Renal function in the newborn
Almost all infants void by 24 hours of life. If it is suspected that urine has not been passed within the first day, it is usually that
voiding has not been recorded, especially immediately after birth. Consider obstruction or intrinsic renal problem, but they are usually detected on antenatal ultrasound screening.
Some key points regarding renal function are listed in Fig. 51.1.
The fetal kidney plays no role in excretion or homeostasis – which is performed by the placenta
In the fetus, the function of the kidney is to produce amniotic fluid. The fetal circulation is in chemical equilibrium with that of the mother. Fetal or cord blood measurements of renal function, e.g. blood urea nitrogen (urea) or creatinine, reflect renal function of the mother, not the fetus
Glomerular filtration rate (GFR) is low in newborns, even if adjusted for body size
Glomerular filtration rate (GFR) in
A preterm infant at 28 weeks – 10 mL/min/1.73 m2 body surface area (BSA) A healthy, term infant – 30 mL/min/1.73 m2
Adult – 120 mL/min/1.73 m2 (range 80–120), reached by the second year of life. Some argue that it is more appropriate to quote GFR in infancy by weight, the mean value being 1 mL/min/kg (range 0.5–1.5 mL/min/kg)
The newborn kidney is optimized for retention of dietary solutes for growth, not for excretion
The healthy newborn infant grows very rapidly, i.e. is strongly anabolic. Breast milk is just sufficient to provide the nutrients needed for this growth. There is little excess dietary solute requiring excretion, so infants can thrive despite biochemical evidence of renal insufficiency that would be inadequate for an adult. There are two practical consequences of this:
The newborn kidney is optimized for retention, not excretion, of essential substances such as sodium and other minerals
If growth ceases, e.g. infection, the low renal reserve of the infant is exposed and
biochemical derangements are common Both these are even more true of the preterm than of the term infant
Term infants produce urine almost free of sodium, and can thrive on human milk that contains
<10 mmol/L of sodium. This is not true of the preterm infant <32 weeks’ gestational age fed mature human milk or an artificial formula of similar composition. Under these circumstances they are prone to become sodium-depleted and hyponatremic, typically at about 10 days postnatal age (late hyponatremia of prematurity). This can be prevented by increasing the dietary sodium intake to 4–6 mmol/kg/day for the vulnerable period of 4–14 postnatal days.
Mature human milk would only provide 1.25 mmol/kg/day. Neonates with renal tract malformations such as dysplasia or obstructive uropathy are also prone to becoming hyponatraemic and acidotic and require sodium and bicarbonate supplements, respectively.
The term kidney conserves sodium, the preterm kidney loses sodium
Term infants are less able to concentrate urine than adults.
This is even more pronounced in preterm infants Reduced urine osmolality in
the newborn is physiologic
Fig. 51.1 Some key points about renal function in newborn infants.
Renal and urinary tract disorders 123 volume depletion with water reabsorption. Also excess IV fluids to
mother during labor; oliguric renal failure (renal impairment with little urine output and fluid overload).
Preterm – marked Na loss in urine, poor at conserving sodium as tubular reabsorptive capacity not fully developed. This results in hyponatremia of prematurity (see Fig. 51.1).
Other causes include:
• insufficient Na supplementation (low FENa)
• gastrointestinal losses – diarrhea, vomiting (low FENa)
• renal losses – diuretics (high FENa), renal dysplasia, congenital adrenal hyperplasia, renal tubulopathies
• SIADH, syndrome of inappropriate antidiuretic hormone (high FENa, low POsm and high UOsm) – probably rare in newborn infants.
Hypernatremia – Na >150 mmol/L
Result of excessive water loss over sodium or excess sodium intake over water.
If detailed assessment required, assess fluid status and measure FENa.
Hypernatraemic dehydration may be from:
• insufficient input of fluids e.g. insufficient breast milk
• excessive water losses, e.g. evaporative through skin in extremely preterm, phototherapy, radiant heater or gastrointes
tinal losses
• excess sodium intake, e.g. sodium containing flushes of lines, sodium bicarbonate, sodium phosphate, etc (high UOsm and high FENa)
Rare causes – diabetes insipidus (central, e.g. septo‐optic dysplasia or nephrogenic, no ADH or ADH effect) (low UOsm, low FENa), deliberate salt poisoning.
Potassium (normal range 3.5–5.5 mmol/L)
Hyperkalemia – K >6.0 mmol/L
Serious condition as can result in arrhythmias and death. But most common reason is hemolyzed blood sample.
Other causes – renal impairment (transient is relatively common in extremely preterm infants), excess K supplementation, congen
ital adrenal hyperplasia.
Neonates tolerate hyperkalemia better than older children, so only treat if K >6.5 mmol/L. ECG monitoring is required.
Treatment involves giving calcium gluconate to stabilize myo
cardium, salbutamol IV or nebulized, correcting acidosis, stopping all K, changing to low K feed, infusion of glucose and insulin, calcium resonium orally or rectally but can cause gastrointestinal obstruction.
Hypokalaemia – K <3.0 mmol/L
Causes include insufficient supplementations, diuretics, diarrhea, vomiting, renal tubular losses (e.g. Bartter syndrome), drugs, e.g.
amphotericin.
Calcium and phosphate
Hypocalcemia
Relatively common problem and can lead to seizures.
Causes: birth trauma/asphyxia, infants of diabetic mothers, exchange transfusion with blood reconstituted in citrate, maternal hyperparathyroidism, Di George syndrome, associated with hypo
magnesemia, maternal vitamin D deficiency.
Hypophosphatemia
Usually results from insufficient supplementation in feeds or parenteral nutrition.
Question
What is the significance of hypernatremia in breast fed babies?
Most breast fed babies have a normal serum sodium.
However, if there is insufficient intake of breast milk, the infant may develop hypernatremic dehydration. On examination the infants may not appear to have severe dehydration as the ante
rior fontanel may not be sunken and skin turgor may be normal as the extracellular fluid volume is relatively well maintained.
However, the baby may be lethargic and quiet and feed poorly because of cerebral intracellular dehydration. Movement of water from brain cells may cause a decrease in brain volume and rupture of intracerebral veins and bridging blood vessels resulting in hemorrhage and seizures. The definitive sign is significant weight loss, often in excess of 12% birth weight.
Once recognized, it is important that the serum sodium is corrected slowly over 2448 hours. Serum sodium may be extremely high (>160 mmol/L). Too rapid correction can result in seizures from too rapid expansion of cells in the brain. Lactation advice and support should be given to try to reestablish successful breastfeeding.
Hypernatremia has also been seen after accidental overconcentration of formula milk feeds or due to deliberate salt poisoning, although both are very rare.
Question
What are the ECG changes in hyperkalemia?
ECG changes progress with increasing potassium con centration:
• Initial changes – prolonged PR interval, peaked T waves
• Progression – absent P waves, ST depression, peaked T waves
• Further progression – QRS widening, ST depression, peaked T waves; danger of ventricular fibrillation and other arrhyth
mias and asystole
Key point
Unexpected hyperkalemia – repeat measurement as often due to hemolyzed blood sample.
Urinary tract infection (UTI)
• Commoner in boys than in girls – the reverse of older children.
• Should be suspected in any infant who is non‐specifically unwell.
Presentation
• Fever or sometimes low temperature or temperature instability
• Poor feeding
• Vomiting
• Prolonged jaundice
• Diarrhea
• Failure to thrive Investigations
Urine – collecting urine samples:
• clean catch specimen
• urethral catheterization
• suprapubic aspiration (see Chapter 76).
Blood culture and sepsis work‐up (with or without lumbar puncture) should be performed as urinary tract infection is often accompanied by septicemia in neonates.
Diagnosis
Is made by culture of a single strain of any organism on a catheter sample or suprapubic aspirate. However, may get false‐positive supra
pubic aspirate result from skin commensal or bowel perforation.
White cells may or may not be present on microscopy or urinalysis.
E. coli is the commonest organism (>75%); remainder caused by Klebsiella, Proteus, Enterobacter.
Management
Intravenous antibiotics – start immediately whilst awaiting the result of the urine culture. Subsequent choice of antibiotics will depend on the sensitivities of the cultured organism. Should be continued at full dosage until the infant has been well for 2–3 days
and a negative follow‐up urine culture obtained. Following treatment of culture positive UTI, oral prophylactic antibiotics, e.g.
trimethoprim or cefalexin, should be given until the results of imaging of the kidneys and urinary tract are known.
Imaging – if culture is positive, ultrasound of the kidneys and urinary tract is performed to detect renal tract abnormalities. A VCUG (voiding cystourethrogram, micturating cystourethrogram) is performed to identify bladder outflow obstruction, e.g. from posterior urethral valves or vesicoureteral reflux (Fig. 51.2).
A radionuclide scan (DMSA, dimercaptosuccinic acid) is per
formed 3 months later to identify renal scarring (Fig. 51.3).
Acute kidney injury, AKI (acute renal failure) In acute kidney injury (acute renal failure) there is sudden impair
ment in renal function leading to inability of the kidney to excrete nitrogenous waste and electrolytes. It is defined as a rise in the plasma creatinine concentration to twice the upper limit of normal, i.e. 1.5 mg/dL (130 mmol/L) accompanied by a reduction in urine flow rate to <1 mL/kg/hour. However, renal failure can occur without oliguria. It results from a significant fall in glomerular filtration rate with failure of tubular reabsorption of salt and water.
Causes
Different in neonates from children and adults as usually prerenal (Table 51.1). Mild renal impairment is not uncommon in the first few days of life, particularly in preterm infants, and is usually transient.
Clinical features
• Creatinine concentration raised – at birth it reflects maternal creatinine, falls over the next 46 weeks; a rising creatinine after day 1 suggests acute kidney injury
• Urinary features – oliguria, hematuria, proteinuria
• Clinical features – edema, dehydration, vomiting, lethargy, seizures, hypertension
Fig. 51.3 Bilateral renal scarring, more severe on right, on DMSA radionuclide scan on investigation following a urinary tract infection.
Fig. 51.2 VCUG (voiding cystourethrogram, micturating cystourethro
gram) showing trabeculation of the bladder wall, hypertrophy of the bladder and dilated posterior urethra from posterior urethral valves.
Renal and urinary tract disorders 125
• Other biochemical features – hyperkalemia, acidosis, hyper
phosphatemia and hypocalcemia Investigations
Ultrasound of kidneys and urinary tract – identifies if there are abnormal kidneys, outflow obstruction, abnormal blood flow in renal arteries and veins.
Management
Prevention
• Monitor the creatinine, blood urea nitrogen (urea) and electro
lytes of newborn infants who have been exposed to risk factors for acute kidney injury, such as birth asphyxia or sepsis
• Early treatment of hypovolemia
• Relief of obstruction
• Avoid nephrotoxic agents if possible Electrolyte and fluid management
• Restrict sodium, potassium and phosphate. Use calcium carbonate as phosphate binder. Correct metabolic acidosis.
• High‐dose furosemide 2–5 mg/kg to convert oliguric into non‐
oliguric renal failure.
• Nutritional support.
• Renal replacement therapy – rarely needed, only if fluid and metabolic abnormalities cannot be corrected. Peritoneal dialysis is preferable but may not be possible (e.g. abdominal wall defects or necrotizing enterocolitis). Hemodialysis is difficult due to vascular access and risks associated with anticoagulation.
Continuous veno‐venous hemofiltration is more gentle and better tolerated, especially in the sick neonate unable to tolerate inter
mittent hemodialysis.
Prognosis
Infants who develop acute kidney injury in the neonatal period have increased mortality, highest in extremely preterm.
Infants who have chronic kidney disease and need to start renal replacement therapy in the neonatal period have a 2‐year survival rate of 81%, with infection being the most common cause of death.
The 5‐year survival rate is 76%. However, there is significant comorbidity in the survivors, with growth problems, anemia and hypertension.
Table 51.1 Causes of acute kidney injury (acute renal failure) in neonates.
Prerenal Renal Postrenal
Hypovolemia
Dehydration, sepsis, necrotizing enterocolitis Blood loss: antepartum, neonatal
Heart failure
Hypoxia including birth asphyxia
Acute tubular necrosis secondary to an uncorrected prerenal cause Congenital renal abnormality, e.g. polycystic kidney disease, renal
agenesis, renal hypodysplasia
Vascular insult – renal vein thrombosis, renal artery thrombosis (associated with use of umbilical arterial lines)
Nephrotoxins, e.g. aminoglycosides
Congenital obstructive uropathy – posterior urethral valves, etc.
Neurogenic bladder
Infection – pyelonephritis
Neonatology at a Glance, Third Edition. Edited by Tom Lissauer, Avroy A. Fanaroff, Lawrence Miall and Jonathan Fanaroff.
© 2016 John Wiley & Sons, Ltd. Published 2016 by John Wiley & Sons, Ltd.
Features of the normal male genitalia are listed in Table 52.1. Most abnormalities arise from abnormal embryology (Fig. 52.1).
Inguinal hernia
This results from the processus vaginalis remaining patent. Much more common in males than females and usually on the right side.
Common in preterm infants, particularly those with broncho‐
pulmonary dysplasia as they have weak muscles and increased intra‐abdominal pressure.
Presents as a swelling in the groin or scrotum on crying (Fig. 52.2). It should be repaired promptly to avoid the risk of strangulation in both term and preterm infants, unless the anes- thetic risk necessitates delaying the operation.
If the hernia becomes irreducible, the lump is firm and tender, the infant vomits or becomes unwell, then an attempt should be made to reduce it after sustained gentle compression together with opioid analgesia. If possible, surgery is delayed for 24–48 hours to allow the edema to resolve. If reduction is unsuccessful, emergency surgery is required to avoid bowel strangulation and damage to the testis.
Hydrocele
This is fluid around the testis from a processus vaginalis that is wide enough to allow peritoneal fluid to flow down it but too narrow to form an inguinal hernia. Tense, transilluminates (Fig. 52.3). Often bilateral. Most resolve spontaneously.