normally high urine flow in the first days of life. For the same reason, with different conclusions, Koralkar et al. [35] proposed to define nAKI exclusively by creatinine criteria, applying a slight modification of the AKIN stage 3. However, the rate of creatinine decline in the first days of life should also be taken into account in order to adequately appreciate how the renal function of the baby is coping with excess maternal creatinine [36]. With the attempt of reconciling all these controversies, an nAKI workgroup on behalf of the National Institute of Diabetes and Digestive and Kidney Diseases recently proposed a definitive nAKI classification (Table 1) [37]. This definition differs from KDIGO in 3 essential points: (1) UO is recorded every 24 h rather than every 6–12 h because most neonatal ICUs do not report on an hourly diuresis. (2) In order to classify a patient with SCr-AKI, each measurement is compared with the lowest previous measurement to detect both an absolute and a percentage rise from “baseline.” This modification is required because serum creatinine values normally decline over the first weeks after birth, such that the baseline value is constantly changing. (3) Stage 3 is reached when a serum creatinine cutoff of 2.5 mg/dL (221 µmol/L), rather than 4.0 mg/dL (353.6 µmol/L) is reached, since a GFR of <10 mL/min/1.73 m2 is calculated in a neonate with such a SCr concentration. The validation of this classification was recently published in a multicentric observational trial, the Assessment of Worldwide Acute Kidney Injury Epidemiology in Neonates, conducted on more than 2,000 neonates [38] (see the pAKI chapter).
Conclusions
AKI is a complex syndrome with specific “endotypes” and pathophysiologies and no single definition will be perfect. Nonetheless, early standard recognition of AKI is crucial, since no specific therapeutic intervention has been demonstrated to be effective and standardized epidemiology and benchmarks are required. The KDIGO definition relies on changes in SCr and UO: 2 universally available and inexpensive markers that although imperfect represent a fundamental step forward in the field of critical care nephrology that has allowed the physicians to better identify AKI patients ahead of time. The KDIGO classification has significantly increased our insights into the epidemiology of the AKI syndrome both in children and adult critically ill patients and allowed clinicians and researchers to communicate in this field. A neonatal KDIGO is currently available and validated in order to definitely conclude the complex pathway of AKI definition in all populations and ages (AKI, pAKI, nAKI). By using a common language, studies and trials can be now compared.
References
1Pickkers P, Ostermann M, Joannidis M, Zarbock A, Hoste E, Bellomo R: The intensive care medicine agenda on acute kidney injury. Intensive Care Med 2017, Epub ahead of print.
2Meersch M, Zarbock A: Renal protection in the 21st century. Curr Opin Crit Care 2016;22:554–559.
3Ricci Z, Ronco C, D’Amico G, De Felice R, Rossi S, Bolgan I, et al: Practice patterns in the management of acute renal failure in the critically ill patient: an international survey. Nephrol Dial Transplant 2006;21:690–696.
4Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P: Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004;8:R204–R212.
5Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, et al: Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007;11:R31.
6Kidney Disease Improving Global Outcomes: Official Journal of the International Society of Nephrology KDIGO clinical practice guideline for anemia in chronic kidney disease. Kidney Int 2012;2:1–138.
7Hoste EA, Bagshaw SM, Bellomo R, Cely CM, Colman R, Cruz DN, et al: Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med 2015;41:1411–1423.
8Ronco C, Bellomo R, Kellum J: Understanding renal functional reserve. Intensive Care Med 2017;43:917–920.
9Traynor J, Mactier R, Geddes CC, Fox JG: How to measure renal function in clinical practice. BMJ 2006;333:733–737.
10van Acker BA, Koomen GC, Koopman MG, de Waart DR, Arisz L: Creatinine clearance with cimetidine for measurement of GFR. Lancet 1993;34:1089–1090.
11Delanaye P, Mariat C, Cavalier E, Maillard N, Krzesinski JM, White CA: Trimethoprim, creatinine and creatinine-based equations. Nephron Clin Pract 2011;119:187–194.
12Delanaye P, Cavalier E, Pottel H: Serum creatinine: not so simple! Nephron 2017;136:302–308.
13Papadakis MA, Arieff AI: Unpredictability of clinical evaluation of renal function in cirrhosis. Prospective study. Am J Med 1987;82:945–952.
14Doi K, Yuen PS, Eisner C, Hu X, Leelahavanichkul A, Schnermann J, et al: Reduced production of creatinine limits its use as marker of kidney injury in sepsis. J Am Soc Nephrol 2009;20:1217–1221.
15Preiss DJ, Godber IM, Lamb EJ, Dalton RN, Gunn IR: The influence of a cooked-meat meal on estimated glomerular filtration rate. Ann Clin Biochem 2007;44(pt 1):35–42.
16Liu KD, Thompson BT, Ancukiewicz M, Steingrub JS, Douglas IS, Matthay MA, et al: Acute kidney injury in patients with acute lung injury: impact of fluid accumulation on classification of acute kidney injury and associated outcomes. Crit Care Med 2011;39:2665–2671.
17Siew ED, Matheny ME: Choice of reference serum creatinine in defining acute kidney injury. Nephron 2015;2372:107–112.
18Schneider A, Ostermann M: The AKI glossary. Intensive Care Med 2017;43:893–897.
19Leedahl DD, Frazee EN, Schramm GE, Dierkhising RA, Bergstralh EJ, Chawla LS, et al: Derivation of urine output thresholds that identify a very high risk of AKI in patients with septic shock. Clin J Am Soc Nephrol 2014;9:1168–1174.
20Stevens LA, Coresh J, Greene T, Levey A: Assessing kidney function – measured and estimated glomerular filtration rate.
