This Article Abstract Résumé de cet Article Full Text (PDF) Submit a scholarly reply Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kutsogiannis, D. J. Articles by Shemie, S. D. Search for Related Content PubMed PubMed Citation Articles by Kutsogiannis, D. J. Articles by Shemie, S. D.

Medical management to optimize donor organ potential: review of the literature

[Traitement médical pour optimaliser le potentiel de don d’organe : une revue documentaire]

Demetrios J. Kutsogiannis, MD^*, Giuseppe Pagliarello, MD, Christopher Doig, MD, Heather Ross, MD and Sam D. Shemie, MD^¶

^* From the Division of Critical Care Medicine and Public Health Sciences,University of Alberta, Edmonton, Alberta; the
Department of Surgery and Critical Care Medicine, University of Ottawa, Ottawa, Ontario;
Adult Critical Care, Foothills Hospital, University of Calgary, Calgary, Alberta;
Cardiac Transplant Program, University Health Network, University of Toronto, Toronto, Ontario; and the
^¶ Division of Pediatric Critical Care, Montreal Children’s Hospital, McGill University Health Centre, Montreal, Quebec, Canada.

Address correspondence to: Dr. Demetrios J. Kutsogiannis, MMC 102-7, Royal Alexandra Hospital, 10240 Kingsway Avenue, Edmonton, Alberta T5H 3V9, Canada. Phone: 780-735-5387; Fax: 780-735-4032; E-mail: dkutsogi{at}telusplanet.net

	Abstract

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Purpose: Over the past two decades, the demand for donor organs continues to outpace the number of organs available for transplantation. Parallel with this has been a change in the demographics of organ donors with an increase in older donors and donors with marginal organs as a proportion of the total organ donor pool. Consequently, efforts have been made to improve the medical care delivered to potential organ donors to improve the conversion rate and graft survival of available organs. The purpose of this literature review is to provide updated recommendations for the contemporary management of organ donors after the neurological determination of death in order to maximize the probability of recipient graft survival.

Sources: A comprehensive review of the literature obtained through searches of MEDLINE/PubMed, and personal reference files.

Principal findings: Contemporary management of the organ donor after neurological determination of death includes therapies to prevent the detrimental effects of the autonomic storm, the use of invasive hemodynamic monitoring and aggressive respiratory therapy including therapeutic bronchoscopy in marginal heart and lung donors, and the use of hormonal therapy including vasopressin, corticosteroids, triiodothyronine or thyroxine, and insulin for the pituitary failure and inflammation seen in brain dead organ donors. The importance of normalizing donor physiology to optimize all available organs is stressed.

Conclusion: Aggressive hemodynamic and respiratory management of solid organ donors, coupled with the use of hormonal therapy improves the rate of conversion and graft survival in solid organ recipients.

	Introduction

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
THE gap between the number of patients awaiting transplantation and those undergoing transplantation widens yearly, and failure to maintain adequate support of cadaveric donors accounts for at least 25% of lost organs.^1,2 Wide variations in the rates of organ procurement and allograft survival between the ten United States Organ Procurement Organizations has motivated clinicians to promote guidelines for the management of cadaveric donors.³ Indeed, consensus on the optimal care of the cadaveric donor may increase the number of organs retrieved for transplantation.^4–6 The purpose of this review is to synthesize the available literature on, and provide recommendations for the medical management of organ donors for the purposes of improving conversion rates and graft survival of recipient organs.

	Literature search strategy

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
A comprehensive search of MEDLINE/PubMed was undertaken, utilizing each and combinations of the MeSH headings, "brain death", "transplantation and heart/lung/liver/kidney/pancreas/pituitary", "organ donor", "hormonal therapy", "pituitary", "thyroid", "adrenal", "corticosteroids", "vasopressin", and "DDAVP". All relevant literature was abstracted and further references were obtained from the abstracted literature, and personal files of members of the executive committee of a recent forum entitled "Medical Management to Optimize Donor Organ Potential: A Canadian Forum".

	Temporal considerations

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
The time between the neurological determination of death (NDD) and the beginning of the cold ischemia time during explantation influence renal allograft survival. Renal allografts retrieved from donors with a duration from NDD over 470 min demonstrated significantly better primary graft function than those procured from donors prior to 470 min after NDD.⁷ In a study of orthotopic liver transplants, longer donor time after NDD was not found to be associated with primary allograft dysfunction.⁸ Data from lung procurement has been conflicting with associations between longer time to donor network referral and a reduced probability of lung procurement demonstrated in a California study in contrast with an Australian study, which successfully delayed lung procurement to provide time for bronchial toilet in marginal lung donors.^9,10

For all solid organs, longer cold ischemia times correlate with worsened allograft survival. Significant negative interactions between ischemia time over six hours and increasing donor age over 45 yr on recipient survival have been demonstrated for lung allografts.^11,12 The major factors contributing to the failure of cardiac allografts include donor age, coronary artery disease, left ventricular hypertrophy, donor-recipient size mismatch, donor hepatitis B status, and cold ischemia time.⁵ In the Collaborative Transplant Study of kidney transplants, a cold ischemia time over 12 hr resulted in progressively worsening recipient graft survival.¹³ A cold ischemia time of over 18 hr, along with reduced size livers, donor age over 49 yr, and moderate to severe fatty changes in the donor liver biopsy have also been found to be independent predictors of primary liver allograft dysfunction.⁸

	The cardiovascular response to brain death

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Brain death results from cerebral herniation following raised intracranial pressure. As intracranial pressure rises, brainstem ischemia progresses in a rostral-caudal fashion and mean arterial pressure rises in an effort to maintain cerebral perfusion pressure. Midbrain ischemia results in parasympathetic activation and sinus bradycardia. Subsequent pontine ischemia results in sympathetic stimulation with superimposed hypertension (Cushing’s reflex).^14,15 Further ischemia of the vagal cardiomotor nucleus in the medulla oblongata occurs, resulting in unopposed sympathetic stimulation and loss of baroreceptor reflexes termed "autonomic storm".^15,16 The vasoconstrictive effect of the autonomic storm compromises end organ blood flow and its severity correlates with the rate of rise in intracranial pressure.^17,18 Following the autonomic storm, a normotensive or hypotensive phase ensues, resulting from reduced sympathetic flow and impairing vascular tone and cardiac output.¹⁹ As a consequence of both the loss of sympathetic nervous system control and concomitant diabetes insipidus (DI), only a minority of cadaveric donors are able to maintain hemodynamic stability.^20–23

	Cardiovascular monitoring and support

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Traditionally, dopamine has been used as the inotrope of choice in the cadaveric donor, however recent studies have not supported the beneficial effect of dopamine on renal or hepatosplanchnic circulation, and dopamine may suppress the function of anterior pituitary hormones.^24,25 Consequently, there has been a move towards the use of medications such as vasopressin for the vasodilatory shock seen in cadaveric donors. Organ donors who require catecholamine support have been shown to be deficient in vasopressin. ²⁶ Several authors have described the successful support and catecholamine sparing effect of iv vasopressin with or without 1-desamino-8-D-arginine vasopressin for up to 14 days after brain death.^27–30 The catecholamine sparing effects of vasopressin have also been shown in several case series of patients in septic shock.^31–33 Consequently, vasopressin has been recommended as initial therapy for hemodynamic support and the treatment of DI in the cadaveric donor by the American College of Cardiology.³⁴

Expert consensus recommends that every cadaveric donor should undergo central venous pressure (CVP) monitoring.^4,35 In studies of hemodynamically unstable cadaveric donors, there is observational evidence to suggest that the use of a pulmonary artery catheter, vasopressin, glucocorticoids, and triiodothyronine (T3) is successful in converting "unsuitable" donor organs into transplantable organs.³⁵ The American College of Cardiology has recommended maintaining a systolic blood pressure 90–140 mmHg, a CVP of 8–12 mmHg, or pulmonary capillary wedge pressure of 12–14 mmHg using a pulmonary artery catheter.³⁴ Other authors recommend a CVP of less than 8 for potential lung donors.¹⁶ Vasopressors, as opposed to inotropic medications should be used in the setting of low systemic vascular resistance and normal or elevated cardiac output.³⁶ In both canine models and humans, right ventricular function appears to be worse than left ventricular function after NDD, and is postulated to be related to both increased pulmonary capillary permeability and from pulmonary overflow injury caused by a reduction in pulmonary vascular resistance.^28,37,38 Care should be taken with respect to aggressive fluid loading as even targeting of CVP to 8–10 mmHg has been demonstrated to increase the alveolar-arterial oxygen gradient as compared to a target of 4–6 mmHg.^4,5,39,40

Echocardiographic parameters have predictive value of the success of cardiac allograft function.⁴¹ However, echocardiographic myocardial dysfunction differs by etiology of cerebral injury and does not correlate well with pathological findings of contraction band necrosis. ⁴² Moreover, improvement in myocardial function has been demonstrated when serial echocardiography has been performed and dobutamine responsive donors may predict successful recovery of myocardial function. ^43,44 Coronary angiography is often performed on donors if they are over 40 yr, require high inotropic support, or have other risk factors for coronary artery disease and recent indications for angiography in the cadaveric donor have been published.^5,45,46 If angiography is performed, numerous studies support the use of acetylcysteine and bicarbonate to prevent the development of contrast nephropathy.^47–53 Changes in catecholamine levels seen in massive subarachnoid hemorrhage and resulting in an increase in peripheral resistance may result in a sudden increase in myocardial work and oxygen consumption leading to myocardial infarction and subsequent elevation of cardiac troponin I and T.⁵⁴ Cadaveric donor levels of troponin I or T have been correlated with pathological findings of subendocardial myocytolysis, higher catecholamine requirements, and increased rates of recipient allograft rejection.^55–58

	Endocrine considerations

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Dysfunction of the posterior pituitary is common with resultant low to undetectable levels of vasopressin manifest clinically as DI, and occurring in up to 90% of adult and pediatric organ donors.^{16,23,59–61} In contrast, variable deficiency of hormones regulated by the anterior pituitary including T3, thyroxine (T4), adrenocorticotropic hormone, thyroid stimulating hormone, and human growth hormone have been described. Moreover, there has been inconsistent improvement in physiological parameters after replacement of these hormones in both animals and humans.^{24,59,60,62–65}

Vasopressin produces its physiological effects through three different receptors: V1, V2, and V3.⁶⁶ The V1 receptors are located within blood vessels and mediate the vasopressor effect. The antidiuretic effect of vasopressin is mediated via V2 receptors found on renal collecting duct epithelia. Stimulation of adrenocorticotropic hormone secretion is mediated by vasopressin via the V3 receptor located in the anterior pituitary. Diabetes insipidus from vasopressin deficiency has been associated with hemodynamic instability in cadaveric donors.^22,23 The vasopressin analogue 1-desamino-8-D-arginine vasopressin is highly selective for the V2 receptor subtype with no significant vasopressor activity in man.⁶⁶ Its duration of action ranges from six to 20 hr and may be given at doses of 2 – 6 µg iv every six to eight hours, as compared to the 15-min half-life of vasopressin.¹⁴ Because of the combined vasopressor and antidiuretic effect of vasopressin, its use has been described in case series of adults and children with DI, and a wide range of doses between 0.5–15 U·hr^–1 have been recommended. ^{4,5,14,28,34,40,67–70} The use of vasopressin at doses greater than 0.04 U·min^–1 may cause coronary, renal, and splanchnic vasoconstriction, potentially jeopardizing cardiac, renal, and hepatic function.³¹ However, the safety and efficacy of using a combination of vasopressin and 1-desamino-8-D-arginine vasopressin in organ donors also remains an option, and has been described in one randomized trial.²⁸

Results from early descriptions of thyroid hormone therapy following brain death were conflicting and could not support the routine use of thyroid hormone after the NDD.^{30,59,61,63–65,71} Results from observational studies and randomized trials using T3 in patients undergoing coronary artery bypass grafting have been equally inconsistent.^72–79 The strongest evidence supporting the use of iv T3 or T4 in organ donors comes from a recent analysis of the United Network for Organ Sharing database.⁶ Hearts procured from donors receiving triple hormonal therapy including T3 or T4 therapy demonstrated a significantly improved one-month survival rate (96.2%) as compared to those donors not receiving triple hormonal therapy. Both corticosteroid and T3/T4 therapy independently resulted in a 46% reduced odds of recipient death within 30 days, and a 48% reduced odds of early cardiac graft dysfunction.

Hyperglycemia is common after NDD and is thought to be secondary to insulin resistance.⁸⁰ No randomized trials exist to evaluate glycemic control in organ donors, however a large randomized trial and an observational study of glycemic control and insulin therapy in critically ill patients demonstrated the survival benefits of tight glycemic control between 6.1 and 8.0 mmol·L^–1 respectively.^81,82

Severe traumatic brain injury results in a "stress" associated rise in serum cortisol and may produce relative adrenal insufficiency.⁵⁹ In critically ill patients in septic shock, the use of corticosteroids has improved survival in those patients with relative adrenal insufficiency. ^83,84 However, it is uncertain whether the beneficial effect of corticosteroids in cadaveric donors is a result of hormonal replacement or a modulatory effect of the inflammatory process described after the NDD.^21,85–88

A recent consensus has recommended that donors with a left ventricular ejection fraction of less than 45% after standard management be treated with a combination of methylprednisolone, T3, and vasopressin.^4,5 This recommendation is supported by an observational study involving 10,292 consecutive brain dead organ donors within the United Network for Organ Sharing database which showed a significant improvement in organ procurement and an increased odds of a donor becoming an organ donor if treated with triple hormonal therapy.⁴⁰

	Pulmonary considerations

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Successful lung procurement is challenging because of the association of brain death with neurogenic pulmonary edema, pneumonia, and systemic inflammation. ^26,89–92 Unfortunately, in less than 20% of cadaveric donors are lungs retrieved.⁹³ Pathological studies of lungs deemed unsuitable for donation have indicated that bronchopneumonia, diffuse alveolar damage, and diffuse lung consolidation are the most common reasons for being deemed unsuitable.⁹⁴ Bronchial colonization or infection with bacteria or yeast is seen in up to 80% of organ donors, correlates with lung recipient survival, and varies by mechanism of brain death.^95–97 Moreover, transplantation mismatch of a cytomegalovirus positive donor lung into a cytomegalovirus negative recipient greatly increases the risk of recipient cytomegalovirus infection.⁹⁸ Given these findings it is recommended that every lung organ donor undergo bronchoscopy for therapeutic bronchial toilet, and to isolate potential pathogens in order to guide antibiotic therapy in both the donor and the recipient.^4,40 However, the benefits of empiric antibiotic administration prior to the diagnosis of pneumonia has only been demonstrated in a canine model.⁹⁹ Corticosteroids have an important role in the management of lung donors. One retrospective study of 118 lung donors administered methylprednisolone at a mean dose of 14.5 mg·kg^–1 compared to 38 donors not receiving methylprednisolone demonstrated a significant improvement in donor oxygenation in the steroid-treated group.¹⁰⁰ A more recent analysis comparing donor factors predicting the procurement of lungs with or without hearts vs the procurement of hearts alone demonstrated an independent beneficial effect of using methylprednisolone in the organ donor.⁹ These findings have been adopted in the recommendation of the use of methylprednisolone as part of a hormonal resuscitation strategy.^5,6 Due to prolonged ventilation in the supine position, microatelectasis is a common finding in the lungs of cadaveric donors. In animals, donor lungs develop microatelectasis and a reduction in pulmonary compliance and functional residual capacity despite positive end expiratory pressure (PEEP) and a relatively short ventilation period. This effect is worsened by preservation solution and ischemia reperfusion injury.^101,102 Shearing forces that produce stress on alveoli, epithelial and endothelial damage, and augmentation of the cytokine response are mechanisms for the alveolar injury seen during mechanical ventilation.¹⁰³ Given the similarity of the lung injury seen in organ donors with the acute respiratory distress syndrome, lung protective strategies used in the treatment of acute respiratory distress syndrome may prevent further lung injury in marginal lung donors.^104,105 However, these strategies have not been formally studied in organ donor populations.¹⁰⁶ Lung recruitment maneuvers utilizing high PEEP or pressure-controlled ventilation for short durations have been proposed as an adjunct to the lung protective strategies used in acute respiratory distress syndrome. However, higher levels of PEEP must be used immediately after recruitment maneuvers in order to produce a sustained effect.^105,107,108 A strategy of aggressive pulmonary care of the organ donor including bronchoscopic bronchial toilet, physiotherapy, and increasing PEEP was able to convert 34% of "unsuitable" lung donors to suitable donors with no difference in lung allograft survival when compared to recipients of lungs from "suitable" donors.¹⁰

	Renal considerations

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Brain death is associated with histologic evidence of both immunological and non-immunological damage to the kidney and the development of delayed allograft function. Delayed allograft function is associated with decreased renal recipient survival, increased rejection rates, and increased renal allograft nephropathy. ^86,109–113 The incidence of acute tubular necrosis and allograft failure increase when high doses of dopamine are used (> 10 µg·kg^–1·min^–1) to support the donor and if donor systolic blood pressure is consistently lower than 80–90 mmHg, as autoregulation of renal blood flow and glomerular filtration declines below this threshold.^14,114,115 Consequently, timely hemodynamic management of the organ donor is important. Although at an increased risk for recipient renal allograft dysfunction, marginal kidneys from donors over 60 yr of age, with cerebrovascular accidents as an etiology of death, with hypertension or diabetes mellitus, or with a serum creatinine greater than 133 µmol·L^–1 should still be considered as candidates for organ donation.^116–121 This is an important consideration, as data from the United Network for Organ Sharing registry have demonstrated a reduction in the annual death rate from 6.3% in those recipients waiting for a renal transplant as compared to 4.7% for those receiving a marginal kidney and 3.3% for those receiving an ideal kidney.¹²⁰

	Hepatic considerations

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Initial poor function of liver allografts result from factors such as the inflammatory process of brain death and preservation-reperfusion injury to the liver.^8,122–124 Cold preservation causes the sinusoidal lining cells of the liver to become edematous and detach, leaving the hepatocyte microvilli exposed to the sinusoidal lumen and resulting in cell death.¹²⁴ The importance of monitoring donor sodium levels and correcting hypernatremia has been emphasized in several observational studies. Both ABO incompatibility and donor plasma sodium > 155 mmol·L^–1 have been independently associated with an increased rate of recipient death and retransplantation.¹²⁵ In a series of 168 liver transplants, a high donor serum sodium concentration, longer cold ischemia time, large platelet transfusion during surgery and prolonged recipient prothrombin time were independently associated with more severe hepatic dysfunction after transplantation.¹²⁶ High donor serum sodium concentrations may promote the accumulation of idiogenic osmoles within liver allograft cells. The subsequent transplantation of these livers into recipients with relatively normal sodium levels may promote intracellular water accumulation, cell lysis and death. Correcting donor serum sodium to levels below 155 mmol·L^–1 has been shown to decrease the incidence of liver allograft loss.¹²⁷

	Infectious considerations

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Several cases of solid organ infection in the donor being transmitted to the recipient with resultant sepsis and poor initial allograft function have been reported.^128–131 However, by using prophylactic antibiotics in recipients immediately after transplantation, two studies totaling 124 organ recipients have demonstrated no transmission of bacterial infection from bacteremic donors to organ recipients.^132,133 In an analysis of all organ donors cared for by the New England Organ bank between 1990 and 1996, only 95 (5.1%) of 1,775 organ donors were identified as being bacteremic.¹³³ No evidence of bacterial transmission could be identified in 212 recipients and there was no difference in allograft or recipient survival for recipients of organs from bacteremic as compared to non-bacteremic donors.

	Transfusion thresholds

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
There are no studies investigating the use of red blood cell transfusions in brain dead donors. Recent consensus has recommended maintaining a hemoglobin level of 10.0 g·dL^–1 or a hematocrit > 30% in organ donors.^5,14 In contrast, current critical care practice advocates a more restrictive transfusion strategy with a hemoglobin threshold of 7.0 g·dL^–1.134,135 Likewise, no guidelines exist in the literature regarding appropriate thresholds for either plasma or platelet transfusions in donors although large platelet transfusion requirements during liver transplant surgery was an independent predictor of severe hepatic dysfunction after transplantation in one cohort study.¹²⁶ However, higher platelet requirements in this study may have been confounded by a more technically complicated procedure.

	Conclusions

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
Our understanding of the pathophysiology of brain death and its effects on donor and recipient organ function has progressed over the last two decades. Several cohort studies have provided valuable information to clinicians regarding donor characteristics predisposing to adverse recipient outcomes and the potential benefits of respiratory, hormonal and hemodynamic therapies. These studies have also been helpful in outlining the risk of allograft failure from marginal donor organs. As the demand for organs increase, future emphasis should be placed on evaluating potential therapies within the context of clinical trials.

	Footnotes

 
Financial support: Funding provided by a grant from The Canadian Council for Donation and Transplantation

Accepted for publication August 23, 2005. Revision accepted February 17, 2006.

Competing interests: None declared.

	References

TOP Abstract Introduction Literature search strategy Temporal considerations The cardiovascular response to... Cardiovascular monitoring and... Endocrine considerations Pulmonary considerations Renal considerations Hepatic considerations Infectious considerations Transfusion thresholds Conclusions References

 
1 Mackersie RC, Bronsther OL, Shackford SR. Organ procurement in patients with fatal head injuries. The fate of the potential donor. Ann Surg 1991; 213: 143–50.[Medline]

2 Nygaard CE, Townsend RN, Diamond DL. Organ donor management and organ outcome: a 6-year review from a level 1 trauma center. J Trauma 1990; 30: 728–32.[Medline]

3 Cho YW, Cecka JM. Organ Procurement Organization and transplant center effects on cadaver renal transplant outcomes. Clinical Transpl 1996: 427–41.

4 Rosengard BR, Feng S, Alfrey EJ, et al. Report of the Crystal City meeting to maximize the use of organs recovered from the cadaver donor. Am J Transplant 2002; 2: 701–11.[Medline]

5 Zaroff JG, Rosengard BR, Armstrong WF, et al. Consensus conference report maximizing use of organs recovered from the cadaver donor: cardiac recommendations, March 28–29, 2001, Crystal City, Va. Circulation 2002; 106: 836–41.[Abstract/Free Full Text]

6 Rosendale JD, Kauffman HM, McBride MA, et al. Hormonal resuscitation yields more transplanted hearts, with improved early function. Transplantation 2003; 75: 1336–41.[Medline]

7 Kunzendorf U, Hohenstein B, Oberbarnscheid M, et al. Duration of donor brain death and its influence on kidney graft function. Am J Transplant 2002; 2: 292–4.[Medline]

8 Ploeg RJ, D’Alessandro AM, Knechtle SJ, et al. Risk factors for primary dysfunction after liver transplantation-- a multivariate analysis. Transplantation 1993; 55: 807–13.[Medline]

9 McElhinney DB, Khan JH, Babcock WD, Hall TS. Thoracic organ donor characteristics associated with successful lung procurement. Clin Transplant 2001; 15: 68–71.[Medline]

10 Gabbay E, Williams TJ, Griffiths AP, et al. Maximizing the utilization of donor organs offered for lung transplantation. Am J Respir Crit Care Med 1999; 160: 265–71.[Abstract/Free Full Text]

11 Snell GI, Rabinov M, Griffiths A, et al. Pulmonary allograft ischemic time: an important predictor of survival after lung transplantation. J Heart Lung Transplant 1996; 15: 160–8.[Medline]

12 Novick RJ, Bennett LE, Meyer DM, Hosenpud JD. Influence of graft ischemic time and donor age on survival after lung transplantation. J Heart Lung Transplant 1999; 18: 425–31.[Medline]

13 Opelz G. Cadaver kidney graft outcome in relation to ischemia time and HLA match. Collaborative Transplant Study. Transplant Proc 1998; 30: 4294–6.[Medline]

14 Van Bakel AB. The cardiac transplant donor: identification, assessment, and management. Am J Med Sci 1997; 314: 152–63.

15 Novitzky D. Detrimental effects of brain death on the potential organ donor. Transplant Proc 1997; 29: 3770–2.[Medline]

16 Tuttle-Newhall JE, Collins BH, Kuo PC, Schoeder R. Organ donation and treatment of the multi-organ donor. Curr Probl Surg 2003; 40: 266–310.[Medline]

17 Shivalkar B, Van Loon J, Wieland W, et al. Variable effects of explosive or gradual increase of intracranial pressure on myocardial structure and function. Circulation 1993; 87: 230–9.[Abstract/Free Full Text]

18 Takada M, Nadeau KC, Hancock WW, et al. Effects of explosive brain death on cytokine activation of peripheral organs in the rat. Transplantation 1998; 65: 1533–42.[Medline]

19 Pratschke J, Wilhelm MJ, Kusaka M, et al. Brain death and its influence on donor organ quality and outcome after transplantation. Transplantation 1999; 67: 343–8.[Medline]

20 Cabrer C, Manyalich M, Valero R, Garcia-Fages LC. Timing used in the different phases of the organ procurement process. Transplant Proc 1992; 24: 22–3.[Medline]

21 Kosieradzki M, Kuczynska J, Piwowarska J, et al. Prognostic significance of free radicals: mediated injury occurring in the kidney donor. Transplantation 2003; 75: 1221–7.[Medline]

22 Lagiewska B, Pacholczyk M, Szostek M, Walaszewski J, Rowinski W. Hemodynamic and metabolic disturbances observed in brain-dead organ donors. Transplant Proc 1996; 28: 165–6.[Medline]

23 Finfer S, Bohn D, Colpitts D, Cox P, Fleming F, Barker G. Intensive care management of paediatric organ donors and its effect on post-transplant organ function. Intensive Care Med 1996; 22: 1424–32.[Medline]

24 Debaveye YA, Van den Berghe GH. Is there still a place for dopamine in the modern intensive care unit? Anesth Analg 2004; 98: 461–8.[Abstract/Free Full Text]

25 Marik PE, Mohedin M. The contrasting effects of dopamine and norepinephrine on systemic and splanchnic oxygen utilization in hyperdynamic sepsis. JAMA 1994; 272: 1354–7.[Abstract]

26 Chen JM, Cullinane S, Spanier TB, et al. Vasopressin deficiency and pressor hypersensitivity in hemodynamically unstable organ donors. Circulation 1999; 100(suppl II): II–244–6.

27 Yoshioka T, Sugimoto H, Uenishi M. Prolonged hemodynamic maintenance by the combined administration of vasopressin and epinephrine in brain death: a clinical study. Neurosurgery 1986; 18: 565–7.[Medline]

28 Pennefather SH, Bullock RE, Mantle D, Dark JH. Use of low dose arginine vasopressin to support brain-dead organ donors. Transplantation 1995; 59: 58–62.[Medline]

29 Kinoshita Y, Yahata K, Yoshioka T, Onishi S, Sugimoto T. Long-term renal preservation after brain death maintained with vasopressin and epinephrine. Transplant Int 1990; 3: 15–8.[Medline]

30 Katz K, Lawler J, Wax J, O’Connor R, Nadkarni V. Vasopressin pressor effects in critically ill children during evaluation for brain death and organ recovery. Resuscitation 2000; 47: 33–40.[Medline]

31 Holmes CL, Patel BM, Russell JA, Walley KR. Physiology of vasopressin relevant to management of septic shock. Chest 2001; 120: 989–1002.[Medline]

32 Landry DW, Levin HR, Gallant EM, et al. Vasopressin pressor hypersensitivity in vasodilatory septic shock. Crit Care Med 1997; 25: 1279–82.[Medline]

33 Malay MB, Ashton RC, Landry DW, Townsend RN. Low-dose vasopressin in the treatment of vasodilatory septic shock. J Trauma 1999; 47: 699–705.[Medline]

34 Hunt SA, Baldwin J, Baumgartner W, et al. Cardiovascular management of a potential heart donor: a statement from the Transplantation Committee of the American College of Cardiology. Crit Care Med 1996; 24: 1599–601.[Medline]

35 Wheeldon DR, Potter CD, Oduro A, Wallwork J, Large SR. Transforming the "unacceptable" donor: outcomes from the adoption of a standardized donor management technique. J Heart Lung Transplant 1995; 14: 734–42.[Medline]

36 Potter CD, Wheeldon DR, Wallwork J. Functional assessment and management of heart donors: a rationale for characterization and a guide to therapy. J Heart Lung Transplant 1995; 14: 59–65.[Medline]

37 Bittner HB, Kendall SW, Chen EP, Van Trigt P. The combined effects of brain death and cardiac graft preservation on cardiopulmonary hemodynamics and function before and after subsequent heart transplantation. J Heart Lung Transplant 1996; 15: 764–77.[Medline]

38 Bittner HB, Chen EP, Biswas SS, Van Trigt P III, Davis RD. Right ventricular dysfunction after cardiac transplantation: primarily related to status of donor heart. Ann Thorac Surg 1999; 68: 1605–11.[Abstract/Free Full Text]

39 Pennefather SH, Bullock RE, Dark JH. The effect of fluid therapy on alveolar arterial oxygen gradient in brain-dead organ donors. Transplantation 1993; 56: 1418–22.[Medline]

40 Rosendale JD, Chabalewski FL, McBride MA, et al. Increased transplanted organs from the use of a standardized donor mangement protocol. Am J Transplant 2002; 2: 761–8.[Medline]

41 Darmon PL, Catoire P, Delaunay L, Wigdorowicz C, Bonnet F. Utility of transesophageal echocardiography in heart collection decision making. Transplant Proc 1996; 28: 2895.[Medline]

42 Dujardin KS, McCully RB, Wijdicks EF, et al. Myocardial dysfunction associated with brain death: clinical, echocardiographic, and pathologic features. J Heart Lung Transplant 2001; 20: 350–7.[Medline]

43 Kono T, Morita H, Kuroiwa T, Onaka H, Takatsuka H, Fujiwara A. Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol 1994; 24: 636–40.[Abstract]

44 Kono T, Nishina T, Morita H, Hirota Y, Kawamura K, Fujiwara A. Usefulness of low-dose dobutamine stress echocardiography for evaluating reversibility of brain death-induced myocardial dysfunction. Am J Cardiol 1999; 84: 578–82.[Medline]

45 McGiffin DC, Savunen T, Kirklin JK, et al. A multivariable analysis of pretransplantation risk factors for disease development and morbid events. J Thorac Cardiovasc Surg 1995; 109: 1081–9.[Abstract/Free Full Text]

46 Young JB, Naftel DC, Bourge RC, et al. Matching the heart donor and heart transplant recipient. Clues for successful expansion of the donor pool: a multivariable, multiinstitutional report. J Heart Lung Transplant 1994; 13: 353–65.[Medline]

47 Tepel M, van der Giet M, Schwarzfeld C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrast- agent-induced reductions in renal function by acetylcysteine. N Engl J Med 2000; 343: 180–4.[Abstract/Free Full Text]

48 Efrati S, Dishy V, Averbukh M, et al. The effect of N-acetylcysteine on renal function, nitric oxide, and oxidative stress after angiography. Kidney Int 2003; 64: 2182–7.[Medline]

49 Shyu KG, Cheng JJ, Kuan P. Acetylcysteine protects against acute renal damage in patients with abnormal renal function undergoing a coronary procedure. J Am Coll Cardiol 2002; 40: 1383–8.[Abstract/Free Full Text]

50 Briguori C, Manganelli F, Scarpato P, et al. Acetylcysteine and contrast agent-associated nephrotoxicity. J Am Coll Cardiol 2002; 40: 298–303.[Abstract/Free Full Text]

51 Diaz-Sandoval LJ, Kosowsky BD, Losordo DW. Acetylcysteine to prevent angiography-related renal tissue injury (the APART trial). Am J Cardiol 2002; 89: 356–8.[Medline]

52 Kay J, Chow WH, Chan TM, et al. Acetylcysteine for prevention of acute deterioration of renal function following elective coronary angiography and intervention. A randomized controlled trial. JAMA 2003; 289: 553–8.[Abstract/Free Full Text]

53 Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate. A randomized controlled trial. JAMA 2004; 291: 2328–34.[Abstract/Free Full Text]

54 Macmillan CS, Grant IS, Andrews PJ. Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management? Intensive Care Med 2002; 28: 1012–23.[Medline]

55 Grant J, Canter CE, Spray TL, et al. Elevated donor cardiac troponin I: a marker of acute graft failure in infant heart recipients. Circulation 1994; 90: 2618– 21.[Free Full Text]

56 Potapov E, Ivanitskaia E, Loebe M, et al. Value of cardiac troponin I and T for selection of heart donors and as predictors of early graft failure. Transplantation 2001; 71: 1394–400.[Medline]

57 Anderson JR, Hossein-Nia M, Brown P, Holt DW, Murday A. Donor cardiac troponin-T predicts subsequent inotrope requirements following cardiac transplantation. Transplantation 1994; 58: 1056–7.[Medline]

58 Vijay P, Scavo VA, Morelock RJ, Sharp TG, Brown JW. Donor cardiac troponin T: a marker to predict heart transplant rejection. Ann Thorac Surg 1998; 66: 1934–9.[Abstract/Free Full Text]

59 Howlett TA, Keogh AM, Perry L, Touzel R, Rees LH. Anterior and posterior pituitary function in brainstem- dead donors. Transplantation 1989; 47: 828– 34.[Medline]

60 Gramm HJ, Meinhold H, Bickel U, et al. Acute endocrine failure after brain death. Transplantation 1992; 54: 851–7.[Medline]

61 Sazontseva IE, Kozlov IA, Moisuc YG, Ermolenko AE, Afonin VV, Ilnitskiy VV. Hormonal response to brain death. Transplant Proc 1991; 23: 2467.[Medline]

62 Powner DJ, Hendrich A, Lagler RG, Ng RH, Madden RL. Hormonal changes in brain dead patients. Crit Care Med 1990; 18: 702–8.[Medline]

63 Novitzky D, Cooper DK, Reichart B. Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors. Transplantation 1987; 43: 852–4.[Medline]

64 Novitzky D, Cooper DK, Morrell D, Isaacs S. Change from aerobic to anaerobic metabolism after brain death, and reversal following triiodothyronine therapy. Transplantation 1988; 45: 32–6.[Medline]

65 Novitzky D, Cooper DK, Chaffin JS, Greer AE, DeBault LE, Zuhdi N. Improved cardiac allograft function following triiodothyronine therapy to both donor and recipient. Transplantation 1990; 49: 311– 6.[Medline]

66 Robinson AG, Verbalis JG. Posterior pituitary gland. In: Larsen PR, Kronenberg HM, Melmed S, Polonsky KS (Eds). Williams Textbook of Endocrinology, 10th ed. Philadelphia: Saunders; 2003: 281–329.

67 Lee YJ, Shen EY, Huang FY, Kao HA, Shyur SD. Continuous infusion of vasopressin in comatose children with neurogenic diabetes insipidus. J Pediatr Endocrinol Metab 1995; 8: 257–62.[Medline]

68 Lee YJ, Yang D, Shyur SD, Chiu NC. Neurogenic diabetes insipidus in a child with fatal Coxsackie virus B₁ encephalitis. J Pediatr Endocrinol Metab 1995; 8: 301–4.[Medline]

69 Chanson P, Jedynak CP, Dabrowski G, et al. Ultralow doses of vasopressin in the management of diabetes insipidus. Crit Care Med 1987; 15: 44–6.[Medline]

70 Ralston C, Butt W. Continuous vasopressin replacement in diabetes insipidus. Arch Dis Child 1990; 65: 896–7.[Abstract]

71 Roels L, Pirenne J, Delooz H, Lauwers P, Vandermeersch E. Effect of triiodothyronine replacement therapy on maintenance characteristics and organ availability in hemodynamically unstable donors. Transplant Proc 2000; 32: 1564–6.[Medline]

72 Salter DR, Dyke CM, Wechsler AS. Triiodothyronine (T₃) and cardiovascular therapeutics: a review. J Card Surg 1992; 7: 363–74.[Medline]

73 Dyke CM, Yeh T Jr, Lehman JD, et al. Triiodothyronine-enhanced left ventricular function after ischemic injury. Ann Thorac Surg 1991; 52: 14–9.[Abstract]

74 Holland FW II, Brown PS Jr, Clark RE. Acute severe postischemic myocardial depression reversed by triiodothyronine. Ann Thorac Surg 1992; 54: 301–5.[Abstract]

75 Klemperer JD, Zelano J, Helm RE, et al. Triiodothyronine improves left ventricular function without oxygen wasting effects after global hypothermic ischemia. J Thorac Cardiovasc Surg 1995; 109: 457–65.[Abstract/Free Full Text]

76 Teiger E, Menasche P, Mansier P, et al. Triiodothyronine therapy in open-heart surgery: from hope to disappointment. Eur Heart J 1993; 14: 629–33.[Abstract/Free Full Text]

77 Bennett-Guerrero E, Jimenez JL, White WD, D‘Amico EB, Baldwin BI, Schwinn DA. Cardiovascular effects of intravenous triiodothyronine in patients undergoing coronary artery bypass graft surgery. A randomized, double-blind, placebo-controlled trial. JAMA 1996; 275: 687–92.[Abstract]

78 Novitzky D, Cooper DK, Barton CI, et al. Triiodothyronine as an inotropic agent after open heart surgery. J Thorac Cardiovasc Surg 1989; 98: 972–8.[Abstract]

79 Mullis-Jansson SL, Argenziano M, Corwin S, et al. A randomized double-blind study of the effect of triiodothyronine on cardiac function and morbidity after coronary bypass surgery. J Thorac Cardiovasc Surg 1999; 117: 1128–35.[Abstract/Free Full Text]

80 Masson F, Thicoipe M, Gin H, et al. The endocrine pancreas in brain-dead donors. Transplantation 1993; 56: 363–7.[Medline]

81 Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med 2001; 345: 1359–67.[Abstract/Free Full Text]

82 Finney SJ, Zekveld C, Elia A, Evans TW. Glucose control and mortality in critically ill patients. JAMA 2003; 290: 2041–7.[Abstract/Free Full Text]

83 Annane D, Sebille V, Troche G, Raphael JC, Gajdos P, Bellissant E. A 3-level prognostic classification in septic shock based on cortisol levels and cortisol response to corticotropin. JAMA 2000; 283: 1038– 45.[Abstract/Free Full Text]

84 Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002; 288: 862–71.[Abstract/Free Full Text]

85 Koo DD, Welsh KI, McLaren AJ, Roake JA, Morris PJ, Fuggle SV. Cadaver versus living donor kidneys: impact of donor factors on antigen induction before transplantation. Kidney Int 1999; 56: 1551–9.[Medline]

86 Zivna H, Navratil PZ, Palicka V, Cerny V, Holeckova M, Pliskova L. The role of cytokines and antioxidant status in graft quality prediction. Transplant Proc 1999; 31: 2094.[Medline]

87 Amado JA, Lopez-Espadas F, Vazquez-Barquero A, et al. Blood levels of cytokines in brain-dead patients: relationship with circulating hormones and acute phase reactants. Metabolism 1995; 44: 812–6.[Medline]

88 Zhai QH, Futrell N, Chen FJ. Gene expression of IL-10 in relationship to TNF-alpha, IL-1 beta and IL-2 in the rat brain following middle cerebral artery occlusion. J Neurol Sci 1997; 152: 119–24.[Medline]

89 Avlonitis VS, Fisher AJ, Kirby JA, Dark JH. Pulmonary transplantation: the role of brain death in donor lung injury. Transplantation 2003; 75: 1928– 33.[Medline]

90 de Perrot M, Keshavjee S. Lung preservation. Curr Opin Organ Transplant 2001; 6: 223–30.

91 Lopau K, Mark J, Schramm L, Heidbreder E, Wanner C. Hormonal changes in brain death and immune activation in the donor. Transpl Int 2000; 13(suppl 1): S282–5.[Medline]

92 Minnear FL, Connell RS. Prevention of aconitineinduced neurogenic pulmonary edema (NPE) with hypovolemia or methylprednisolone. J Trauma 1982; 22: 121–8.[Medline]

93 Sundaresan S, Semenkovich J, Ochoa L, et al. Successful outcome of lung transplantation is not compromised by the use of marginal donor lungs. J Thorac Cardiovasc Surg 1995; 109: 1075–80.[Abstract/Free Full Text]

94 Aziz TM, El-Gamel A, Saad RA, Migliore M, Campbell CS, Yonan NA. Pulmonary vein gas analysis for assessing donor lung function. Ann Thorac Surg 2002; 73: 1599–605.[Abstract/Free Full Text]

95 Harjula A, Baldwin JC, Starnes VA, et al. Proper donor selection for heart-lung transplantation. The Stanford experience. J Thorac Cardiovasc Surg 1987; 94: 874–80.[Abstract]

96 Avlonitis VS, Krause A, Luzzi L, et al. Bacterial colonization of the donor lower airways is a predictor of poor outcome in lung transplantation. Eur J Cardiothorac Surg 2003; 24: 601–7.[Abstract/Free Full Text]

97 Waller DA, Thompson AM, Wrightson WN, et al. Does the mode of donor death influence the early outcome of lung transplantation? A review of lung transplantation from donors involved in major trauma. J Heart Lung Transplant 1995; 14: 318–21.[Medline]

98 Griffith BP, Bando K, Armitage JM. Lung transplantation at the University of Pittsburgh. Clin Transplant 1992; 13: 149–59.

99 Dowling RD, Zenati M, Yousem SA, et al. Donor-transmitted pneumonia in experimental lung allogafts. Successful prevention with donor antibiotic therapy. J Thorac Cardiovasc Surg 1992; 103: 767–72.[Abstract]

100 Follette DM, Rudich SM, Babcock WD. Improved oxygenation and increased lung donor recovery with high-dose steroid administration after brain death. J Heart Lung Transplant 1998; 17: 423–9.[Medline]

101 Koletsis E, Chatzimichalis A, Fotopoulos V, et al. Donor lung pretreatment with surfactant in experimental transplantation preserves graft hemodynamics and alveolar morphology. Exp Biol Med (Maywood) 2003; 228: 540–5.[Abstract/Free Full Text]

102 Taskar V, John J, Evander E, Wollmer P, Robertson B, Jonson B. Healthy lungs tolerate repetitive collapse and reopening during short periods of mechanical ventilation. Acta Anaesthesiol Scand 1995; 39: 370– 6.[Medline]

103 Dreyfuss D, Ricard JD, Saumon G. On the physiologic and clinical relevance of lung-borne cytokines during ventilator-induced lung injury. Am J Respir Crit Care Med 2003; 167: 1467–71.[Free Full Text]

104 Anonymous. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000; 342: 1301–8.[Abstract/Free Full Text]

105 Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004; 351: 327–36.[Abstract/Free Full Text]

106 Christie JD, Bavaria JE, Palevski HI, et al. Primary graft failure following lung transplantation. Chest 1998; 114: 51–60.[Medline]

107 Moran I, Zavala E, Fernandez R, Blanch L, Mancebo J. Recruitment manoeuvres in acute lung injury/acute respiratory distress syndrome. Eur Respir J Suppl 2003; 42: 37s–42s.[Medline]

108 Crotti S, Mascheroni D, Caironi P, et al. Recruitment and derecruitment during acute respiratory failure. A clinical study. Am J Respir Crit Care Med 2001; 164: 131–40.[Abstract/Free Full Text]

109 Melk A, Gourishankar S, Halloran PF. Long-term effects of nonimmune tissue injury in renal transplantation. Curr Opin Organ Transplant 2002; 7: 171–7.

110 Nagareda T, Kinoshita Y, Tanaka A, et al. Clinicopathology of kidneys from brain-dead patients treated with vasopressin and epinephrine. Kidney Int 1993; 43: 1363–70.[Medline]

111 Pratschke J, Wilhelm MJ, Kusaka M, et al. Accelerated rejection of renal allografts from brain-dead donors. Ann Surg 2000; 232: 263–71.[Medline]

112 Kusaka M, Pratschke J, Wilhelm M, et al. Activation of inflammatory mediators in rat renal isografts by donor brain death. Transplantation 2000; 69: 405– 10.[Medline]

113 van der Hoeven JA, Ploeg RJ, Postema F, et al. Induction or organ dysfunction and activation of inflammatory markers in donor liver and kidney during hypotensive brain death. Transplant Proc 1999; 31: 1006–7.[Medline]

114 Szostek M, Gaciong Z, Danielelewicz R, et al. Influence of thyroid function in brain stem death donors on kidney allograft function. Transplant Proc 1997; 29: 3354–6.[Medline]

115 Walaszewski J, Rowinski W, Pacholczyk M, et al. Multiple risk factor analysis of delayed graft function (ATN) after cadaveric transplantation: positive effect of lidocaine donor pretreatment. Transplant Proc 1991; 23: 2475–6.[Medline]

116 Port FK, Bragg-Gresham JL, Metzger RA, et al. Donor characteristics associated with reduced graft survival: an approach to expanding the pool of kidney donors. Transplantation 2002; 74: 1281–6.[Medline]

117 Carter JT, Lee CM, Weinstein RJ, Lu AD, Dafoe DC, Alfrey EJ. Evaluation of the older cadaveric kidney donor: the impact of donor hypertension and creatinine clearance on graft performance and survival. Transplantation 2000; 70: 765–71.[Medline]

118 Sola R, Guirado L, Diaz JM, Lopez-Navidad A, Caballero F, Gich I. Elderly donor kidney grafts into young recipients: results at 5 years. Transplantation 2002; 73: 1673–5.[Medline]

119 Becker YT, Leverson GE, D‘Alessandro AM, Sollinger HW, Becker BN. Diabetic kidneys can safely expand the donor pool. Transplantation 2002; 74: 141–5.[Medline]

120 Ojo AO, Hanson JA, Meier-Kriesche H, et al. Survival in recipients of marginal cadaveric donor kidneys compared with other recipients and wait-listed transplant candidates. J Am Soc Nephrol 2001; 12: 589– 97.[Abstract/Free Full Text]

121 Tullius SG, Volk HD, Neuhaus P. Transplantation of organs from marginal donors. Transplantation 2001; 72: 1341–9.[Medline]

122 Brokelman W, Stel AL, Ploeg RJ. Risk factors for primary dysfunction after liver transplantation in the University of Wisconsin solution era. Transplant Proc 1999; 31: 2087–90.