J Pediatr Intensive Care 2024; 13(01): 080-086
DOI: 10.1055/s-0041-1736549
Original Article

Urinary Chloride Excretion Postcardiopulmonary Bypass in Pediatric Patients—A Pilot Study

Sophie Fincher
1   Department of Pediatric Intensive Care, Queensland Children's Hospital, Brisbane, Australia
2   Pediatric Critical Care Research Group, Brisbane, Australia
,
Kristen Gibbons
2   Pediatric Critical Care Research Group, Brisbane, Australia
3   Child Health Research Centre, The University of Queensland, Brisbane, Australia
,
Kerry Johnson
1   Department of Pediatric Intensive Care, Queensland Children's Hospital, Brisbane, Australia
2   Pediatric Critical Care Research Group, Brisbane, Australia
3   Child Health Research Centre, The University of Queensland, Brisbane, Australia
,
Peter Trnka
4   School of Medicine, The University of Queensland, Brisbane, Australia
5   Queensland Child and Adolescent Renal Service, Queensland Children's Hospital, Brisbane, Australia
,
Adrian C. Mattke
1   Department of Pediatric Intensive Care, Queensland Children's Hospital, Brisbane, Australia
2   Pediatric Critical Care Research Group, Brisbane, Australia
3   Child Health Research Centre, The University of Queensland, Brisbane, Australia
4   School of Medicine, The University of Queensland, Brisbane, Australia
› Author Affiliations
Funding The study received in-kind support from the Pediatric Intensive Care Unit, Queensland Children's Hospital, South Brisbane, Australia.

Abstract

The aim of this study was to describe renal chloride metabolism following cardiopulmonary bypass (CPB) surgery in pediatric patients. A prospective observational trial in a tertiary pediatric intensive care unit (PICU) with 20 recruited patients younger than 2 years following CPB surgery was conducted. Urinary electrolytes, plasma urea, electrolytes, creatinine, and arterial blood gases were collected preoperatively, on admission to PICU and at standardized intervals thereafter. The urinary and plasma strong ion differences (SID) were calculated from these results at each time point. Fluid input and output and electrolyte and drug administration were also recorded. Median chloride administration was 67.7 mmol/kg over the first 24 hours. Urinary chloride (mmol/L; median interquartile range [IQR]) was 30 (19, 52) prior to surgery, 15 (15, 65) on admission, and remained below baseline until 24 hours. Plasma chloride (mmol/L; median [IQR]) was 105 (98, 107) prior to surgery and 101 (101, 106) on admission to PICU. It then increased from baseline, but remained within normal limits, for the remainder of the study. The urinary SID increased from 49.8 (19.1, 87.2) preoperatively to a maximum of 122.7 (92.5, 151.8) at 6 hours, and remained elevated until 48 hours. Plasma and urinary chloride concentrations were not associated with the development of acute kidney injury. Urinary chloride excretion is impaired after CPB. The urinary SID increase associated with the decrease in chloride excretion suggests impaired production and/or excretion of ammonium by the nephron following CPB, with gradual recovery postoperatively.

Note

This study was performed at the Queensland Children's Hospital.


Ethical Approval

Ethical approval for this study was received from the Children's Health Queensland Human Research Ethics Committee (HREC/17/QRCH/310).




Publication History

Received: 06 June 2021

Accepted: 10 September 2021

Article published online:
22 October 2021

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  • References

  • 1 Yunos NM, Bellomo R, Glassford N, Sutcliffe H, Lam Q, Bailey M. Chloride-liberal vs. chloride-restrictive intravenous fluid administration and acute kidney injury: an extended analysis. Intensive Care Med 2015; 41 (02) 257-264
  • 2 Suetrong B, Pisitsak C, Boyd JH, Russell JA, Walley KR. Hyperchloremia and moderate increase in serum chloride are associated with acute kidney injury in severe sepsis and septic shock patients. Crit Care 2016; 20 (01) 315
  • 3 Yessayan L, Neyra JA, Canepa-Escaro F, Vasquez-Rios G, Heung M, Yee J. Acute Kidney Injury in Critical Illness Study Group. Effect of hyperchloremia on acute kidney injury in critically ill septic patients: a retrospective cohort study. BMC Nephrol 2017; 18 (01) 346
  • 4 Self WH, Semler MW, Wanderer JP. et al; SALT-ED Investigators. Balanced crystalloids versus saline in noncritically ill adults. N Engl J Med 2018; 378 (09) 819-828
  • 5 Stenson EK, Cvijanovich NZ, Allen GL. et al. Hyperchloremia is associated with acute kidney injury in pediatric patients with septic shock. Intensive Care Med 2018; 44 (11) 2004-2005
  • 6 Kimura S, Iwasaki T, Shimizu K. et al. Hyperchloremia is not an independent risk factor for postoperative acute kidney injury in pediatric cardiac patients. J Cardiothorac Vasc Anesth 2019; 33 (07) 1939-1945
  • 7 Barhight MF, Lusk J, Brinton J. et al. Hyperchloremia is independently associated with mortality in critically ill children who ultimately require continuous renal replacement therapy. Pediatr Nephrol 2018; 33 (06) 1079-1085
  • 8 Oh TK, Kim CY, Jeon YT, Hwang JW, Do SH. Perioperative hyperchloremia and its association with postoperative acute kidney injury after craniotomy for primary brain tumor resection: a retrospective, observational study. J Neurosurg Anesthesiol 2019; 31 (03) 311-317
  • 9 Oh TK, Song IA, Kim SJ. et al. Hyperchloremia and postoperative acute kidney injury: a retrospective analysis of data from the surgical intensive care unit. Crit Care 2018; 22 (01) 277
  • 10 Yunos NM, Bellomo R, Taylor DM. et al. Renal effects of an emergency department chloride-restrictive intravenous fluid strategy in patients admitted to hospital for more than 48 hours. Emerg Med Australas 2017; 29 (06) 643-649
  • 11 Mamikonian LS, Mamo LB, Smith PB, Koo J, Lodge AJ, Turi JL. Cardiopulmonary bypass is associated with hemolysis and acute kidney injury in neonates, infants, and children*. Pediatr Crit Care Med 2014; 15 (03) e111-e119
  • 12 Wilcox CS. Regulation of renal blood flow by plasma chloride. J Clin Invest 1983; 71 (03) 726-735
  • 13 Weiner ID, Verlander JW. Recent advances in understanding renal ammonia metabolism and transport. Curr Opin Nephrol Hypertens 2016; 25 (05) 436-443
  • 14 Batlle DC, Hizon M, Cohen E, Gutterman C, Gupta R. The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. N Engl J Med 1988; 318 (10) 594-599
  • 15 Gattinoni L, Carlesso E, Cadringher P, Caironi P. Strong ion difference in urine: new perspectives in acid-base assessment. Crit Care 2006; 10 (02) 137
  • 16 Halperin ML, Richardson RM, Bear RA, Magner PO, Kamel K, Ethier J. Urine ammonium: the key to the diagnosis of distal renal tubular acidosis. Nephron 1988; 50 (01) 1-4
  • 17 Singh SP. Acute kidney injury after pediatric cardiac surgery. Ann Card Anaesth 2016; 19 (02) 306-313
  • 18 Li S, Krawczeski CD, Zappitelli M. et al; TRIBE-AKI Consortium. Incidence, risk factors, and outcomes of acute kidney injury after pediatric cardiac surgery: a prospective multicenter study. Crit Care Med 2011; 39 (06) 1493-1499
  • 19 Yuan SM. Acute kidney injury after pediatric cardiac surgery. Pediatr Neonatol 2019; 60 (01) 3-11
  • 20 Boehne M, Sasse M, Karch A. et al. Systemic inflammatory response syndrome after pediatric congenital heart surgery: incidence, risk factors, and clinical outcome. J Card Surg 2017; 32 (02) 116-125
  • 21 Balsorano P, Romagnoli S, Evans SK, Ricci Z, De Gaudio AR. Urinary strong ion difference as a marker of renal dysfunction. A retrospective analysis. PLoS One 2016; 11 (06) e0156941
  • 22 Schreuder MF, Bökenkamp A, van Wijk JAE. Interpretation of the fractional excretion of sodium in the absence of acute kidney injury: a cross-sectional study. Nephron 2017; 136 (03) 221-225
  • 23 Kellum JA, Lameire N. KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (part 1). Crit Care 2013; 17 (01) 204
  • 24 Kwiatkowski DM, Krawczeski CD. Acute kidney injury and fluid overload in infants and children after cardiac surgery. Pediatr Nephrol 2017; 32 (09) 1509-1517
  • 25 Weiner ID, Verlander JW. Role of NH3 and NH4+ transporters in renal acid-base transport. Am J Physiol Renal Physiol 2011; 300 (01) F11-F23
  • 26 Weiner ID, Verlander JW. Renal ammonia metabolism and transport. Compr Physiol 2013; 3 (01) 201-220
  • 27 Ring T, Frische S, Nielsen S. Clinical review: renal tubular acidosis–a physicochemical approach. Crit Care 2005; 9 (06) 573-580
  • 28 Corey HE, Vallo A, Rodríguez-Soriano J. An analysis of renal tubular acidosis by the Stewart method. Pediatr Nephrol 2006; 21 (02) 206-211
  • 29 Murray D, Grant D, Murali N, Butt W. Unmeasured anions in children after cardiac surgery. J Thorac Cardiovasc Surg 2007; 133 (01) 235-240
  • 30 Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA 2012; 308 (15) 1566-1572
  • 31 Yunos NM, Bellomo R, Story D, Kellum J. Bench-to-bedside review: chloride in critical illness. Crit Care 2010; 14 (04) 226
  • 32 Yunos NM, Kim IB, Bellomo R. et al. The biochemical effects of restricting chloride-rich fluids in intensive care. Crit Care Med 2011; 39 (11) 2419-2424
  • 33 Diedericks BJ, Roelofse JA, Shipton EA, Gray IP, de Wet JI, Hugo SA. The renin-angiotensin-aldosterone system during and after cardiopulmonary bypass. S Afr Med J 1983; 64 (24) 946-949
  • 34 Verbrugge FH, Tang WH, Mullens W. Renin-angiotensin-aldosterone system activation during decongestion in acute heart failure: friend or foe?. JACC Heart Fail 2015; 3 (02) 108-111
  • 35 Lorenz JN, Weihprecht H, Schnermann J, Skøtt O, Briggs JP. Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport. Am J Physiol 1991; 260 (4 Pt 2): F486-F493
  • 36 Goldstein SL. A new pediatric AKI definition: implications of trying to build the perfect mousetrap. J Am Soc Nephrol 2018; 29 (09) 2259-2261
  • 37 Ricci Z, Di Nardo M, Iacoella C, Netto R, Picca S, Cogo P. Pediatric RIFLE for acute kidney injury diagnosis and prognosis for children undergoing cardiac surgery: a single-center prospective observational study. Pediatr Cardiol 2013; 34 (06) 1404-1408
  • 38 Morgan CJ, Zappitelli M, Robertson CM. et al; Western Canadian Complex Pediatric Therapies Follow-Up Group. Risk factors for and outcomes of acute kidney injury in neonates undergoing complex cardiac surgery. J Pediatr 2013; 162 (01) 120-7.e1
  • 39 Ichimura T, Bonventre JV, Bailly V. et al. Kidney injury molecule-1 (KIM-1), a putative epithelial cell adhesion molecule containing a novel immunoglobulin domain, is up-regulated in renal cells after injury. J Biol Chem 1998; 273 (07) 4135-4142
  • 40 Han WK, Bailly V, Abichandani R, Thadhani R, Bonventre JV. Kidney injury molecule-1 (KIM-1): a novel biomarker for human renal proximal tubule injury. Kidney Int 2002; 62 (01) 237-244
  • 41 Kullmar M, Saadat-Gilani K, Weiss R. et al. Kinetic changes of plasma renin levels predict acute kidney injury in cardiac surgery patients. Am J Respir Crit Care Med 2021; 203 (09) 1119-1126
  • 42 Hirsch R, Dent C, Pfriem H. et al. NGAL is an early predictive biomarker of contrast-induced nephropathy in children. Pediatr Nephrol 2007; 22 (12) 2089-2095