INTRODUCTION — Acute kidney injury (AKI), formerly referred to as acute renal failure (ARF), is defined as an acute reduction in kidney function that results in a decline in glomerular filtration rate (GFR), leading to retention of urea and other nitrogenous waste products and loss of fluid, electrolyte, and acid-base regulation. AKI is an important contributing factor to the morbidity and mortality of critically ill neonates.
The pathogenesis, etiology, presentation, and diagnosis of neonatal AKI is presented in this topic review. The diagnostic evaluation, management, and prognosis of neonatal AKI in children are presented separately. (See "Neonatal acute kidney injury: Evaluation, management, and prognosis".)
DEFINITION — AKI is typically defined as a decrease in glomerular filtration rate (GFR), which is traditionally defined by an increase in serum creatinine (SCr). Clinically, neonatal AKI has been most commonly defined as an SCr greater than 1.5 mg/dL (133 micromol/L) or an increase of at least 0.2 to 0.3 mg/dL (17 to 27 micromol/L) per day from a previous lower value. Of note, the SCr value at birth reflects the maternal SCr and normally decreases over time. (See 'Normal neonatal kidney function' below.)
However, this definition underestimates the prevalence because during early AKI, a reduction in GFR has a modest effect on creatine excretion and the level may remain unchanged. In addition, SCr may also be underestimated due the effects of gestational age (GA) and postnatal age. Efforts have been made to reach a more accurate consensus definition based on normative data; however, it has been challenging to obtain this information, especially in very preterm infants (GA <32 weeks).
Despite these limitations, definitions of neonatal AKI used in research studies have been published that rely on SCr, including the following:
●Modified Kidney Disease Improving Global Outcomes (KDIGO) for newborns classifies the severity of AKI into stages based on changes in SCr [1,2]:
•Stage 0 – No significant change in SCr
•Stage 1 – Increase in SCr by ≥0.3 mg/dL (≥26.5 micromol/L) within 48 hours
•Stage 2 – Increase in SCr by 150 to <200 percent from previous trough level
•Stage 3 – Increase in SCr by 200 to <300 percent from previous trough level or SCr ≥2.5 mg/dL (221 micromol/L)
●In a report from the AWAKEN (Assessment of Worldwide Acute Kidney Injury Epidemiology in Neonates) database, the absolute rise of SCr ≥0.3 mg/dL (≥26.5 micromol/L) more accurately predicted mortality in the first week of life than ≥50 percent increase in SCr for infants ≤29 weeks gestation . However, specificity was poor for both measures.
●For preterm infants, AKI is based on exceeding critical SCr [4,5]:
•GA 24 to 27 weeks – >1.6 mg/dL
•GA 28 to 29 weeks – >1.1 mg/dL
•GA 30 to 32 weeks – >1.0 mg/dL
In our center, we continue to use the more practical clinical definition of an SCr greater than 1.5 mg/dL (133 micromol/L) or an increase of at least 0.2 to 0.3 mg/dL (17 to 27 micromol/L) per day.
NORMAL NEONATAL KIDNEY FUNCTION — The neonate is more vulnerable to AKI than older individuals due to functional and developmental immaturity of the neonatal kidney that affects glomerular filtration and tubular function (eg, concentrating ability), hemodynamic changes that occur at delivery, and risk of hypovolemia due to large insensible water losses because of relatively larger body surface area to mass compared with older children and adults.
Glomerular filtration rate — It is challenging to ascertain normal neonatal glomerular filtration rate (GFR) due to variability based on gestational age (GA) and postnatal physiological changes and the difficulty of performing accurate clearance measurements [6,7]. Although measurement of inulin clearance is the gold standard to determine GFR, it is difficult to use as it requires an intravenous priming dose followed by continuous infusion (see "Assessment of kidney function", section on 'Assessment of GFR'). As a result, neonatal GFR values are based on creatinine clearance measurements.
The following are reference values from a prospective cohort study of preterm infants between 27 to 31 weeks of age compared with term infants .
●At birth, GFR is lower with lower GA. Very preterm infants (GA less than 32 weeks) had a reduced GFR because renal embryogenesis is not completed until 35 weeks gestation.
Reported average GFR based on creatinine clearance measurements at birth or within the first three days of life varied by GA:
•27 weeks gestation: 13.4 mL/min per 1.73 m2
•28 weeks gestation: 16.2 mL/min per 1.73 m2
•29 weeks gestation: 19.1 mL/min per 1.73 m2
•30 weeks gestation: 21.9 mL/min per 1.73 m2
•31 weeks gestation: 24.9 mL/min per 1.73 m2
•Term infants: 26 mL/min per 1.73 m2
●GFR increased postnatally in all infants with the following reported average GFR based on creatinine clearance measurements at two weeks of age by GA:
•27 weeks gestation: 16.2 mL/min per 1.73 m2
•28 weeks gestation: 19.1 mL/min per 1.73 m2
•29 weeks gestation: 21.9 mL/min per 1.73 m2
•30 weeks gestation: 24.8 mL/min per 1.73 m2
•31 weeks gestation: 27.6 mL/min per 1.73 m2
•Term infants: 54 mL/min per 1.73 m2
Serum creatinine — Clinically, serum creatinine (SCr) values are the most convenient method to estimate GFR. Similar to GFR, SCr normally varies with gestational and postnatal age. SCr at birth is equal to the concentration in the mother (approximately 1 mg/dL [88 micromol/L]). In term infants, SCr declines rapidly in the first or two weeks of life to nadir values (SCr 0.2 to 0.4 mg/dL [18 to 35 micromol/L]), which remain stable through the first year of life [8-10], whereas in preterm infants, the decline is slower and nadir values are reached over the first one to two months. In VPT infants (GA <32 weeks), SCr may increase after birth, most likely due to low GFR and tubular reabsorption of creatinine, followed by a slower decline over two months [8,10]. SCr values for VPT infants and extremely preterm infants (GA<28 weeks) over the first months of life are inversely related to decreasing GA [10,11]. As a result, SCr levels remain higher in EPT and VPT infants compared with term infants in the first months of life (table 1). (See "Assessment of kidney function".)
Time of first void and urine volume — Although the time of the first void is variable, at least 50 percent of newborns void by eight hours of age and nearly all before 24 hours . Urine output is not affected by gestational or postnatal age during the first week of life, averaging 3 to 4 mL/kg per hour . Similar to older patients, neonatal AKI may be oliguric (urine volume less than 1 mL/kg per hour) or nonoliguric, depending upon the severity of the reduction in GFR and the degree of tubular reabsorption.
●Urinary concentration – Urine concentrating ability is limited in the newborn compared with the older individuals. The maximum urine concentration that can be achieved increases from 400 mosmol/kg in the first few days after birth to 1200 mosmol/kg at one year of age. The reasons for poor urine concentrating ability in infants include low corticomedullary solute gradient, decreased formation of cyclic adenosine monophosphate (cAMP) in response to antidiuretic hormone (ADH), a short loop of Henle, and interference by prostaglandins [13-15].
●Sodium reabsorption – Similar to GFR, tubular reabsorption is lower in neonates compared with older individuals and is affected by gestational and postnatal age. In particular, tubular function is immature in VPT infants (GA <32 weeks) with decreasing sodium reabsorption as GA decreases . As a result, the use of fractional excretion of sodium to differentiate between prerenal and intrinsic AKI has limited utility in VPT infants. In addition, the value used to differentiate between prerenal and intrinsic disease is higher in term or late preterm infants. (See "Neonatal acute kidney injury: Evaluation, management, and prognosis", section on 'FENa'.)
●Bicarbonate reabsorption – Neonates have a lower threshold for proximal renal tubular bicarbonate reabsorption, resulting in smaller proportion of reabsorbed filtered bicarbonate than in older children and adults. As a result, infants have a lower normal serum/plasma bicarbonate (HCO3-) than older children and adults (20 versus 24 mEq/L) .
●Acid excretion – The maximum net acid excretion by the distal nephron is limited in newborn infants, especially preterm infants .
INCIDENCE — The reported incidence of neonatal AKI varies and is dependent on the definition of neonatal AKI used, the characteristics of the study population (eg, term versus preterm infants, severity of illness), and whether or not proactive surveillance of kidney function was performed (see 'Definition' above). The risk of AKI is higher in very preterm (VPT) infants and increases with the severity of illness. Previous studies most likely underestimated the incidence of AKI .
Observational studies from the United States report an incidence that ranges from 20 to 40 percent for infants cared for in neonatal intensive care units (NICUs) [18-23]. The incidence, including severe AKI, increases with lower gestational age (GA) and appears to be greater in extremely preterm (EPT) infants (GA <28 weeks) than in more mature infants [24-26]. In the Preterm Epo Neuroprotection trial, severe AKI occurred in 19 percent of the entire study cohort (168 of 900 infants) and stage 3 AKI occurred in 60 neonates (7 percent) and was associated with mortality .
Other high-risk neonatal groups include very preterm infants with the following :
●Congenital diaphragmatic hernia
●Complex cardiac disease requiring cardiac surgery
●Treatment with extracorporal membrane oxygenation (ECMO)
PATHOGENESIS AND ETIOLOGY — Determining the underlying pathogenesis and etiology is important to help guide management decisions (see "Neonatal acute kidney injury: Evaluation, management, and prognosis", section on 'Directed therapy based on etiology'). The causes of neonatal AKI can be divided into pathophysiologic categories based on the anatomical location of the initial injury (table 2) :
●Prerenal AKI due to inadequate renal perfusion – 85 percent
●Intrinsic AKI due to intrarenal pathology – 11 percent
●Postrenal AKI due to obstruction to the flow of urine – 3 percent
Prerenal disease — Prerenal disease, also referred to as volume-responsive or functional AKI, is caused by reduced renal perfusion and is the most common form of neonatal AKI. It is typically due to hypovolemia or reduction of effective circulation.
●Hypovolemia – Neonates are at increased risk for hypovolemia due to their increased insensible water loss, limited urinary concentration ability, and concomitant conditions that result in excessive fluid loss such as:
•Increased evaporative fluid loss due to use of radiant warmers, some phototherapy devices, compromise of skin integrity (eg, abdominal wall defect), or thinness of the skin seen in extremely low birth weight (ELBW) infants (BW <1000 g).
●Reduction of effective circulation – Neonatal conditions associated with reduced effective circulation include:
•Impaired cardiac output (eg, myocardial injury [perinatal asphyxia], critical congenital heart defects (table 3), complete heart block).
•Third spacing (movement of fluid from the vascular space into the interstitium) from acute intestinal injury (eg, necrotizing enterocolitis), hypoalbuminemia due to nephrotic syndrome or hepatic failure, and/or capillary leak (eg, perinatal asphyxia, and hydrops fetalis).
Risk factors — Neonates are more vulnerable to prerenal AKI than older patients because of the following:
●Urine concentrating ability is limited in the newborn compared with the older children, which increases the risk of volume depletion if intake is reduced and/or fluid loss is increased. (See 'Tubular function' above.)
●Insensible water loss through the skin is higher in newborns who have a greater body surface area for their mass compared with older children and adults. Insensible losses are increased by radiant warmers or some phototherapy devices.
●At birth, changes in fetal to postnatal circulation include a substantial increase in renal blood flow (RBF) as renal vascular resistance decreases and systemic blood pressure (BP) increases. As a proportion of cardiac output, RBF increases from 2 to 4 percent in the fetus to approximately 10 percent by one week after birth (the normal adult value is approximately 20 percent). Interference with this transition, as may occur with congenital heart disease or perinatal asphyxia, may lead to diminished kidney function.
●Autoregulation of RBF, in which small changes in systemic BP produce parallel changes in afferent renal vascular resistance so that a constant RBF is maintained over a range of systemic BP, is set at a lower range of BP for infants compared with adults. This reduces a newborn's ability to compensate for significant hemodynamic changes and may lead to compromised kidney function. Impaired autoregulation predisposes to acute kidney injury (AKI) when the BP is reduced [28-30].
Intrinsic renal disease — Intrinsic or intrarenal AKI is caused by a renal pathology that results in:
●Tubular and/or interstitial injury
●Renal vasculature disease
●Glomerular and cystic renal disease
Tubular and interstitial disease — Acute tubular necrosis (ATN) is the most common cause of intrinsic neonatal AKI. Tubular injury can be multifactorial and include the following mechanisms:
•Prolonged and/or severe renal hypoperfusion – Although hypoperfusion usually results in prerenal AKI, prolonged hypoperfusion causes direct tubular endothelial and epithelial cell injury from ischemia and inflammation [31-34].
•Perinatal asphyxia – Perinatal asphyxia can lead to hypoxia (lack of oxygen). Severe asphyxia results in diffuse tubular damage and dysfunction with impaired reabsorption of sodium and water, and decreased glomerular filtration rate (GFR). For infants with milder asphyxia, there may be a loss of renal concentrating ability. (See "Perinatal asphyxia in term and late preterm infants", section on 'Renal manifestations'.)
●Prenatal and postnatal nephrotoxic exposures:
•Maternal drug use – Maternal use of drugs that may affect the renal blood flow of the fetus and neonate include nonsteroidal inflammatory drugs (NSAIDs). NSAIDs inhibit cyclooxygenase (COX) enzymes with subsequent reduction in prostaglandin synthesis leading to reduced neonatal peritubular blood flow, thereby increasing the risk of ischemic ATN . (See "Safety of rheumatic disease medication use during pregnancy and lactation", section on 'NSAIDs' and "NSAIDs: Acute kidney injury", section on 'Mechanism of acute kidney injury'.)
•Postnatal nephrotoxic exposure – In the neonate, the most common nephrotoxic drugs resulting in renal tubular damage include aminoglycosides, prostaglandin synthesis inhibitors (eg, indomethacin), amphotericin B, and vancomycin [2,35-37].
●Sepsis – Although, sepsis is often associated with prerenal AKI due to renal hypoperfusion, there is evidence that sepsis also results in direct tubular injury. (See "Pathophysiology of sepsis", section on 'Kidney' and "Pathogenesis and etiology of ischemic acute tubular necrosis", section on 'Sepsis'.)
Renal vasculature disease — In the neonate, bilateral renal vascular thrombosis can result in intrinsic renal failure. A more common manifestation of less severe renal vascular thrombosis is hypertension. (See "Etiology, clinical features, and diagnosis of neonatal hypertension".)
●Renal artery thrombosis — Although thrombi are common in newborns with umbilical artery catheters and usually are asymptomatic [38,39], severe bilateral renal artery thrombosis can cause AKI [40,41]. Thrombi that form on the tip or surface of the catheter can partially or completely occlude the abdominal aorta, thereby decreasing renal perfusion. These thrombi may embolize to the renal artery, resulting in areas of infarction and increased renin release . (See "Neonatal thrombosis: Clinical features and diagnosis", section on 'Catheter-associated thrombosis'.)
●Renal vein thrombosis — Renal vein thrombosis (RVT) is uncommon, with an incidence estimated as 2.2 per 100,000 live births . Approximately one-half of affected infants are preterm . Bilateral RVT is generally associated with irreversible renal failure. RVT typically presents with a palpable flank mass, often accompanied by hypertension and reduced urine output if bilateral. Affected infants have gross or microscopic hematuria, proteinuria, and diminished kidney function if bilateral. (See "Neonatal thrombosis: Clinical features and diagnosis", section on 'Renal vein thrombosis'.)
Glomerular and cystic renal disease — Intrinsic AKI due to glomerular disease in the newborn is rare. More commonly, neonatal kidney dysfunction due to glomerular disorders is due to chronic kidney disease (CKD) caused by congenital anomalies of the kidney and urinary tract (CAKUT), genetic disorders (polycystic kidney), and congenital nephrotic syndrome, which can present in a similar manner as AKI. (See 'Differential diagnosis' below and "Overview of congenital anomalies of the kidney and urinary tract (CAKUT)" and "Autosomal recessive polycystic kidney disease in children", section on 'Neonatal' and "Autosomal dominant polycystic kidney disease (ADPKD) in children" and "Congenital nephrotic syndrome".)
Postrenal disease — Postrenal or obstructive AKI is due to obstruction of urinary flow from both kidneys or obstruction of the upper urinary tract of a solitary kidney. Therefore, postrenal neonatal AKI is usually due to anatomic bladder obstruction (eg, posterior urethral valves) or bilateral anomalies of the renal pelvis or ureter. (See "Clinical presentation and diagnosis of posterior urethral valves".)
CLINICAL PRESENTATION — Neonatal AKI can present in one of the following clinical settings:
●Kidney function monitoring of at-risk asymptomatic patients – Monitoring serum creatinine (SCr) in at-risk asymptomatic infants identifies those with AKI due to an abnormally high SCr.
●Symptomatic patients – Signs and symptoms due to alterations of renal function, including edema (due to progressive fluid accumulation), decreased or no urine output, and/or hypertension.
●Other abnormal laboratory tests – AKI may be first recognized because of associated electrolyte and acid-base abnormalities.
At-risk asymptomatic patients — Routine testing of kidney function using SCr for at-risk neonates is the most common presentation of neonatal AKI.
We obtain SCr for all patients admitted to the neonatal intensive care unit. SCr is also obtained for any neonate with the following clinical conditions [2,44]:
●Very preterm (VPT) infants (gestational age [GA] <32 weeks or birth weight [BW] <1500 g)
●Perinatal asphyxia (see "Perinatal asphyxia in term and late preterm infants")
●Critical congenital heart disease (see "Identifying newborns with critical congenital heart disease")
●Antenatal bilateral hydronephrosis (see "Postnatal evaluation and management of hydronephrosis")
●Hydrops fetalis (see "Postnatal care of hydrops fetalis")
●Septic infants treated with parenteral antibiotics
●Infants who receive total parenteral nutrition
●Following surgical procedure
●Infants who are treated with ECMO (extracorporeal membrane oxygenation)
Symptomatic patients — Symptoms of neonatal AKI include:
●Edema is common in newborns with AKI. This can result from fluid overload due to kidney dysfunction. Alternatively, other comorbid conditions can contribute to edema, such as capillary leak, heart failure, or hypoalbuminemia.
●Oligoanuria or anuria defined as no urine output noted by 48 hours of age or a diminished urine output (urine volume less than 1 mL/kg per hour). However, the presence of urine does not rule out AKI since some infants are nonoliguric [45,46]. (See 'Time of first void and urine volume' above.)
●Hypertension defined as persistent systolic and/or diastolic blood pressure (BP) that exceeds the 95th percentile for postmenstrual (sometimes referred to as postconceptional) age may be seen in some patients with AKI (figure 1 and figure 2 and figure 3). However, assessing BP is challenging, especially in extremely preterm (EPT) infants, due to technical difficulties and a great variability of BP due to effects from gestational age (GA) and postnatal age. (See "Etiology, clinical features, and diagnosis of neonatal hypertension" and "Assessment and management of low blood pressure in extremely preterm infants".)
Presentation due to other laboratory abnormalities — In addition to changes in serum creatinine, AKI also may be associated with a number of electrolyte or acid-base test abnormalities. In many cases, these abnormal results are seen in conjunction with an abnormally elevated SCr. In other patients, these findings may lead to further testing, including SCr, which may be abnormal. These abnormal laboratory results include:
●Hyponatremia – Hyponatremia almost always results from an inability to excrete free water by the kidneys.
●Hyperkalemia – Several factors may contribute to hyperkalemia in patients with AKI. These include a reduced glomerular filtration rate (GFR), decreased tubular secretion of potassium, tissue breakdown with release of intracellular potassium, and metabolic acidosis resulting in transcellular movement of potassium (each 0.1 unit reduction in arterial pH raises serum potassium by 0.3 mEq/L).
●Metabolic acidosis – AKI impairs the neonates' ability to regulate acid-base status due to tubular immaturity. (See 'Tubular function' above.)
●Hyperphosphatemia – The kidney plays a major role in phosphate excretion. Thus, AKI, particularly if moderate to severe, can lead to hyperphosphatemia.
●Hypocalcemia – Hypocalcemia is a less common problem that can be caused by hyperphosphatemia and other factors in patients with AKI. (See "Neonatal hypocalcemia".)
Late-onset AKI — Late-onset neonatal AKI occurs in infants who are greater than 7 days of age. In a retrospective report from the AWAKEN database, infants with late-onset AKI often had an earlier episode of AKI (28 percent) . They had a longer birth hospitalizations and higher mortality compared with infants without late-onset AKI, and were more likely to have additional comorbidities (eg, congenital heart disease, kidney anomalies, and necrotizing enterocolitis).
DIAGNOSIS — Neonatal AKI is clinically suspected in a newborn with no urine output by 48 hours of age, a diminished urine output (less than 1 mL/kg per hour), edema, or high blood pressure. The diagnosis of neonatal AKI is confirmed with an abnormally elevated serum creatinine (SCr) for gestational age (GA) and postnatal age or increasing SCr from a previous baseline. SCr at birth is equal to the concentration in the mother (approximately 1 mg/dL [88 micromol/L]) and declines rapidly in the first one or two weeks of life in term infants and over the first one to two months in preterm infants to nadir values (SCr 0.2 to 0.4 mg/dL [18 to 35 micromol/L]). The rate of decline decreases with decreasing GA, especially in very preterm (VPT) infants (GA <32 weeks) (table 1). (See 'Serum creatinine' above.)
Investigational urinary biomarkers — Research efforts are in progress to define urinary markers of kidney injury in infants so that a diagnosis of AKI is made before the onset of biochemical changes (SCr) and clinical symptoms . These markers include neutrophil gelatinase-associated lipocalin (NGAL), urinary interleukin-18, kidney injury molecule-1 (KIM-1), and cystatin-C [49-51]. However, further testing is need to establish whether any of these markers will provide beneficial clinical guidance in the diagnosis and management of AKI regardless of the age of the patient. In addition, both gestational and postnatal age appear to effect the normal range of many of these markers [7,52]. As a result, it will also be imperative for studies to account for these effects before any of these markers can be used clinically. (See "Investigational biomarkers and the evaluation of acute kidney injury", section on 'Overview'.)
DIFFERENTIAL DIAGNOSIS — At birth, the distinction between acute and chronic kidney disease (CKD) may be difficult, as presentations are similar. Abnormal antenatal renal ultrasound examination or the presence of dysmorphic features on physical examination is suggestive of CKD. Differentiating between the two entities is also based on the duration of kidney dysfunction. For infants with AKI, the kidney dysfunction resolves over days and weeks, whereas kidney dysfunction persists for months to years for those with CKD.
Identifying the underlying cause of kidney dysfunction is useful as it provides information on the probability of kidney function recovery. Renal ultrasound is helpful as some neonates with CKD may have identifiable congenital anomalies (eg, renal hypodysplasia) or bilateral cystic disease (eg, autosomal polycystic kidney disease). In addition, other physical findings may suggest an underlying genetic or syndromic condition associated with CKD. (See "Overview of congenital anomalies of the kidney and urinary tract (CAKUT)" and "Neonatal acute kidney injury: Evaluation, management, and prognosis", section on 'Identifying the underlying cause'.)
OUTCOME — Observational studies have reported that neonates with AKI have a higher mortality rate than infants without AKI [18,19,21,26]. In addition, longer length of birth hospitalization is observed for infants with AKI .
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute kidney injury in children".)
SUMMARY AND RECOMMENDATIONS
●Definition – Acute kidney injury (AKI) is defined as an acute reduction in kidney function due to a decline in glomerular filtration rate (GFR), which recovers over days to weeks.
●Incidence – The incidence of neonatal AKI varies depending on the definition used and the characteristics of the study population. The incidence of AKI is higher in very preterm (VPT) infants (gestational age [GA] <32 weeks) compared with older children and adults and for infants cared for in the neonatal intensive care unit (NICU). (See 'Incidence' above and 'Definition' above.)
●Increased susceptibility to AKI – Newborns are more susceptible to kidney injury than older infants and children because of the functional and developmental immaturity of the neonatal kidney, affecting glomerular filtration and tubular function (urine concentrating ability), hemodynamic changes that occur at delivery, and risk of hypovolemia due to large insensible water losses. Both GFR and tubular function vary based on gestational and postnatal age. (See 'Normal neonatal kidney function' above and 'Pathogenesis and etiology' above.)
●Etiology – Causes of neonatal AKI are categorized as follows (table 2):
•Prerenal failure is caused by decreased renal perfusion due to hypovolemia or a reduced effective circulation. (See 'Prerenal disease' above.)
•Intrinsic renal failure is caused by renal tubular or interstitial injury, renal vascular disease, or, rarely, glomerular disorders. (See 'Intrinsic renal disease' above.)
•Postrenal failure is caused by obstructive uropathy. (See 'Postrenal disease' above.)
●Presentation – Neonatal AKI can present due to:
•An abnormal serum creatinine (SCr) value obtained by screening at-risk asymptomatic patients. (See 'At-risk asymptomatic patients' above.)
•Symptomatic patients who present with edema, oliguria or anuria, or hypertension. (See 'Symptomatic patients' above.)
•Electrolyte or acid-base test abnormalities that are associated with AKI, including hyponatremia, hyperkalemia, metabolic acidosis, hyperphosphatemia and hypocalcemia. Although these abnormal results are often observed in conjunction with an abnormally elevated SCr, in some cases, these findings may lead to further testing including SCr, which may be abnormal.
●Diagnosis – AKI is clinically suspected in newborns with no urine output by 48 hours of age, a diminished urine output (less than 1 mL/kg per hour), edema, or high blood pressure. The diagnosis of neonatal AKI is confirmed by an abnormally elevated SCr. (See 'Clinical presentation' above and 'Diagnosis' above.)
●Differential diagnosis – The differential diagnosis for AKI is the initial presentation of chronic kidney disease (CKD). At birth, the distinction between acute and chronic kidney disease is difficult, as presentations are similar. Abnormal antenatal renal ultrasound examination or the presence of dysmorphic features on physical examination is suggestive of CKD. Differentiating between the two entities is based on the duration of kidney dysfunction. For infants with AKI, the kidney recovers over days and weeks, whereas kidney dysfunction persists for months to years for those with CKD. (See 'Differential diagnosis' above.)
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