Renal failure (neonatology)

From WikiLectures

Renal failure in newborns is a life-threatening condition caused by acute or gradually developing impairment of kidney function. Acute kidney failure is significantly more common in newborns.[1]

Acute kidney failure (acute kidney injury, AKI) is a condition accompanied by a sudden decrease in glomerular filtration. There is no clear definition of ARF in newborns, but from a practical point of view kidney damage can be considered if the creatinine level does not decrease after birth or if the creatinine level > 130 µmol/L (> 1.5 mg/dl) persists. According to diuresis, AKI can be divided into oliguric (diuresis < 1 ml/kg) and non-oliguric (diuresis > 1 ml/kg). AKI can also be accompanied by completely normal diuresis (ie 1-3 ml/kg/h), for example in newborns after asphyxia. In newborns, prerenal failure is the most common type, while renal and postrenal failure are less common.[2][3] Acute kidney failure can progress to chronic failure.

Acute Renal Failure[edit | edit source]

Pathophysiology[edit | edit source]

Prerenal causes
  • occurs as a result of impaired kidney perfusion, which leads to deterioration of normal kidney function;
  • causes: bleeding, dehydration, septic shock, congestive heart failure, patent Botall duct (PDA), necrotizing enterocolitis, respiratory distress syndrome, hypoxia, congenital heart defects, hypoalbuminemia, perinatal asphyxia, ECMO and hypotension, drugs: indomethacin ibuprofen, ACE inhibitors; drugs used by the mother: NSAIDs, ACE inhibitors, COX-2 inhibitors.
Renal causes
  • arises as a result of structural kidney damage that leads to renal tubular dysfunction;
  • causes: acute tubular necrosis (most common; causes are prolonged kidney hypoperfusion, ischemia or hypoxia, sepsis, cardiac surgery - transfusion of blood derivatives, aminoglycosides, NSAIDs, amphotericin B, contrast agents, acyclovir), congenital kidney defects (bilateral renal agenesis, polycystic kidney disease, congenital nephrotic syndrome, renal hypoplasia/dysplasia), vascular lesions (bilateral venous/arterial renal thrombosis, cortical necrosis, DIC), infections (congenital syphilis, toxoplasmosis, candidiasis, pyelonephritis) and toxins (myoglobinuria, hemoglobinuria).
Postrenal/obstructive causes
  • arises as a result of obstruction of the urinary tract;
  • causes: posterior valve of the urethra, strictures and stenosis of the urinary tract, etc.[3]

Clinical picture[edit | edit source]

  • positive family history
  • oligohydramnios, pulmonary hypoplasia (in severe oligohydramnios)
  • palpable resistance when palpating the abdomen
  • reduced diuresis
  • Prune belly syndrome, meningomyelocele, Potter facies.[3]

Diagnosis[edit | edit source]

  • insertion of a urinary catheter
  • serum level of urea and creatinine
  • urinalysis: osmolality, sodium and creatinine (serum vs. urine)
  • blood count (sepsis, thrombocytopenia - renal venous thrombosis), serum potassium level (increased in renal insufficiency), urine examination (hematuria - renal venous thrombosis, tumors, DIC; pyuria - urinary tract infection)
  • fluid challenge: i.v. crystalloid bolus and then furosemide bolus - if diuresis does not increase, look for obstruction proximal to the bladder (ultrasound), once obstruction is ruled out intrinsic renal failure is the most likely cause
  • imaging methods: abdominal ultrasound.[3]

Treatment[edit | edit source]

  • treatment of the underlying cause
  • fluid balance, compensation of fluid losses
  • monitoring of serum sodium and potassium levels (risk of hypoNa and hyperK)
  • protein intake restriction < 2 g/kg/day
  • monitoring of phosphorus and calcium levels (risk of hyperP and hypoCa)
  • correction of metabolic acidosis - chronic oral bicarbonate supplementation at pH < 7.25 and serum bicarbonate level < 12 mmol/l
  • blood pressure monitoring (risk of hypertension)
  • peritoneal dialysis (method of choice), hemodialysis, hemofiltration.[3]

Chronic renal failure[edit | edit source]

Causes[edit | edit source]

Clinical picture[edit | edit source]

  • failure to thrive, accidental detection of elevated serum creatinine level
  • increased excretion of sodium in the urine - tendency to hyponatremia
  • arterial hypertension.[2]

Treatment[edit | edit source]

  • ensuring sufficient energy supply (optimally 150-180 kcal/kg/day)
  • uremia leads to loss of appetite, nausea and vomiting, therefore nasogastric tube feeding is often necessary
  • substitution with sodium bicarbonate to achieve a plasma bicarbonate level of 22-24 mmol/l
  • in case of hyponatremia and failure to benefit from NaCl supplementation
  • calcium supplementation (Ca gluconicum) to maintain a normal plasma level of phosphorus.[2]

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References[edit | edit source]

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External links[edit | edit source]

Reference[edit | edit source]

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  2. a b c d e