Therapeutic Options for Neonatal Acute Kidney Injury (AKI)

Abstract

Neonatal acute kidney injury (AKI) I Renal failure I CRRT I CVVH I Peritoneal dialysis I Renal support therapy I Fluid overload I Renal recovery I Dialysis I Theophylline I Nephrotoxic I Prevention I CARPEDIEM I NIDUS Opinion statement Acute kidney injury (AKI) occurs commonly in neonates and is associated with increased mortality. Recent advances in neonatal intensive care have resulted in improved patient survival, but this had not been paralleled by improved outcomes for neonates with AKI. Management of AKI remains supportive with no effective pharmacologic therapy to hasten the recovery process. Emphasis is placed on the prevention and minimization of further renal insults once AKI is established. Routine, regular assessments of renal function with identification of high risk patients and those with incipient AKI are essential so prevention strategies can be promptly initiated. Effective prevention strategies include prompt restoration/preservation of organ perfusion with fluid resuscitation to ensure an adequate effective circulating volume and inotropic support as needed to maintain hemodynamic stability while also avoiding/minimizing nephrotoxin exposure. In established AKI, efforts are focused on maintaining organ perfusion while closely monitoring cumulative fluid balance from admission and remaining cognizant of the need to minimize the degree of fluid overload as this has also been associated with poor outcomes. Continuous renal replacement therapy (CRRT) has become the preferred therapy for managing fluid overload and metabolic disturbances in critically ill children and adults but is still considered by many to be a heroic intervention for neonates due in large part to numerous technical challenges. The recent development of two miniaturized machines specifically designed to deliver CRRT and hemodialysis (HD) to neonates will hopefully change this paradigm making it easier for nephrologists and intensivists to safely offer and provide this therapy to neonates. Prospective studies are needed to assess whether early initiation of RRT with correction of fluid imbalance results in improved patient survival and renal recovery.

Incidence, risk and risk factors for acute kidney injury associated with the use of intravenous indomethacin in neonatal patent ductus arteriosus: A 16-year retrospective cohort study

“…Likewise, vasopressors and inotropes seemed to increase the AKI risk, the association was still imprecise. A retrospective cohort study conducted by 27,28 The present study, however did not find the dose-dependent effects (data not shown).…”

Neonatal AKI profile using KDIGO guidelines: A cohort study in tertiary care hospital ICU of Lahore, Pakistan

“…Similar results have been reflected in our study that show that these drugs have a negligible contribution to AKI. The supporting data from other studies highlight that AKI is associated with poor outcomes [1][2][3][4][5][6][7][8][9][10][11][12][13]. Jetton et al analysis shows that neonates with AKI have 8.8 times longer duration of stay and 4.6 times higher mortality as compared to the non-AKI group [5].…”

“…6 Our study highlights the association between intraventricular hemorrhage and disseminated intravascular coagulation with acute renal insult. Both DIC and IVH lead to a decrease in effective circulatory volume resulting in renal hypo-perfusion and failure [3].…”

“…Acute kidney injury (AKI) is a condition characterized by an acute decline in kidney functions affecting fluid and electrolyte homeostasis and elimination of waste products [1]. Neonate are at increased risk of developing acute kidney injury because of relatively immature kidneys and low glomerular filtration rate [2,3]. In neonates, oliguria (urine output < 0.5 – 1.0 ml/kg/hr) may or may not be present in case of AKI [4].…”

Modern View on Diagnostics and Treatment of Acute Kidney Injury in Full-Term Newborns With Hypoxic-Ischemic Encephalopathy

“…В діапазоні від 40 до 90 мл/хв/1,73м2 немає пропорційності між підвищення концентрації креатиніну та зниженням ШКФ. Підвищення рівню креатиніну починається тільки після зниження ШКФ на 50 % і нижче [43]. На відміну від цистатину С, сироватковий креатинін має значну кореляцію з масою тіла.…”