Non-cardiogenic pulmonary edema during basiliximab induction in three adolescent renal transplant patients

Fatai O. Bamgbola, Marcela Del Rio, Frederick J. Kaskel, Joseph T. Flynn

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background: Introduction of the anti-CD-25 mAb basiliximab into renal transplant protocols has reduced the incidence of acute rejection. However, its side-effect profile is still unfolding. We report three adolescents who developed severe non-cardiogenic PE within 2 days of renal transplantation. Methods: Pretransplant cardiorespiratory evaluation was normal in all cases. Transplant immunosuppression consisted of basiliximab induction, corticosteroids, and tacrolimus. Patients received standard fluid management during and after the transplant surgery. Case reports: Patients 1 and 2 were 17- and 21-yr-old females. Pretransplant Hct values were 35 and 25% respectively. Each received 5-L normal saline during surgery. EBL was 200 and 500 mL in patients 1 and 2, respectively. There was immediate post-operative diuresis. Both developed non-cardiogenic PE by POD no. 2. BIPAP and PRVC were administered respectively. In both cases PE resolved within 1 wk. Patient 3 was a 19-yr-old male with pretransplant Hct of 43% who received a cadaveric renal transplant after 23.5-h cold-ischemia; 3.5 L normal saline was given during surgery. EBL was 100 mL. Non-cardiogenic PE ensued on POD no. 2 warranting assisted ventilation. The patient died following a sudden cardiopulmonary arrest on POD no. 3. Conclusions: Potential mechanisms for the development of PE include cytokine release from basiliximab with increased capillary permeability, volume overload and ischemic-reperfusion injury. Improved awareness of this potential complication, prudent fluid management, and efforts to minimize graft-ischemia are recommended to prevent further cases.

Original languageEnglish (US)
Pages (from-to)315-320
Number of pages6
JournalPediatric Transplantation
Volume7
Issue number4
DOIs
StatePublished - Aug 2003

Fingerprint

Pulmonary Edema
Transplants
Kidney
Cold Ischemia
Diuresis
Capillary Permeability
Tacrolimus
Heart Arrest
Reperfusion Injury
Kidney Transplantation
Immunosuppression
Ventilation
Adrenal Cortex Hormones
Ischemia
basiliximab
Cytokines
Incidence

Keywords

  • Acute lung injury
  • Basiliximab
  • Capillary leak syndrome
  • Children
  • Monoclonal antibody
  • Renal transplant

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Transplantation

Cite this

Non-cardiogenic pulmonary edema during basiliximab induction in three adolescent renal transplant patients. / Bamgbola, Fatai O.; Del Rio, Marcela; Kaskel, Frederick J.; Flynn, Joseph T.

In: Pediatric Transplantation, Vol. 7, No. 4, 08.2003, p. 315-320.

Research output: Contribution to journalArticle

@article{ae935a0715254292b71ff55945a16e73,
title = "Non-cardiogenic pulmonary edema during basiliximab induction in three adolescent renal transplant patients",
abstract = "Background: Introduction of the anti-CD-25 mAb basiliximab into renal transplant protocols has reduced the incidence of acute rejection. However, its side-effect profile is still unfolding. We report three adolescents who developed severe non-cardiogenic PE within 2 days of renal transplantation. Methods: Pretransplant cardiorespiratory evaluation was normal in all cases. Transplant immunosuppression consisted of basiliximab induction, corticosteroids, and tacrolimus. Patients received standard fluid management during and after the transplant surgery. Case reports: Patients 1 and 2 were 17- and 21-yr-old females. Pretransplant Hct values were 35 and 25{\%} respectively. Each received 5-L normal saline during surgery. EBL was 200 and 500 mL in patients 1 and 2, respectively. There was immediate post-operative diuresis. Both developed non-cardiogenic PE by POD no. 2. BIPAP and PRVC were administered respectively. In both cases PE resolved within 1 wk. Patient 3 was a 19-yr-old male with pretransplant Hct of 43{\%} who received a cadaveric renal transplant after 23.5-h cold-ischemia; 3.5 L normal saline was given during surgery. EBL was 100 mL. Non-cardiogenic PE ensued on POD no. 2 warranting assisted ventilation. The patient died following a sudden cardiopulmonary arrest on POD no. 3. Conclusions: Potential mechanisms for the development of PE include cytokine release from basiliximab with increased capillary permeability, volume overload and ischemic-reperfusion injury. Improved awareness of this potential complication, prudent fluid management, and efforts to minimize graft-ischemia are recommended to prevent further cases.",
keywords = "Acute lung injury, Basiliximab, Capillary leak syndrome, Children, Monoclonal antibody, Renal transplant",
author = "Bamgbola, {Fatai O.} and {Del Rio}, Marcela and Kaskel, {Frederick J.} and Flynn, {Joseph T.}",
year = "2003",
month = "8",
doi = "10.1034/j.1399-3046.2003.00083.x",
language = "English (US)",
volume = "7",
pages = "315--320",
journal = "Pediatric Transplantation",
issn = "1397-3142",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Non-cardiogenic pulmonary edema during basiliximab induction in three adolescent renal transplant patients

AU - Bamgbola, Fatai O.

AU - Del Rio, Marcela

AU - Kaskel, Frederick J.

AU - Flynn, Joseph T.

PY - 2003/8

Y1 - 2003/8

N2 - Background: Introduction of the anti-CD-25 mAb basiliximab into renal transplant protocols has reduced the incidence of acute rejection. However, its side-effect profile is still unfolding. We report three adolescents who developed severe non-cardiogenic PE within 2 days of renal transplantation. Methods: Pretransplant cardiorespiratory evaluation was normal in all cases. Transplant immunosuppression consisted of basiliximab induction, corticosteroids, and tacrolimus. Patients received standard fluid management during and after the transplant surgery. Case reports: Patients 1 and 2 were 17- and 21-yr-old females. Pretransplant Hct values were 35 and 25% respectively. Each received 5-L normal saline during surgery. EBL was 200 and 500 mL in patients 1 and 2, respectively. There was immediate post-operative diuresis. Both developed non-cardiogenic PE by POD no. 2. BIPAP and PRVC were administered respectively. In both cases PE resolved within 1 wk. Patient 3 was a 19-yr-old male with pretransplant Hct of 43% who received a cadaveric renal transplant after 23.5-h cold-ischemia; 3.5 L normal saline was given during surgery. EBL was 100 mL. Non-cardiogenic PE ensued on POD no. 2 warranting assisted ventilation. The patient died following a sudden cardiopulmonary arrest on POD no. 3. Conclusions: Potential mechanisms for the development of PE include cytokine release from basiliximab with increased capillary permeability, volume overload and ischemic-reperfusion injury. Improved awareness of this potential complication, prudent fluid management, and efforts to minimize graft-ischemia are recommended to prevent further cases.

AB - Background: Introduction of the anti-CD-25 mAb basiliximab into renal transplant protocols has reduced the incidence of acute rejection. However, its side-effect profile is still unfolding. We report three adolescents who developed severe non-cardiogenic PE within 2 days of renal transplantation. Methods: Pretransplant cardiorespiratory evaluation was normal in all cases. Transplant immunosuppression consisted of basiliximab induction, corticosteroids, and tacrolimus. Patients received standard fluid management during and after the transplant surgery. Case reports: Patients 1 and 2 were 17- and 21-yr-old females. Pretransplant Hct values were 35 and 25% respectively. Each received 5-L normal saline during surgery. EBL was 200 and 500 mL in patients 1 and 2, respectively. There was immediate post-operative diuresis. Both developed non-cardiogenic PE by POD no. 2. BIPAP and PRVC were administered respectively. In both cases PE resolved within 1 wk. Patient 3 was a 19-yr-old male with pretransplant Hct of 43% who received a cadaveric renal transplant after 23.5-h cold-ischemia; 3.5 L normal saline was given during surgery. EBL was 100 mL. Non-cardiogenic PE ensued on POD no. 2 warranting assisted ventilation. The patient died following a sudden cardiopulmonary arrest on POD no. 3. Conclusions: Potential mechanisms for the development of PE include cytokine release from basiliximab with increased capillary permeability, volume overload and ischemic-reperfusion injury. Improved awareness of this potential complication, prudent fluid management, and efforts to minimize graft-ischemia are recommended to prevent further cases.

KW - Acute lung injury

KW - Basiliximab

KW - Capillary leak syndrome

KW - Children

KW - Monoclonal antibody

KW - Renal transplant

UR - http://www.scopus.com/inward/record.url?scp=0042736126&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0042736126&partnerID=8YFLogxK

U2 - 10.1034/j.1399-3046.2003.00083.x

DO - 10.1034/j.1399-3046.2003.00083.x

M3 - Article

C2 - 12890011

AN - SCOPUS:0042736126

VL - 7

SP - 315

EP - 320

JO - Pediatric Transplantation

JF - Pediatric Transplantation

SN - 1397-3142

IS - 4

ER -