Renal replacement therapy (RRT) is an effective therapy for treating neonates with acute kidney injury (AKI) and inborn errors of metabolism with hyperammonemia.
Peritoneal dialysis is used most frequently to treat AKI in neonates, although intermittent hemodialysis and continuous renal replacement therapy (CRRT) are important alternatives.
Timely initiation of RRT may improve outcomes in neonates with AKI and volume overload.
RRT can be an important temporizing option in infants with chronic issues such as congenital anomalies of the kidney and urinary tract and inherited cystic diseases until transplantation is possible/available.
Treatment of hyperammonemia with dialysis may help reduce neurotoxicity.
CRRT can be useful in various combinations of ultrafiltration with hemodialysis.
Recent advances in the safe application and availability of renal replacement therapy (RRT) have changed the management of premature and young infants with acute kidney injury (AKI) or severe congenital anomalies of the kidney and urinary tracts. In the 1990s, only 41% of infants younger than 1 month of age were eligible to receive RRT. This number has steadily increased. This article reviews the available RRT options for neonates to treat AKI, inborn errors of metabolism with hyperammonemia, and renal structural anomalies until more definitive treatment becomes available.
Renal Replacement Therapy in Infants With Acute and Chronic Renal Failure
As described in other chapters in this section, the survival of infants with AKI and chronic renal failure is increasing. AKI is being recognized in up to 18% of very low birth weight infants, 23% to 52% of neonates being treated with cardiopulmonary bypass, and 71% of infants receiving extracorporeal membrane oxygenation (ECMO). The survival rates of infants with congenital anomalies of the kidney and the urinary tract (CAKUTs) and inherited cystic anomalies are also increasing. Encouragingly, many of these infants can be supported using RRT.
In RRT, the primary idea is to mimic the normal, physiologic renal system, where blood in the afferent arteriole enters the glomerular system for filtration and then exits through the efferent arteriole ( Fig. 59.1 ). Three RRT systems are currently available to support these infants with AKI and/or chronic renal failure. These systems include acute peritoneal dialysis (PD), intermittent hemodialysis (HD), and continuous renal replacement therapy (CRRT; Fig. 59.2 ). RRT can efficiently remove endogenous and exogenous toxins and maintain fluid, electrolyte, and acid-base balance in safe ranges until renal function recovers or a kidney transplantation is feasible/available ( Table 59.1 ).
|PD||Hemodialysis||Continuous Veno-Venous Hemofiltration/Hemodiafiltration|
|Ease of access||+++||−||−|
|Need for hemodynamic stability||−||+++||−(+)|
|Removal of potassium||++||++++||+(++)|
|Removal of ammonia||+||++++||+(+++)|
|Need for anticoagulation||−||++||−/+(−/+)|
|Reverse osmosis water||−||++++||−(−)?|
In neonates, the determinants of the efficacy of RRT in AKI or chronic kidney disease (CKD) are still being determined. Factors such as gestation, birth weight, the cause of kidney injury, the severity of metabolic derangements, hemodynamic changes, and nutritional needs are important. There is a need to understand the severity of renal failure and its progression to predict the need for RRT. The cause, the overall disease severity, its tempo, secondary changes in the fluid/electrolyte balance, and nutritional deficits are important. The renal injury may be underestimated because the lower muscle mass found in neonates may cause baseline levels of the traditional indicators such as blood urea nitrogen (BUN) and serum creatinine to be lower. These infants may also be less responsive to diuretics to excrete fluids and electrolytes and may develop fluid overload. The need for enteral feedings/hyperalimentation to support nutritional needs may be an important consideration for the initiation of RRT.
PD is an important therapy for AKI and CKD in neonates, even extremely low birth weight infants, in whom stable vascular access can be difficult to maintain. PD is relatively easy to perform; it only requires surgical insertion of a PD catheter, an intact peritoneal membrane that functions as the filter for dialysis, dialysis fluids, and connecting tubing and drainage bags. There is infrequent need for heparinization, and hemodynamic stability is not an absolute need. If needed, PD can be initiated soon after placement of the catheter using low-fill volumes such as 10 to 20 mL/kg, and the volumes can be increased as needed, although a period of catheter immobilization and healing of approximately 2 weeks is most ideal. The procedure can be used for long periods of time. The efficiency can be increased by increasing the frequency of exchanges as often as every hour and using dialysate with higher glucose concentrations.
The peritoneal cavity is accessed using a Tenckhoff catheter. Very low birth weight neonates can also be dialyzed using a 14-gauge vascular catheter to access the peritoneal fluid. Commercially available 1.5%, 2.5%, and 4.25% glucose solutions that have been warmed to body temperature should be used in PD ( Table 59.2 ). PD can be started in neonates with volumes of 5 to 10 mL/kg body weight, and the volumes can be gradually increased based on the need for solute and fluid removal and with safety based on the cardiovascular and respiratory status. Neonates with lactate acidosis should be dialyzed using a bicarbonate-buffered dialysate solution.
|Amino acids||1.1 g/dL|