were significantly decreased following 24 h of CRRT treatment and urine output was significantly increased. At 24 h and following CRRT treatment, the levels of serum creatinine of AKI stage 2-3 neonates were higher than those of AKI stage 0-1 neonates (F=3.013, 5.005; P<0.05), and at all time-points, the urine output of AKI stage 0-1 was higher than that of AKI stage 2-3 (F=13.785, 4.008, 0.965; P<0.05). A total of four cases of thrombocytopenia, two cases of obstruction, and two cases of hypotension were noted in the course of CRRT treatment (the occurrence rate was 8/25). Therefore, it was concluded that CRRT could be an effective measure for the treatment of AKI neonates. Thus, ideally CRRT treatment of AKI neonates should be initiated in cases characterized as AKI stages 0-1.

Neonatal acute kidney injury and serum cystatin C as its early predictor

Aim: To assess cystatin-C as an early biomarker for identifying AKI in newborns at risk for the condition. Methodology: Prospective cohort study in neonates with preterm and term admitted to NICU. The study group comprised of 24 Neonates with risk of AKI &amp; 24 Neonates with no risk of AKI. The Biochemical investigations were done. Collected data was subjected to statistical analysis using SPSS. Results: In this study, there is no significant correlation between gestational age and Creatinine &amp; Cystatin C levels of day 1 &amp; day 5/ death.There is no significant correlation between birth weight and Creatinine day 1, Creatinine &amp; Cystatin C levels of day 5/ death. But positive correlation between birth weight and Cystatin C levels of day 1. Serum Cystatin C can predict development of AKI in at cutoff point of &gt;1.41 mg/l, AUC= 1.000 with sensitivity of 93.3 % and specificity of 97.4 %. Conclusion : The rate of rise of serum cystatin C was earlier and the absolute number was also higher than serum creatinine. Cystatin C levels can predict AKI earlier than serum creatinine value. It can predict AKI atleast 1 or 2 days earlier than serum creatinine.