Renal failure (neonatology)

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.

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. Acute kidney failure can progress to chronic failure.

Pathophysiology

 * 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.

Clinical picture

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

Diagnosis

 * 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.

Treatment

 * 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.

Clinical picture

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

Treatment

 * 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.

Related Articles

 * Acute renal failure (pediatrics) • Chronic renal dysfunction (pediatrics)
 * Renal failure • Acute renal failure • Treatment of acute renal failure • Chronic kidney disease
 * Kidney • Nephron • Kidney function • Kidney function in maintaining acid-base balance