Renal Disorders in Newborn infants

Renal Disorders in Newborn infants Safaa ELMeneza MD, DTQM, DHPE, DGSHH, Professor of Paediatrics, Faculty of Medicine for Girls, AL Azhar University

Prof Dr.Safaa ELMeneza

Educational Objectives • Enumerate most common renal disorders in newborn infants. • Highlight the anatomy and physiology • Enumerate pathogenesis/presentation of some disorders • Describe pathogenesis and clinical picture of acute kidney injury. • Plan for management of acute kidney injury. Prof Dr.Safaa ELMeneza

Pretest 1

• 1- Baby B is a FT delivered by C/S for severe fetal distress associated with placenta abruption. • Apgar's scores were 2 & 4. Vigorous resuscitation, including intubation, ventilation and volume expansion for hypotension. • At 24 hours of age, she is severely oliguric, edematous, & urine is grossly bloody • • • •

A. Post renal disease B. Prerenal renal disease C. Intrinsic renal disease D. A and C Prof Dr.Safaa ELMeneza

Pretest 2 • 2- Among Non-excretory functions of kidney ; Excretes nitrogenous end products ( true or false ) • 3- Nephrogenesis starts at • A. 20 weeks of gestation • B. 18 weeks of gestation • C. 8 weeks of gestation • D. 34 weeks of gestation Prof Dr.Safaa ELMeneza

Pretest 3 • 4- In newborn infants polyurea is passing – A. more than 7 mL/kg/h of urine flow. – B. more than 10 mL/kg/h of urine flow – C. more than 5 mL/kg/h of urine flow – D. more than 12 mL/kg/h of urine flow

• 5- Normal newborn infant may excrete up to 1 g albumin/L during the first 24– 48 hours of life. (true or false ) Prof Dr.Safaa ELMeneza

Pretest 4 • 6- In newborn with obstructive uropathy the gold standard for diagnosis is • A. Voiding cystourethrogram • B. Plain xray • C. pelvic Ultrasound • D.A and B


Pretest 5 • 7- To diagnose ARI which one is true • A. Plasma creatinine > 1.5 mg/dL for at least 24 to 48 hrs , if mother’s renal function is normal • B. Serum creatinine raised > 0.3 mg/dL over 48 hours • C. Serum creatinine fails to fall below maternal plasma creatinine within 5-7 days. • D. All of above Prof Dr.Safaa ELMeneza

Pretest 6 • 8- Response to fluid challenge test defined a • • • •

A. Urine output > 2 ml/kg/hr B. Urine output > 1 ml/kg/hr C. Urine output > 1.5 ml/kg/hr D. Urine output > 2.5 ml/kg/hr


Children are not small adults Newborn infants are not little children too


Introduction • • • • •

Different sizes, and shapes Different disorders and pathogenesis Common presence of anomalies Different treatment and doses Most important the need to grow and quality of life as well as safety of care.



Renal function • Non-excretory functions – Produces renin – Produces erythropoietin – Metabolizes vitamin D – Degrades insulin – Produces prostaglandins

• Excretory functions • Maintain plasma osmolarity • Maintain electrolyte balance – Maintain water balance – Excretes nitrogenous end products


Nephron • Functional unit of kidney – Nephrogenesis – Begins at 7-8 weeks EGA – Completed by 34 wks. EGA • Three major functions – Filtration

– Reabsorption – Secretion Prof Dr.Safaa ELMeneza

Renal function • Time of urination • Most babies pass urine: – at or immediately after birth – 97% have done so within 24 hours –all normal babies have passed urine within 48 hours.


Renal function • Amount of urine : • About 40–60 mL/kg/24 h is produced.

• Oliguria : • If passing < 12 mL/kg/24 h (0.5 mL/kg/h) on day 1 • If passing < 24 mL/kg/24 h (1 mL/ kg/h) thereafter • it is abnormal and requires investigation. Prof Dr.Safaa ELMeneza

Renal function • Polyuria is defined as more than 7 mL/kg/h of urine flow. • Polyuria can be caused by – reduced antidiuretic hormone concentration (diabetes insipidus) – resistance to ADH in the renal tubules (nephrogenic diabetes insipidus) – but is more commonly seen in the polyuric phase of renal failure – or in the diuretic phase of respiratory distress syndrome (RDS) Prof Dr.Safaa ELMeneza

Renal function • Urine concentration : • about 500 mosmol/L (preterm) • about 700 mosmol/L (term), but this is much less than the adult value of 1400 mosmol/L. • The reasons are : – shorter loop of Henle – reduced tonicity of the medullary interstitium – reduced expression of aquaporins Prof Dr.Safaa ELMeneza

Renal function • Specific gravity • When there is no glycosuria, proteinuria or haematuria, this corresponds to a specific gravity of 1002–1030. • The pH of neonatal urine is usually between 5 and 8.


Renal function • GFR is reflective of renal function • Plasma creatinine is best clinical measure of GFR • But new markers ------


Renal function • Although nephrogeneis is complete in humans by 34-36 weeks of gestation, glomerular filtration rate (GFR) is approximately 10–20 ml/min/1.73m2 demonstrating the immaturity of the kidney. • Premature infants have an even lower GFR. Prof Dr.Safaa ELMeneza

Renal Disorders


Renal Disorders • 1- diseases • 2-Abnormal urine


Renal Disorders 1 • • • • • • • • •

Renal malformations Congenital nephrotic syndrome Acute renal failure/Acute kidney injury Urinary tract infection Renal vascular thrombosis Nephrocalcinosis Renal tubular acidosis Renal masses Syndrome of inappropriate secretion of antidiuretic hormone Prof Dr.Safaa ELMeneza

Renal Disorders • -Abnormal urine – Haematuria – Haemoglobinuria – Proteinuria


Haematuria 1 • Neonatal hematuria can be broadly classified into gross and microscopic hematuria. • Microscopic hematuria is defined as >5 RBCs/HPF and is more common in premature or low birth weight infants than healthy term neonates. Prof Dr.Safaa ELMeneza

Haematuria 2 • Exclude other causes e.g. • Urate crystals in the diaper present as a reddish-brown or pink discoloration and is more commonly seen in states of volume depletion especially in breast fed neonates . • Vaginal discharge due to maternal hormonal withdrawal can be mistaken for gross hematuria. Prof Dr.Safaa ELMeneza

Haematuria 3 • Exclude other causes e.g. • Diaper rash causing skin break down or rectal bleeding. • In rare instances porphyria can present with pink discoloration of the diaper. • HDN in health newborn may present with haematuria Prof Dr.Safaa ELMeneza

Haematuria 4 • Common in very sick infants • 1. Bleeding tendency, particularly DIC –This is probably the most common cause of haematuria in very sick infants with RDS, septicaemia or necrotizing enterocolitis receiving intensive care. –2. Emboli from umbilical artery catheters or with coagulase-negative staphylococci sepsis (endocarditis) in association with long lines. Prof Dr.Safaa ELMeneza

Haematuria 5 • 3. Trauma, particularly after suprapubic bladder aspiration. • 4. HIE with associated tubular or cortical necrosis. • 5. Renal artery or vein thrombosis • 6. Urinary tract infection • 7. Malformation, as from the wall of a trabeculated bladder in the presence of post urethral valves , or with hydronephrosis. Prof Dr.Safaa ELMeneza

Haematuria 6 • 8. Other very rare causes include – drugs – tumors – or polycystic kidney disease (the kidneys are often palpable and uraemia may be present – Glomerulonephritis – Neonatal hemolytic uremic syndrome – congenital thrombotic thrombocytopenic purpura (Upshaw Shulman syndrome), – inborn errors of cobalamin metabolism, methylmalonic aciduria associated HUS, or drugs Prof Dr.Safaa ELMeneza

Haematuria 7 • 11.Nephrocalcinosis has been reported to occur in 7–40% of preterm infants. • Nephrocalcinosis can also be seen in term neonates who have distal renal tubular acidosis, primary hyperparathyroidism or Dents disease and they are associated with hypercalciuria. Prof Dr.Safaa ELMeneza

Haemoglobinuria • Haemoglobinuria is very rare in the newborn except in –the presence of DIC with intravascular haemolysis. – ABO blood group incompatibility from intravascular hemolysis • Urinalysis will be positive for blood but urine microscopy will be negative for red blood cells. Prof Dr.Safaa ELMeneza

Myoglobinuria • Myoglobinuria is rarely seen in neonates but has been reported in a patient with severe perinatal asphyxia. • Urinalysis will be positive for blood but urine microscopy will be negative for red blood cells.


Proteinuria 1 • The normal newborn infant may excrete up to 1 g albumin/L during the first 24–48 hours of life, but the level falls rapidly after that period. • Normal protein excretion in a full term neonate is 68–309 mg/m2/24hrs . • Proteinuria in the neonatal period is rare as a primary finding. Prof Dr.Safaa ELMeneza

Proteinuria 2 • Neonatal proteinuria can be due to : • Glomerular or tubular – genetic causes – structural anomalies – infections – immune mediated

• Severity of proteinuria can vary based on the etiology and will determine the clinical presentation in the neonate. Prof Dr.Safaa ELMeneza

Proteinuria 3 • It is common in the severe illnesses which compromise renal perfusion and in some cases also cause haematuria such as : – septicaemia – HIE – hypotension – DIC

• Massive proteinuria occurs in congenital nephrotic syndrome. Prof Dr.Safaa ELMeneza

Proteinuria 4 • Congenital nephrotic syndrome 1 • Rare ,baby present with proteinuria that may be severe enough to cause fetal hydrops. •Causes •Genetic causes •Non genetic

•The treatment is to maintain serum albumin and try diuretics. • The prognosis is poor Prof Dr.Safaa ELMeneza

Proteinuria 5 Nephrotic syndrome 2

• Genetic causes: • genetic mutations of proteins that are components of the glomerular filtration barrier. • Homozygous mutations of nephrin and podocin.(gene NPHS1 , NPHS2) • WT1 protein and Laminin β2 (gene WTI, LAMB2) • ‘Finnish’ congenital nephrotic syndrome, an Prof Dr.Safaa ELMeneza

Proteinuria 6 Nephrotic syndrome 3 • Non genetic causes. Infections include congenital syphilis, rubella, CMV, toxoplasmosis, hepatitis B and HIV . • Neonatal lupus has been reported in the presence and in the absence of maternal lupus. • RVT • Nephrotic syndrome has also been described in neonates due to placental transfer of NeutralEndopeptidase (NEP) antibodies from fetomaternal alloimmunization. Prof Dr.Safaa ELMeneza

Proteinuria 7 • Acute Kidney Injury/Acute Tubular Necrosis: • Acute tubular necrosis (ATN) is a common cause for acute kidney injury especially in the NICU and as a consequence, proteinuria can be seen in the setting of ATN. Prof Dr.Safaa ELMeneza

Proteinuria 8 • The premature infant nephronogenesis is incomplete at the time of birth is particularly at risk for – low nephron number, – glomerular hyperfiltration and – proteinuria in childhood which in turn can lead to CKD .


Proteinuria 9 • If there is nephron loss due to AKI, the premature infant is at an even higher risk for CKD. • In these infants, persistent proteinuria can be an early marker for the development of chronic kidney disease.


Proteinuria 10 • Tubular proteinuria • Tubular immaturity, neonates tend to have generalized aminoaciduria that is compounded in the face of prematurity . • Hereditary conditions associated with tubular low molecular weight proteinuria include hereditary forms of Fanconi syndrome including cystinosis, Dent’s disease, Lowes Syndrome and Prof Dr.Safaa ELMeneza mitochondropathies.

Renal Malformations


Renal Malformations • • • • •

Pelvi-ureteric junction obstruction Vesico-ureteric junction obstruction Urethral valves Vesico-ureteric reflux Hydronephrosis


Renal Malformations • Renal malformations are identified by antenatal ultrasound in about 1:800 pregnancies. • All babies with an antenatally diagnosed problem should have a renal ultrasound scan within a week. • if dilatation of the renal pelvis (pyelectasis) was 15 mm or more this scan should be done urgently, before the baby goes home Prof Dr.Safaa ELMeneza

Urethral Valves 1 • Posterior Urethral valves are aberrant folds of tissue that extend from verumontanum to the external sphincter, creating a urethral obstruction.


Urethral Valves 2 • Clinical presentations • Prenatally with bilateral hydroureteronephrosis and megacystis, with or without oligohydramnios • Postnally wide spectrum, from mild bladder outlet obstruction to severe obstructive uropathy with renal insufficiency ,and pulmonary hypoplasia. –symptoms of severe metabolic disorders related to renal failure –respiratory problems ,spontaneous pneumothorax or pneumomediastinum –urinary tract infections Prof Dr.Safaa ELMeneza

Urethral Valves 3 • Diagnosis. • Voiding cystourethrogram (VCUG) is the gold standard for diagnosis • Classically shows – a thickened bladder wall – a dilated posterior urethra – decreased urethral caliber beyond the verumontanum. Prof Dr.Safaa ELMeneza

Urethral Valves 4 •Management. •Prenatally, in utero decompression of the bladder has limited success. •Postnatal treatment consists of –placement of an indwelling catheter, a transurethral or a suprapubic catheter. –initiating antibiotic prophylaxis –Surgical incision of the valve endoscopically within the first week of life /elective cystoscopic ablation of the valves –Serial chemistries are needed to monitor Prof Dr.Safaa ELMeneza

Hydronephrosis (Prenatal and Postnatal) 1 • Hydronephrosis is dilatation of the renal pelvis and calyces. • Mild dilation of the renal pelvis is defined as an anteroposterior diameter of 5–10 mm between weeks 18 and 23 of gestation. • Severe dilation is generally defined as an anteroposterior diameter >15 mm. • Postnatally, hydronephrosis is classified as grade 1–4 Prof Dr.Safaa ELMeneza

Hydronephrosis 4 • All infants with severe unilateral or bilateral hydronephrosis should be started on antibiotic prophylaxis and evaluated with a VCUG under current guidelines.


RENAL MASSES


Renal Masses 1 • Majority of neonatal abdominal masses arise from the kidney. • Unilateral or bilateral, solid or cystic


Renal Masses 2 • • • • • • •

Multicystic dysplastic kidney Infantile polycystic kidney disease Renal vein thrombosis Wilms tumor Mesoblastic nephroma Adrenal haemorrhage or tumour Hydronephrosis Prof Dr.Safaa ELMeneza

Multicystic dysplastic kidney • Most common renal cystic disease of the newborn. • It is usually unilateral. • Ultrasonography can define the nature of the disorder, and CT/nuclear renal scans are useful in assessing the remainder of the urinary system. • Management ;Nephrectomy may be warranted. Prof Dr.Safaa ELMeneza

Infantile polycystic kidney disease 3 • There are two types: • A. Autosomal recessive polycystic kidney disease presents with – abdominal masses – hypertension – renal insufficiency – hepatic biliary fibrosis

• May be too pulmonary failure from lung hypoplasia. Prof Dr.Safaa ELMeneza

Infantile polycystic kidney disease 4 • B. Autosomal dominant polycyctic kidney disease usually : • onset in the 3rd to 5th decade of life. • In some newborns, it can present with – bilateral flank masses –hypertension –renal insufficiency –and cystic involvement of other organs Prof Dr.Safaa ELMeneza

Mesoblastic Nephroma • A mesoblastic nephroma is embryonic solid renal tissue that is not usually malignant. • II. Clinical presentation. • A palpable mass is found on abdominal examination in first few months of life • or a solid kidney mass is seen on prenatal ultrasound. Prof Dr.Safaa ELMeneza

Mesoblastic Nephroma 3 • Management • A. Surgery. Nephrectomy is indicated and includes lymph node sampling to assess for rare malignant degeneration.


Wilms Tumor /Nephroblastoma1 • Definition. • It is an embryonal renal neoplasm in which blastemic, stromal, and epithelial cell types are present. • Renal involvement is usually unilateral but may be bilateral (5% of cases).


Wilms Tumor 2 • II. Clinical presentation. • A palpable abdominal mass extending from beneath the costal margin is the usual mode of presentation


Wilms Tumor 4 • Management. Multimodality therapy combining surgery, radiation, and chemotherapy is the standard. • A. Unilateral renal involvement. – Radical nephrectomy with lymph node sampling is indicated. – Surgical staging determines the need for radiotherapy and chemotherapy. Both are effective. Prof Dr.Safaa ELMeneza

Wilms Tumor 5 • B. Bilateral renal involvement. • Treatment of bilateral tumors is highly individualized. • Neoadjuvant therapy followed by nephronsparing resection may be attempted.


Renal vascular thrombosis 1 • Clinical picture : • classically presents with haematuria in first 3 days , loin mass and thrombocytopenia • The affected kidney usually becomes atrophic • Risk factors maternal diabetes, dehydration, asphyxia or congenital heart disease. • 50% of cases the thrombus extends into the inferior vena cava. • RVT is the most common • Non-catheter-related thrombosis in infancy Prof Dr.Safaa ELMeneza

Renal vascular thrombosis 2 • Conservative management is generally recommended. • Low molecular weight heparin can be considered and may prevent spread of the thrombus to the other renal vein.


Renal vascular thrombosis 3 • The outcome • Unilateral disease is good • Bilateral renal vein thrombi , up to half of the babies will die. • Hypertension occurs in 20% • Permanent renal failure is rare (3% ) • Babies who have experienced RVT must be followed up. Prof Dr.Safaa ELMeneza

Renal Tubular Acidosis • Caused by defects in reabsorption of HCO3- and secretion of H+ ions, generally presents systemic metabolic acidosis and inappropriately high urine pH (>6.0). • This occurs frequently in preterm infants and is transient. • RTA can also be associated with a wide variety of other conditions Prof Dr.Safaa ELMeneza

Renal Tubular Acidosis 2 • Renal tubular acidosis can occur as a genetic defect, secondary to nephrocalcinosis, or be due to drugs. • Treatment is with sodium bicarbonate orally.


Syndrome of Inappropriate Secretion of Antidiuretic Hormone • It is a very infrequent disorder of fluid and electrolyte balance due to excessive release of antidiuretic hormone leading to water retention and hyponatremia. • Findings include oliguria, low serum osmolality, hyponatremia, concentrated urine and elevated urine sodium. • Treatment is strict restriction of fluid intake Prof Dr.Safaa ELMeneza

Potter’s Syndrome 1 • There is oligohydramnios and the fetal membranes show amnion nodosum. • Renal agenesis plus pulmonary hypoplasia • The baby has a squashed face, hypertelorism, epicanthic folds, micrognathia, low-set ears and large, floppy hands and feet. • This condition presents at birth with severe dyspnoea due to pulmonary hypoplasia and the infants usually die within 2–3 hours.

Nephrocalcinosis • Nephrocalcinosis is commonly diagnosed in VLBW babies on diuretics, particularly those who have received total parenteral nutrition. • The crystals are calcium oxalate or calcium urate and eventually resolve. • In term babies nephrocalcinosis can occur secondary to renal tubular acidosis or primary oxalosis Prof Dr.Safaa ELMeneza

Acute Renal Failure (Acute Kidney Injury) Difficulties to define acute kidney injury in neonatal period


Why? • During the first 48–72 h of life, neonatal SCr still reflects maternal levels . • These values may decline at varying rates over days, depending on gestational age. • Thereby, the levels of SCr during the first week after birth and its changes (or lack of change) may be difficult to interpret. Prof Dr.Safaa ELMeneza

Why? • Moreover, SCr concentrations may not change until 25–50% of the kidney function has already been lost . • At lower GFR, SCr will overestimate renal function due to tubular secretion of creatinine.


Acute Kidney Injury • The term acute renal failure has now been replaced with the term acute kidney injury.

• It is a complex disorder , clinical manifestations ranging from mild injury to complete kidney failure, • Generally could require renal replacement therapy, peritoneal dialysis or hemodialysis. Prof Dr.Safaa ELMeneza

Acute Kidney Injury • ARF is an acute reduction in glomerular filtration rate with both failure to remove solutes and water leading to concurrent net solute and water retention – oligo-anuric renal failure .


Acute Kidney Injury • Also is defined as an acute and reversible increment in serum creatinine levels associated or not with a reduction in urine output oliguria/anuria.


Acute Kidney Injury • AKI is classically defined as a sudden decline in kidney function resulting in derangements in fluid balance, electrolytes, and waste products.


Acute Kidney Injury • Currently, the diagnosis of AKI is dependent on a rise in serum creatinine (SCr) or decrease in urine output. • Unfortunately, SCr is a suboptimal biomarker as it is a marker of kidney function, not damage. • As a result, there is a significant delay in the rise of SCr after an insult (48–72 hours) and a significant amount of function has to be lost before SCr will rise (.50% of the GFR) Prof Dr.Safaa ELMeneza

Acute Kidney Injury • In neonates, ARF/AKI is defined as a serum creatinine >1.5 mg/dL (132.6 μmol/L), regardless of age or urine output, with normal maternal renal function. • ARF/AKI can be anuric (absence of urinary output by 24–48 hours of age), oliguric (urine output of 1.0 mL/kg). Prof Dr.Safaa ELMeneza

Creatinine Interpretation •1. Plasma creatinine > 1.5 mg/dL for at least 24 to 48 hrs , if mother’s renal function is normal •2. Serum creatinine raised > 0.3- 0.5 mg/dL over 48 hours •3. Serum creatinine fails to fall below maternal plasma creatinine within 5-7 days. •4. Creatinine increases two times between any two measurementsProf Dr.Safaa ELMeneza

Plasma Creatinine • In preterm neonates, there is a transient increase in serum creatinine, peaking on day 4, followed by a progressive decline to normal neonatal levels by a postnatal age of 3 to 4 weeks. • This occurs due to re-absorption of creatinine across the permeable tubules. • Further, in VLBW infants without ARF, there could be oliguric phase that resolve spontaneously inProf the first few days of life. Dr.Safaa ELMeneza

Incidence of Acute Renal Injury • Incidence varies between 8 – 24% • • • •

37% of infants > 28 weeks 8% of infants between 28-32 weeks 4% of infants between 33-36 weeks 2% of term infants


Incidence of Acute Renal Injury Population

AKI incidence

AKI definition

Pre-term VLBW

18%

Modified KDIGO

Pre-term ELBW

12.5%

Modified KDIGO

Sick near-term/term

18%

Modified KDIGO

Asphyxiated newborn

38%

Modified KDIGO

ECMO

71%

RIFLE criteria

Sepsis

26%

Cardiac surgery

62%

AKIN criteria Prof Dr.Safaa ELMeneza

Incidence of Acute Renal Injury • Prerenal is the most common type in the neonate, up to 85% of cases. • Renal incidence is 6–8% • Postrenal 3–5%. • Persistence of insult can convert pre renal or post renal failure to intrinsic renal failure. Prof Dr.Safaa ELMeneza

Risk Factors 1 • Multifactorial – Sepsis (39%) – Perinatal asphyxia (17%) – Hypotension not associated with sepsis (10%)

– “Just being premature” (32%) 79% cases of ARF 0.5 mg/dL

< 0.3 mL/kg/h (24 h) OR Anuric (12 h)



Limitation (L)

Loss of kidney function for 4 weeks

End stage (E)

Loss of kidney function > 3 months

Etiology Of Neonatal Renal Failure


Clinical Presentation • A. Decreased or absent urine output is usually the presenting problem. • B. Family history. – History of urinary tract disease in other family members – Oligohydramnios, which frequently accompanies urinary outflow obstruction or severe renal dysplasia or agenesis – Maternal diabetes Prof Dr.Safaa ELMeneza

Clinical Presentation • B. Family history. –Increased maternal alpha-fetoprotein – Hypertrophied placenta –Hearing disorders – Maternal drugs – Vesico-ureteral reflux – Umbilical cord anomalies – ? Void Prof Dr.Safaa ELMeneza – Spontaneous pneumothorax

Clinical Presentation

• C. Physical examination 1. Abdominal mass may be due to a distended bladder, polycystic kidneys, hydronephrosis, or tumors 2. Potter facies is associated with renal agenesis 3. Meningomyelocele is associated with neurogenic bladder 4. Pulmonary hypoplasia is due to severe oligohydramnios in utero Prof Dr.Safaa ELMeneza

Clinical Presentation • C. Physical examination • 5. Urinary ascites may be seen with posterior urethral valves and severe upper urinary tract obstruction. • 6. Prune belly syndrome. Hypoplasia of the abdominal wall musculature, cryptorchidism, and dilated upper urinary tracts. • Others as Hydrops or ascites or isolated ear anomalies Prof Dr.Safaa ELMeneza

Diagnosis • A. Urethral catheterization • Use a 5F or 8F feeding tube to measure volume of retained urine of monitor output. • B. Laboratory studies –A. Blood urea nitrogen a. BUN. 15–20 mg/dL. suggests dehydration or renal insufficiency Prof Dr.Safaa ELMeneza

Diagnosis • B. Laboratory studies –b. Creatinine –Best clinical measure of GFR –indicative of renal impairment in the newborn – Five days to reflect neonatal values –Levels > 130 mcmol/l (1.5mg/dl) considered Prof Dr.Safaa ELMeneza

Diagnosis • B. Laboratory studies • b. Creatinine – Normal serum creatinine values are 0.8–1.0 mg/dL at 1 day – 0.7–0.8 mg/dL at 3 days – < 0.6 mg/dL by 7 days of life

–Higher values suggest renal disease except in low birthweight infants, in whom a creatinine level of 2 ml/kg/hr • If there is no response, give furosemide, 1 mg/kg IV. • If there is still no increase in urine output, obstruction above the level of the bladder must be ruled out by ultrasound examination. Prof Dr.Safaa ELMeneza

Diagnostic fluid challenge • If there is no evidence of obstruction, and the patient does not respond to these maneuvers, the most likely cause of anuria or oliguria is intrinsic renal failure.


D. Imaging studies • 1. Abdominal ultrasonography • May identify –hydronephrosis –dilated ureters –abdominal masses –distended bladder –renal vein thrombosis Prof Dr.Safaa ELMeneza

D. Imaging studies • 2. Abdominal radiograph studies • May show –spina bifida – an absent sacrum, which may be associated with a neurogenic bladder –Displaced bowel loops suggest the presence of a space-occupying mass Prof Dr.Safaa ELMeneza

D. Imaging studies • 3. Radionuclide scanning • May be used to assess function of renal parenchymal but is less accurate in neonates due to immature kidneys • VCUG


Management Prevention • After the diagnosis of AKI, it becomes important to prevent the development of sequelae. – monitor drug levels and avoid nephrotoxic exposures –Strict documentation of all fluid input and output, serum electrolytes, and weight is essential to optimize fluid status. Prof Dr.Safaa ELMeneza

Management Prevention • There are sparse data documenting interventions that can prevent AKI in atrisk patients or ameliorate AKI once it is established. • In neonates with perinatal asphyxia, adenosine receptor antagonists (theophylline) may prevent AKI by inhibiting the adenosine-induced vasoconstriction.Prof Dr.Safaa ELMeneza

Management Prevention • As a result, the KDIGO guidelines recommend a single dose of theophylline for asphyxiated infants at risk for AKI.


Management Prevention • Other drugs that have been studied to prevent the development of AKI and improve renal blood flow include dopaminergic agonists (dopamine and fenoldopam).No Evidence based yet • Diuretics are frequently used in patients with AKI in attempts to maintain urine output. Studies in critically ill patient populations have not demonstrated a beneficial effect of Prof Dr.Safaa ELMeneza

Management Outlines • Prerenal – Volume resuscitation – Treat specific causes

• Postrenal – Drain bladder with indwelling catheter – Consult urology

• Intrinsic – supportive care Prof Dr.Safaa ELMeneza

Management General 1

• 1- Maintenance of state of euvolemia –Replace insensible fluid losses + fluid output (urine and gastrointestinal tract). • Full term: 30 ml/kg /d + ml/ml UOP • Premature: 50 up to 70 ml/kg /d + ml/ml UOP Prof Dr.Safaa ELMeneza

Management General 1

• Insensible fluid losses

• Based on the weights, • newborns < 750 g would have 100-150 mL/kg/day of insensible losses • weighing 750 g to 1000 g would receive 60-70 mL/kg/day. • More mature preterm newborn weighing between 1000-1250 g would have 30-65 mL/kg/day of insensible losses Prof Dr.Safaa ELMeneza

Maintenance of State of Euvolemia • Extravasation of the intravascular fluid (third-spacing) is common in fluid overloaded neonates due to combination of – fluid overload – low oncotic pressure –and leaky capillaries secondary to sepsis and inflammation.

Maintenance of State of Euvolemia • The extravasated fluid : – depletes the intravascular fluid volume –causes skin breakdown – chest wall edema –in extreme cases, fluid overload may lead to abdominal compartment syndrome.

Maintenance of State of Euvolemia • The extravasated fluid : – pulmonary edema, –increased respiratory requirements – resulting in higher ventilatory requirements – worsening of the PDA, –dilutional hyponatremia due to excessive free water

Management General 2 • 2- Keep strict intake and output and frequent weights. • 3. Monitor serum sodium and potassium levels frequently, and replace losses cautiously as needed. • Hyperkalemia may be lethal Prof Dr.Safaa ELMeneza

Management General 3 • 4. Restrict protein to