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859 84 Hackbarth R, Bunchman TE, Chua AN, et al The effect of vascular access location and size on circuit survival in pediatric continuous renal replacement therapy a report from the PPCRRT registry[.]

43  Diagnosis and Treatment of Acute Kidney Injury in Children and Adolescents 84 Hackbarth R, Bunchman TE, Chua AN, et  al The effect of vascular access location and size on circuit survival in pediatric continuous renal replacement therapy: a report from the PPCRRT registry Int J Artif Organs 2007;30(12):1116–21 85 Garzotto F, Zanella M, Ronco C.  The evolution of pediatric continuous renal replacement therapy Nephron Clin Pract 2014;127(1–4):172–5 86 Flores FX, Brophy PD, Symons JM, et  al Continuous renal replacement therapy (CRRT) after stem cell transplantation A report from the prospective pediatric CRRT Registry Group Pediatr Nephrol 2008;23(4):625–30 87 Brophy PD, Mottes TA, Kudelka TL, et  al AN-69 membrane reactions are pH-dependent and preventable Am J Kidney Dis 2001;38(1):173–8 88 Pasko DA, Mottes TA, Mueller BA.  Pre dialysis of blood prime in continuous hemodialysis normalizes pH and electrolytes Pediatr Nephrol 2003;18(11):1177–83 89 Yessayan L, Yee J, Frinak S, Szamosfalvi B.  Treatment of severe hyponatremia in patients with kidney failure: role of continuous venovenous hemofiltration with low-sodium replacement fluid Am J Kidney Dis 2014;64(2):305–10 90 Askenazi DJ, Goldstein SL, Chang IF, Elenberg E, Feig DI.  Management of a severe carbamazepine overdose using albumin-enhanced continuous venovenous hemodialysis Pediatrics 2004;113(2):406–9 91 Collins KL, Roberts EA, Adeli K, Bohn D, Harvey EA. Single pass albumin dialysis (SPAD) in fulminant Wilsonian liver failure: a case report Pediatr Nephrol 2008;23(6):1013–6 92 Palevsky PM, Zhang JH, O’Connor TZ, et al Intensity of renal support in critically ill patients with acute kidney injury N Engl J Med 2008;359(1):7–20 93 Bellomo R, Cass A, Cole L, et al Intensity of continuous renal-replacement therapy in critically ill patients N Engl J Med 2009;361(17):1627–38 94 Liu C, Mao Z, Kang H, Hu J, Zhou F. Regional citrate versus heparin anticoagulation for continuous renal replacement therapy in critically ill patients: a meta-­ analysis with trial sequential analysis of randomized controlled trials Crit Care 2016;20(1):144 95 Raymakers-Janssen P, Lilien M, van Kessel IA, Veldhoen ES, Wosten-van Asperen RM, van Gestel 859 JPJ.  Citrate versus heparin anticoagulation in continuous renal replacement therapy in small children Pediatr Nephrol 2017;32(10):1971–8 96 Davenport A, Tolwani A.  Citrate anticoagulation for continuous renal replacement therapy (CRRT) in patients with acute kidney injury admitted to the intensive care unit NDT Plus 2009;2(6):439–47 97 Santiago MJ, Lopez-Herce J, Urbano J, et  al Complications of continuous renal replacement therapy in critically ill children: a prospective observational evaluation study Crit Care 2009;13(6):R184 98 Wang P-L, Meyer MM, Orloff SL, Anderson S. Bone resorption and “relative” immobilization hypercalcemia with prolonged continuous renal replacement therapy and citrate anticoagulation Am J Kidney Dis 2004;44(6):1110–4 99 Hauschild DB, Ventura JC, Mehta NM, Moreno YMF.  Impact of the structure and dose of protein intake on clinical and metabolic outcomes in critically ill children: a systematic review Nutrition 2017;41:97–106 100 Zuppa AF.  Understanding renal replacement therapy and dosing of drugs in pediatric patients with kidney disease J Clin Pharmacol 2012;52(1 Suppl):134s–40s 101 Veltri MA, Neu AM, Fivush BA, Parekh RS, Furth SL.  Drug dosing during intermittent hemodialysis and continuous renal replacement therapy: special considerations in pediatric patients Paediatr Drugs 2004;6(1):45–65 102 Harris RC, Breyer MD.  Update on cyclooxygenase-­ inhibitors Clin J Am Soc Nephrol 2006;1(2):236–45 103 Perazella MA. Onco-nephrology: renal toxicities of chemotherapeutic agents Clin J Am Soc Nephrol 2012;7(10):1713–21 104 Perazella MA.  Pharmacology behind common drug nephrotoxicities Clin J Am Soc Nephrol 2018;13(12):1897–908 105 Carvounis CP, Nisar S, Guro-Razuman S.  Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure Kidney Int 2002;62(6):2223–9 106 Fivez T, Kerklaan D, Mesotten D, et al Early versus late parenteral nutrition in critically ill children N Engl J Med 2016;374(12):1111–22 Neonatal Acute Kidney Injury 44 Cherry Mammen and David Askenazi Introduction Critically ill neonates admitted to neonatal and cardiac intensive care units are at high risk for acute kidney injury (AKI) In theory, the potential benefits to providing renal replacement therapy (RRT) for neonates with severe AKI are similar to larger pediatric and adult populations Performing peritoneal dialysis is possible even in the smallest of infants The use of extracorporeal therapies to provide RRT has been limited as the devices that are commonly used are not designed for small infants and carry added risks to the patient Fortunately, several novel machines with smaller extracorporeal volumes have been introduced into clinical practice in select centers around the world In this chapter, we will describe a case of a critically ill neonate admitted to the neonatal intensive care unit to illustrate the diagnosis of neonatal AKI, delineate consequences and medical management of AKI, discuss indications for RRT, compare and contrast options for care, and provide specifics of RRT in neonates Chapter contents directly relevant to the case are C Mammen (*) Department of Pediatrics, Division of Nephrology, BC Children’s Hospital, Vancouver, BC, Canada e-mail: cmammen@cw.bc.ca D Askenazi Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA provided in italics We conclude by reporting on the novel devices which promise to change the approach to the care of neonates who can benefit from RRT Case Presentation A term male infant is born via spontaneous vaginal delivery at 37  weeks gestational age to a 31-year-old G1P0 mother with history of maternal fever and prolonged rupture of membranes The infant is assessed in the nursery on the first day of life (DOL) with poor latching, shallow respirations, and lethargy With concerns of sepsis, he is transferred to the Neonatal Intensive Care Unit (NICU) Vital signs reveal elevated heart rate of 180 beats/minute, increased respiratory rate of 64 breaths/minute, increased temperature of 38.5 degrees Celsius, and low blood pressure (BP) of 42/20 mmHg (mean arterial pressure 30) Physical exam reveals poor peripheral pulses and prolonged capillary refill Initial labs include neutropenia (1.0 × 109/L) and lactic acidosis (HCO3 17  mmol/L, lactate 5.0  mmol/L) Chest X-ray shows normal heart size and lung fields Umbilical venous and arterial catheters are placed Boluses of 20 cc/kg of normal saline (NS) are administered with no improvement in blood pressure and no documented urine output Broad-­ spectrum intravenous antibiotics are started (ampicillin 50  mg/kg/dose q8h and gentamycin 2.5 mg/kg/dose q12h) With ongoing hypotension, © Springer Nature Switzerland AG 2021 B A Warady et al (eds.), Pediatric Dialysis, https://doi.org/10.1007/978-3-030-66861-7_44 861 C Mammen and D Askenazi 862 dopamine is started at mcg/kg/min, and 20 cc/ kg of NS was administered again to optimize ­perfusion Blood pressure stabilized at this point with a mean arterial pressure maintained above 40 mmHg Over the next 12 hours, dopamine is stopped due to stable BP. Blood cultures are positive for Group B Streptococcus (GBS) at 36 hours Infant is kept NPO, and standard total parenteral nutrition was commenced with an ongoing total fluid intake of 80 cc/kg/day and protein intake of 2.5 g/kg/day Gentamycin trough level before the third dose is elevated at 5.0 mg/L, and antibiotics are switched to IV penicillin (sensitive to GBS) A Foley catheter is inserted due to ongoing oliguria Renal ultrasound showed two normal-sized echogenic kidneys On the third DOL, severe body wall edema and ascites are noted, and the infant develops worsening respiratory distress requiring intubation and ventilation Chest X-ray is consistent with pulmonary edema and a slightly large cardiac silhouette Intravenous furosemide (1 mg/kg dose) is attempted with no increase in urine output Chemistry on DOL #3 reveals sodium (Na+) 127  mmol/L, potassium (K+) 6.4  mmol/L, bicarbonate (HCO3) 15  mmol/L (lactate normal), phosphate (PO4) 9.1  mg/dL (2.94  mmol/L), ionized calcium (Ca++) 1.0 mmol/L, uric acid 12 mg/dL (713 umol/L), and serum albumin of 1.8  g/dL.  Pediatric nephrology is consulted for further management of acute kidney injury Table 44.1 provides trends of renal function (blood urea nitrogen, and serum creatinine), weight, and urine output from birth till DOL Table 44.1  Renal function, weight, and urine output trends from case example Day of life BUN in mg/dL (urea in mmol/L) SCr in mg/dL (umol/L) Weight (kg) Urine output (ml/kg/hour) N/A N/A 3.4 22 (7.9) 0.7 (62) 3.7 0.2 42 (15) 1.1 (97) 4.0 0.3 70 (25) 2.1 (186) 4.3 0.3 BUN blood urea nitrogen, SCr serum creatinine, N/A not available Defining Neonatal AKI Acute kidney injury (AKI) has replaced the previous term “acute renal failure” in order to represent the entire spectrum of injury severity ranging from mild increases in serum creatinine (SCr) to severe oligoanuria requiring renal replacement therapy (RRT) Consequently, there has been a steady evolution of severity graded AKI definitions based on changes in serum creatinine (SCr) and/or urine output including RIFLE (Risk, Injury, Failure, Loss, and End Stage Renal Disease), AKIN (Acute Kidney Injury Network), and most recently the KDIGO (Kidney Disease: Improving Global Outcomes) definition in 2013 [1–3] These staged definitions were first validated for older pediatric and adult cohorts and more recently have been applied empirically to single- and multi-center neonatal studies Beyond the traditional challenges to using SCr to define AKI, there is added complexity in the first perinatal weeks due to the complex physiology surrounding adaptation and transition into the extrauterine environment Neonatal SCr around birth represents maternal creatinine and achieves a steady-state value over several days as the innate renal function equilibrates Preterm infants of approximately 30 weeks gestational age (GA) have a GFR

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