Sections

Sections Pediatric Kidney Transplantation
Overview
Workup
Treatment
Media Gallery
Tables
References

Overview

Practice Essentials

In children and adolescents younger than 18 years, the adjusted incidence of end-stage kidney disease (ESKD) in the United States in 2020 was 11 cases per million population, down slightly from 13 cases per million population in 2010.^[1]Current treatment options for ESKD include hemodialysis, peritoneal dialysis, and kidney transplantation. Of those, kidney transplantation offers children with ESKD the best opportunity for survival, growth, and development. Consequently, kidney transplantation has become the primary method of treating ESKD in the pediatric population, with 1-year all-cause mortality rates significantly lower than with either form of dialysis.^[1]

Unfortunately, the demand for kidney transplants continues to exceed the supply of donor organs. In 2020, 715 pediatric kidney transplantations were performed, but a lack of donor kidneys saw the prevalent pediatric transplant waitlist reach 2637 by the end of the year 2020.^[2]

Over the past decade, the age of pediatric candidates on the list has shifted, with an increase in those aged 1–5 years (14.9% to 20.9%) and a slight decrease in those aged 11–17 years (63.4% to 61.9%). However, teenagers still represent the largest t proportion of those waiting kidney transplant^[3](See Table 1, below.)

Table 1. Demographics of pediatric patients awaiting kidney transplant: United States, 2020. (OPTN/SRTR Annual Data Report 2020) (Open Table in a new window)

Patient Characteristics	Percentage
Age < 1 year	0.3
Age 1-5 years	20.9
Age 6-10 years	17.0
Age 11-17 years	61.9
White	37.1
African American	26.5
Hispanic	31.8
Asian	3.0
Other or unknown	1.5

The leading cause of ESKD changes with age: congenital anomalies of the kidney and urinary tract (CAKUT) are most common in children younger than 6 years of age, while focal segmental glomerulosclerosis and glomerulonephritis are more common in older children (see Table 2, below).^[2]Congenital anomalies of the lower urinary tract that lead to ESKD pose significant difficulty for kidney transplantation; treatment of these urologic disorders may require additional procedures, such as open vesicostomy and bladder augmentation.^[4]

Table 2. Primary causes of ESKD in pediatric patients on the kidney transplant waiting list: OPTN/SRTR Annual Data Report 2020 (Open Table in a new window)

Etiology of ESKD	Percentage
Focal segmental glomerulosclerosis	7.4
Glomerulonephritis	5.1
Congenital anomalies	38.3
Other or unknown	49.2

In pediatric recipients of kidney transplants from deceased donors, the graft failure rate was 1.9% at 6 months and 2.8% at 1 year for transplants in 2018-2019, 6.4% at 3 years for transplants in 2016-2017, 15.2% at 5 years for transplants in 2014-2015, and 32.1% at 10 years for transplants in 2010-2011. The graft failure after living-donor pediatric transplantation was better at 0.8% at 6 months and 1.6% at 1 year for transplants in 2018-2019, 2.7% at 3 years for transplants in 2016-2017, 8.2% at 5 years for transplants in 2014-2015, and 21.7% at 10 years for transplants in 2010-2011.^[2](See Table 3, below.)

Table 3. Graft failure rates in pediatric kidney transplant recipients (Open Table in a new window)

	After deceased donor transplant	After living donor transplant
6 months	1.9%	0.8%
1 Year	2.8%	1.6%
3 years	6.4%	2.7%
5 years	15.2%	8.2%
10 years	32.1%	21.7%

Both allograft and patient survival have demonstrated consistent improvement in the 5 decades during which kidney transplantation has been available. This has been the result of improved understanding of the immune response to allograft and the development of increasingly specific strategies to protect a kidney transplant from the body's natural defenses while leaving the recipient protected from infection. Further, in children, technical advances in surgical technique, strict perioperative fluid management, and avoidance of small allografts with small vessels have also improved allograft survival.

For patient education information, see the Kidney Transplant Directory.

Background

Until the 1950s, ESKD from any cause was uniformly lethal. Hope for treating kidney failure grew with the development of surgical techniques that allowed the anastomosis of blood vessels, in the early 20th century, and elucidation of the pathophysiology of rejection, starting in the mid-20th century.

In 1902, Ullman successfully autotransplanted a canine kidney to the dog's neck^[5]. Later that year, he also conducted dog-to dog allotransplants as well as a dog-to-goat kidney xenotransplants that both produced urine. Ullmann used Payr’s method, whereby the blood vessels are connected by tubes of absorbable magnesium metal.

In 1906, Jaboulay, in whose laboratory Carrel had worked, performed the first human kidney transplant, a xenograft between a pig and human. This kidney made urine for only a short time.^{[6, 7]}

In 1909, Ernst Unger transplanted an ape's kidney to a young girl with kidney failure. The failure of this attempt convinced Unger that a nonsurgical barrier to transplantation existed.^[8]

Other early attempts at the transplantation of kidneys were unsuccessful. Within hours or days, transplanted kidneys became swollen, ceased urine production, became ischemic, and, in some cases, ruptured.

In a series of experiments, Medawar and colleagues demonstrated that skin grafts from non-identical rabbits were rejected and sloughed by a reaction involving leukocyte invasion of the graft.^[9]This reaction increased in severity and rapidity when the recipient had received a previous transplant from the same donor. Medawar won the 1960 Nobel Prize in Medicine for this work. Researchers began to look for ways to prevent this response. Ionizing radiation, known to suppress bone marrow production of leukocytes, was used in an attempt to prevent the immune reaction to allografts.

Armed with new information about the immune response to allograft, researchers revived interest in kidney transplantation. In 1954, Joseph Murray (winner of the 1990 Nobel Prize in Medicine) performed the first successful kidney transplant in Boston between identical twins, thus skirting the problems of immune compatibility.^[10]Several transplants between twins followed. However, the possibility of kidney transplantation for patients with kidney failure who did not have a twin donor remained unrealized until 1959, when Gordon Murray in Toronto performed the first successful non-twin sibling transplant.^{[11, 12]}

In the early 1960s, Calne found that a derivative of 6-mercaptopurine (azathioprine) increased the success of experimental kidney transplantation in dogs.^[13] Human use of azathioprine followed, and long-term graft survival from non–identical-donor kidneys became a possibility. The success of kidney transplantation increased significantly when Goodwin and Starzl added prednisolone to azathioprine.^{[14, 15]}Encouraged by this success, transplant centers began performing non–identical living donor kidney transplantation.

Simultaneously, dialysis became available as a pre-transplant therapy for patients with ESKD and as a life-preserving measure for recipients of transplants whose allograft had failed. This increased the number of individuals who were candidates for kidney transplantation. Terasaki reported a marked decrease in early allograft failure from hyperacute rejection when a crossmatch between donor lymphocytes and recipient serum was performed.^[16]A negative crossmatch (no reaction against donor lymphocytes when incubated with recipient serum) indicated that the recipient did not harbor antibody directed against the donor's organ.

In 1968, the Harvard Committee on Irreversible Coma described the features of brain death and made the important observation that patients who had lost basic brainstem function were dead despite the persistence of a heartbeat sustained by artificial ventilator support.^[17]

In 1970, Kansas became the first state in the United States to enact legislation defining brain death. Within several years, such statutes were widely established in other places. This provided a legal framework for families to donate the organs of deceased loved ones for use in transplantation. The number of kidney transplants dramatically increased because of the combination of this legislation and the contemporary advances in immunosuppression.

Concurrently, in 1973 the Medicare program in the United States was expanded to provide insurance coverage for patients with ESKD, meaning that individuals were provided kidney transplantation or dialysis regardless of their health insurance coverage or their ability to pay. From a relatively rare procedure performed in research centers, kidney transplantation became available in most major cities.

During the 1970s, a 1-year allograft survival rate of 75% was typical for kidneys donated by living relatives; a rate of 50% was typical for organs from cadavers.^[18]Improvement in graft survival followed the routine use of human leukocyte antigen (HLA) tissue matching and the use of anti-lymphocyte antibodies as a temporary adjunct to immunosuppression regimens.^[19]

In 1978, Calne reported improvement in allograft survival with the use of a new immunosuppressive agent, cyclosporine.^[20]Widespread use of cyclosporine led to a dramatic improvement in allograft survival. New protocols incorporating cyclosporine and other drugs have increased the specificity of immunosuppression and decreased the prevalence of infectious complications in transplant recipients.

Pathophysiology

Despite numerous attempts and prolific experimentation, kidney transplantation (except between identical twins) was not successful until the 1960s. Early experimenters understood the outcome of the unmodified response to allograft (ie, a rapid or gradual decrease in urine output and ultimate demise of the transplanted kidney) but not its mechanism.

In the 1940s, through a series of elegant animal experiments, Medawar demonstrated that skin grafts between non-identical rabbits were ultimately sloughed.^[21]He found that this reaction occurred much more rapidly in animals that had previously been grafted from the same donor and that the process involved a leukocytic infiltration in the allograft. Medawar reasoned that exposure to foreign tissue resulted in an activation of the immune system and that it induced specific memory that allowed rapid reaction to subsequent exposure to similar grafts. Modulation of that response became the goal of transplant investigators in the subsequent decades. Although understanding of the immune response to allografts has dramatically increased over the 50 years since Medawar's experiments, it remains incomplete.

Major histocompatibility complex (MHC) proteins are cell surface proteins that are important for self-recognition, tolerance, and antigen presentation. The key MHC genes are the class I genes (HLA-A, -B, and -C genes), which are expressed on all nucleated cells, and the class II genes (HLA-DP, -DQ, and -DR), which are expressed on antigen-presenting cells (APC): dendritic cells, macrophages, and B-cells. MHC-I is important for intracellular antigen presentation and MHC-II is responsible for presentation of extracellular antigens. MHC mismatch is a risk factor for allograft rejection and MHCs A, B, and DR are used as donor-recipient matching criteria for kidney transplantation.

The immune system lies at the nexus of immune tolerance and graft intolerance. Both innate (non-specific) and adaptive immunity (antigen-specific) activate each other and play key roles in transplant rejection.

Phagocytic leukocytes (neutrophils, monocytes, eosinophils, and basophils), natural killer cells, and dendritic cells form the backbone for innate immunity. Ischemia-reperfusion injury during transplantation recruits neutrophils and macrophages, resulting in release of proteases, free radicals, and pro-inflammatory molecules such as interleukin 6 (IL-6), interleukin 8 (IL-8), and tumor necrosis factor alpha (TNF-α) within the graft. Macrophages present peptides to alloreactive T cells in peripheral lymph nodes and establish communication between innate and adaptive immunity.

Dendritic cells, macrophages, and B-lymphocytes present peptide fragments of antigens in association with MHC molecules and activate specific T cells. These antigen presenting cells also express costimulatory molecules (B7-1 (CD-80) and B7-2 (CD86) to optimally activate T lymphocytes (interacting with T-cell CD28 receptors). B-cells produce anti-graft antibodies that can act by fixing complement or targeting cells. CD8 T lymphocyte (cytotoxic T cells) cause tissue injury by releasing membrane-damaging proteins such as perforin and granzyme from intracellular granules.

There are subtle differences between adult and pediatric immune responses to the allograft, with greater alloreactivity in adults. Due to thymic atrophy, the thymic response in adults is not as active as it is in children; that leads to changes in the T-cell pool from naive to memory T cells. In children, reduced T-cell effector function, lower titers of anti-HLA antibodies, lower expression of CD40 co-stimulatory ligands, and fewer T- lymphocytes with specific antigen affiliation make the allograft more tolerable, with better post-transplant outcomes.^[22]

Once stimulated, the immune response results in an attack on the vascular endothelium of the allograft, resulting in rejection. The attack may be rapid or gradual. If the allograft expresses antigens against which the recipient has already developed antibodies, rejection occurs rapidly. This is called hyperacute rejection, and it involves swelling, rupture, and loss of the allograft within minutes or hours. Current pre-transplant cross-matching techniques (between recipient serum and donor lymphocytes) have dramatically reduced the occurrence of this type of rejection.

Acute rejection occurs within days or weeks, when stimulated cytotoxic T lymphocytes, specifically directed against the mismatched tissue, and natural killer cells attack target cells. This response can vary in severity from mild allograft dysfunction to a dramatic rise in serum creatinine with loss of urine output.

Some recipients of transplants experience a gradual reduction in allograft function over years, typified by a gradual obliteration of the lumen of small arteries in the graft caused by endothelial thickening, along with interstitial fibrosis and tubular atrophy. This response occurs more commonly, but not exclusively, in recipients who have experienced an acute rejection. Therefore, these chronic changes may be a long-term consequence of acute rejection, a low-grade indolent immune reaction, toxicity of immunosuppressive medications, or a combination of those processes.^[23]Consequently, the term chronic allograft dysfunction is preferred over chronic rejection to describe these chronic changes.

Indications

Any child with measured or calculated glomerular filtration rate < 20 mL/min/1.732 m² without hope of recovery or ESKD can be considered for kidney transplantation. Selection criteria in pediatric patients have subtle differences from those in adults. All of the following need to be taken into consideration when determining whether a child is appropriate for rkidney transplantation:

Symptoms of uremia
Failure to thrive (due to limited caloric intake, impaired growth hormone–activated post-receptor Janus kinase/signal transducer and activator of transcription [JAK/STAT] signaling, and reduced levels of free IGF-1 due to increased inhibitory IGF-binding proteins)
Delayed psychomotor development
Metabolic bone disease
Reliability of the child's social situation

Contraindications

There are few absolute contraindications for kidney transplantation in children. Acute or chronic active infection, active malignancy, unaddressed outflow obstruction, are absolute contraindications due to the need for long-term significant immunosuppression post-transplant. Patients with hepatitis- and HIV-related kidney disease may receive a transplant once they no longer have active disease.

Children with treated malignancy can be eligible for kidney transplant after a disease-free waiting period. The length of time will depend on the type of malignancy.^[24]

There can be many relative, and transient, contraindications to kidney transplant. Kidney transplantation should be delayed in those with ongoing active infections, or if the disease responsible for kidney failure is active and rapidly progressive. Transplantation is also deferred in any child with active anti–glomerular basement membrane (GBM) disease with elevated levels of circulating anti-GBM antibodies, active hemolytic-uremic syndrome, active lupus and active anti-neutrophil cytoplasmic antibody (ANCA) vasculitis, because those processes can damage an allograft. Transplantation should not be performed until those conditions have been successfully treated, so that they do not negatively affect the allograft.

Children with kidney failure from primary glomerulonephritis, such as focal segmental glomerulosclerosis (FSGS) or membranoproliferative glomerulonephritis, are at increased risk of recurrence following transplantation. Patients with FSGS can receive a transplant once they are no longer nephrotic. These patients may undergo medical or surgical nephrectomy before transplantation and thus are not candidates for a preemptive transplant. Many registry studies suggested obesity as a contraindication at a body mass index (BMI) >35 mg/kg².^[25]

Transplantation in children with progressive central neurodegenerative disease is not advised, if survival and quality of life are not expected to be substantially improved by transplantation. Non-progressive intellectual, developmental, or cognitive disability are not contraindications for kidney transplantation. Children with developmental delay and their caregivers may benefit from an improved quality of life.

Generally, younger children are transplanted once they reach a length of 65 cm or a weight of 10 kg, to minimize the risk of vascular thrombosis and to accommodate the adult-sized kidney.^[26]

The responsibility for the selection of transplant candidates ultimately lies with the evaluating team, which must assess the risk versus benefit.

Prognosis

For pediatric kidney transplantation dperformed after 2002, patient survival is much greater than graft survival at 10 years (deceased donor recipients: 95% vs. 57%, live donor recipients: 96% vs 78%).^[27]In contrast, adults have a much lower patient survival.

Graft survival

The 2018 annual report of the Organ Procurement and Transplantation Network/Scientific Registry of Transplant Recipients (OPTN/SRTR) notes that graft survival was highest for living-donor recipients younger than 11 years (93.1% at 5 years) and lowest for deceased-donor recipients aged 11–17 years (77.2% at 5 years). The incidence of acute rejection in the first year was 11.4% overall—highest, at 12.5%, for ages younger than 6 years and lowest, at 7.9% for ages 6-10 years.^[2]

Using data from the United Network for Organ Sharing (UNOS) database, one study evaluated the impact of age at transfer to adult-oriented care on kidney allograft failure rates. The data noted that graft failures were 58% higher among those who had transferred early (aged < 21 y) compared with those who were transferred late (aged ≥21 y).^[28]

Patient survival

Common causes of death in pediatric kidney transplant recipients are cardiovascular issues, infections, and cancer (including post-transplant lymphoproliferative disorder [PTLD]).^[29]Cardiovascular disease accounts for a mortality rate of 36% among all pediatric patients with ESKD, 34% in those undergoing dialysis and 11% after transplantation.^[30]The youngest children have reported causes similar to those in older children and adolescents.^[2]

Managing chronic kidney disease and related cardiovascular morbidity should be an essential component to the care of pediatric transplant patients. Timely identification of any irregularities, such as albuminuria and hypertension, aid in the early detection of kidney damage and increase the probability of restoring lost kidney function.^[31]

Analysis of North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) data from 1988 to 2010 on pediatric patients with PTLD showed that in the most recent cases, patient survival was 87.4% at 5 years post-PTLD, compared with 48% cross-sectional survival reported in the 1990s. Recent graft survival post-PTLD was 81.8% at 1 year and 65% at 5 years. Interventions for PTLD included reduction of immunosuppression; use of anti-CD20 antibody, interferon alpha, or antiviral therapy; and surgical reduction.^[32]

In a study of 18,911 patients who received a first transplant before age 21 years, mortality was highest in the first year post transplantation. After the first year of the first transplant, mortality rates and age-, sex-, and race-standardized mortality ratios decreased slightly. The age-adjusted all-cause mortality rate decreased by 1% and the cardiovascular mortality rate by 16% for every year after the first post-transplantation year; the infection-related mortality rate did not change. Those results suggest that exposure to the "transplantation milieu" does not negatively affect long-term cardiovascular health.^{[33, 30]}

Workup

Johansen KL, Chertow GM, Gilbertson DT, Herzog CA, Ishani A, Israni AK, et al. US Renal Data System 2021 Annual Data Report: Epidemiology of Kidney Disease in the United States. Am J Kidney Dis. 2022 Apr. 79 (4 Suppl 1):A8-A12. [QxMD MEDLINE Link].
Lentine KL, Smith JM, Hart A, Miller J, Skeans MA, Larkin L, et al. OPTN/SRTR 2020 Annual Data Report: Kidney. Am J Transplant. 2022 Mar. 22 Suppl 2:21-136. [QxMD MEDLINE Link].
Shapiro R, Sarwal MM. Pediatric kidney transplantation. Pediatr Clin North Am. 2010 Apr. 57 (2):393-400, table of contents. [QxMD MEDLINE Link].
Cho MH. Pediatric kidney transplantation is different from adult kidney transplantation. Korean J Pediatr. 2018 Jul. 61 (7):205-209. [QxMD MEDLINE Link].
Ullman E. [Experimental kidney transplantation. 1902]. Wien Klin Wochenschr. 2002 Feb 28. 114 (4):126-7. [QxMD MEDLINE Link].
Rodger D, Hurst DJ. Mathieu Jaboulay's (1860-1913) contribution to xenotransplantation. Xenotransplantation. 2022 Sep. 29 (5):e12765. [QxMD MEDLINE Link].
Jaboulay M. Greffe de reins au pli du coude par soudures arterielles et veineuses. Lyon Méd. 1906;107(39):575-583.
Unger E. Nierentransplantation. Berlin Dlin Wochenschr. 1909. Vol 1: 1057.
Medawar PB. The behaviour and fate of skin autografts and skin homografts in rabbits: A report to the War Wounds Committee of the Medical Research Council. J Anat. 1944 Oct. 78 (Pt 5):176-99. [QxMD MEDLINE Link].
HUME DM, MERRILL JP, MILLER BF, THORN GW. Experiences with renal homotransplantation in the human: report of nine cases. J Clin Invest. 1955 Feb. 34 (2):327-82. [QxMD MEDLINE Link].
MURRAY JE, MERRILL JP, HARRISON JH. Kidney transplantation between seven pairs of identical twins. Ann Surg. 1958 Sep. 148 (3):343-59. [QxMD MEDLINE Link].
Verghese PS. Pediatric kidney transplantation: a historical review. Pediatr Res. 2017 Jan. 81 (1-2):259-264. [QxMD MEDLINE Link].
CALNE RY, ALEXANDRE GP, MURRAY JE. A study of the effects of drugs in prolonging survival of homologous renal transplants in dogs. Ann N Y Acad Sci. 1962 Oct 24. 99:743-61. [QxMD MEDLINE Link].
GOODWIN WE, MIMS MM, KAUFMAN JJ. Human renal transplantation III. Technical problems encountered in six cases of kidney homotransplantation. Trans Am Assoc Genitourin Surg. 1962. 54:116-25. [QxMD MEDLINE Link].
STARZL TE, MARCHIORO TL, WADDELL WR. THE REVERSAL OF REJECTION IN HUMAN RENAL HOMOGRAFTS WITH SUBSEQUENT DEVELOPMENT OF HOMOGRAFT TOLERANCE. Surg Gynecol Obstet. 1963 Oct. 117:385-95. [QxMD MEDLINE Link].
Terasaki PI, Vredevoe DL, Porter KA, Mickey MR, Marchioro TL, Faris TD, et al. Serotyping for homotransplantation. V. Evaluation of a matching scheme. Transplantation. 1966 Nov. 4 (6):688-99. [QxMD MEDLINE Link].
Cranford RW. Brain death. Organ Procurement, Preservation and Distribution in Transplantation. Richmond, Va: UNOS; 1991. 23-31. [package insert].
Banowsky LH. Current results and future expectations in renal transplantation. Urol Clin North Am. 1983 May. 10 (2):337-46. [QxMD MEDLINE Link].
Ting A, Morris PJ. Matching for B-cell antigens of the HLA-DR series in cadaver renal transplantation. Lancet. 1978 Mar 18. 1 (8064):575-7. [QxMD MEDLINE Link].
Calne RY, White DJ, Thiru S, Evans DB, McMaster P, Dunn DC, et al. Cyclosporin A in patients receiving renal allografts from cadaver donors. Lancet. 1978 Dec 23-30. 2 (8104-5):1323-7. [QxMD MEDLINE Link].
Medawar PB. The behaviour and fate of skin autografts and skin homografts in rabbits: A report to the War Wounds Committee of the Medical Research Council. J Anat. 1944 Oct. 78 (Pt 5):176-99. [QxMD MEDLINE Link].
Dharnidharka VR, Fiorina P, Harmon WE. Kidney transplantation in children. N Engl J Med. 2014 Aug 7. 371 (6):549-58. [QxMD MEDLINE Link].
Bröcker V, Mengel M. Histopathological diagnosis of acute and chronic rejection in pediatric kidney transplantation. Pediatr Nephrol. 2014 Oct. 29 (10):1939-49. [QxMD MEDLINE Link].
Knoll G, Cockfield S, Blydt-Hansen T, Baran D, Kiberd B, Landsberg D, et al. Canadian Society of Transplantation consensus guidelines on eligibility for kidney transplantation. CMAJ. 2005 Nov 8. 173 (10):1181-4. [QxMD MEDLINE Link].
Nicoletto BB, Fonseca NK, Manfro RC, Gonçalves LF, Leitão CB, Souza GC. Effects of obesity on kidney transplantation outcomes: a systematic review and meta-analysis. Transplantation. 2014 Jul 27. 98 (2):167-76. [QxMD MEDLINE Link].
Jalanko H, Mattila I, Holmberg C. Renal transplantation in infants. Pediatr Nephrol. 2016 May. 31 (5):725-35. [QxMD MEDLINE Link].
Chinnakotla S, Verghese P, Chavers B, Rheault MN, Kirchner V, Dunn T, et al. Outcomes and Risk Factors for Graft Loss: Lessons Learned from 1,056 Pediatric Kidney Transplants at the University of Minnesota. J Am Coll Surg. 2017 Apr. 224 (4):473-486. [QxMD MEDLINE Link].
Foster BJ, Platt RW, Dahhou M, Zhang X, Bell LE, Hanley JA. The impact of age at transfer from pediatric to adult-oriented care on renal allograft survival. Pediatr Transplant. 2011 Nov. 15 (7):750-9. [QxMD MEDLINE Link].
Francis A, Johnson DW, Melk A, Foster BJ, Blazek K, Craig JC, et al. Survival after Kidney Transplantation during Childhood and Adolescence. Clin J Am Soc Nephrol. 2020 Mar 6. 15 (3):392-400. [QxMD MEDLINE Link]. [Full Text].
Kaidar M, Berant M, Krauze I, Cleper R, Mor E, Bar-Nathan N, et al. Cardiovascular risk factors in children after kidney transplantation--from short-term to long-term follow-up. Pediatr Transplant. 2014 Feb. 18 (1):23-8. [QxMD MEDLINE Link].
Filler G. Challenges in pediatric transplantation: the impact of chronic kidney disease and cardiovascular risk factors on long-term outcomes and recommended management strategies. Pediatr Transplant. 2011 Feb. 15 (1):25-31. [QxMD MEDLINE Link].
Dharnidharka VR, Martz KL, Stablein DM, Benfield MR. Improved survival with recent Post-Transplant Lymphoproliferative Disorder (PTLD) in children with kidney transplants. Am J Transplant. 2011 Apr. 11 (4):751-8. [QxMD MEDLINE Link].
Foster BJ, Dahhou M, Zhang X, Platt RW, Hanley JA. Change in mortality risk over time in young kidney transplant recipients. Am J Transplant. 2011 Nov. 11 (11):2432-42. [QxMD MEDLINE Link].
Hart A, Smith JM, Skeans MA, Gustafson SK, Wilk AR, Castro S, et al. OPTN/SRTR 2018 Annual Data Report: Kidney. Am J Transplant. 2020 Jan. 20 Suppl s1:20-130. [QxMD MEDLINE Link].
Brophy PD, Thomas SE, McBryde KD, Bunchman TE. Comparison of polyclonal induction agents in pediatric renal transplantation. Pediatr Transplant. 2001 Jun. 5 (3):174-8. [QxMD MEDLINE Link].
Hardinger KL, Rhee S, Buchanan P, Koch M, Miller B, Enkvetchakul D, et al. A prospective, randomized, double-blinded comparison of thymoglobulin versus Atgam for induction immunosuppressive therapy: 10-year results. Transplantation. 2008 Oct 15. 86 (7):947-52. [QxMD MEDLINE Link].
Ashoor IF, Martz K, Galbiati S, Beyl RA, Dharnidharka VR. Reassessing Rabbit Antithymocyte Globulin Induction in Kidney Transplantation (RETHINK): An Analysis of the North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) Registry. Transplant Direct. 2020 Sep. 6 (9):e598. [QxMD MEDLINE Link].
Kahan BD, Rajagopalan PR, Hall M. Reduction of the occurrence of acute cellular rejection among renal allograft recipients treated with basiliximab, a chimeric anti-interleukin-2-receptor monoclonal antibody. United States Simulect Renal Study Group. Transplantation. 1999 Jan 27. 67 (2):276-84. [QxMD MEDLINE Link].
Webster AC, Woodroffe RC, Taylor RS, Chapman JR, Craig JC. Tacrolimus versus ciclosporin as primary immunosuppression for kidney transplant recipients: meta-analysis and meta-regression of randomised trial data. BMJ. 2005 Oct 8. 331 (7520):810. [QxMD MEDLINE Link].
Neu AM, Ho PL, Fine RN, Furth SL, Fivush BA. Tacrolimus vs. cyclosporine A as primary immunosuppression in pediatric renal transplantation: a NAPRTCS study. Pediatr Transplant. 2003 Jun. 7 (3):217-22. [QxMD MEDLINE Link].
Hymes LC, Warshaw BL. Linear growth in pediatric renal transplant recipients receiving sirolimus. Pediatr Transplant. 2011 Sep. 15 (6):570-2. [QxMD MEDLINE Link].
Archdeacon P, Dixon C, Belen O, Albrecht R, Meyer J. Summary of the US FDA approval of belatacept. Am J Transplant. 2012 Mar. 12 (3):554-62. [QxMD MEDLINE Link].
Summers DM, Watson CJ, Pettigrew GJ, Johnson RJ, Collett D, Neuberger JM, et al. Kidney donation after circulatory death (DCD): state of the art. Kidney Int. 2015 Aug. 88 (2):241-9. [QxMD MEDLINE Link].
Hosgood SA, Saeb-Parsy K, Wilson C, Callaghan C, Collett D, Nicholson ML. Protocol of a randomised controlled, open-label trial of ex vivo normothermic perfusion versus static cold storage in donation after circulatory death renal transplantation. BMJ Open. 2017 Jan 23. 7 (1):e012237. [QxMD MEDLINE Link].
Lentine KL, Kasiske BL, Levey AS, Adams PL, Alberú J, Bakr MA, et al. KDIGO Clinical Practice Guideline on the Evaluation and Care of Living Kidney Donors. Transplantation. 2017 Aug. 101 (8S Suppl 1):S1-S109. [QxMD MEDLINE Link].
Kidney Donor Profile Index (KDPI) Guide for Clinicians. Organ Procurement & Transplantation Network. Available at https://optn.transplant.hrsa.gov/professionals/by-topic/guidance/the-new-kidney-allocation-system-kas-frequently-asked-questions/#bookmark5. Accessed: March 15, 2023.
Barry JM. Unstented extravesical ureteroneocystostomy in kidney transplantation. J Urol. 1983 May. 129 (5):918-9. [QxMD MEDLINE Link].
Howe A, Kozel Z, Palmer L. Robotic surgery in pediatric urology. Asian J Urol. 2017 Jan. 4 (1):55-67. [QxMD MEDLINE Link].
Bowen DK, Casey JT, Cheng EY, Gong EM. Robotic-assisted laparoscopic transplant-to-native ureteroureterostomy in a pediatric patient. J Pediatr Urol. 2014 Dec. 10 (6):1284.e1-2. [QxMD MEDLINE Link].
Heap SL, Webb NJ, Kirkman MA, Roberts D, Riad H. Extraperitoneal renal transplantation in small children results in a transient improvement in early graft function. Pediatr Transplant. 2011 Jun. 15 (4):362-6. [QxMD MEDLINE Link].
Tydén G, Kumlien G, Berg UB. ABO-incompatible kidney transplantation in children. Pediatr Transplant. 2011 Aug. 15 (5):502-4. [QxMD MEDLINE Link].
Gill IS, Hayes JM, Hodge EE, Novick AC. Clean intermittent catheterization and urinary diversion in the management of renal transplant recipients with lower urinary tract dysfunction. J Urol. 1992 Nov. 148 (5):1397-400. [QxMD MEDLINE Link].
Hatch DA, Koyle MA, Baskin LS, Zaontz MR, Burns MW, Tarry WF, et al. Kidney transplantation in children with urinary diversion or bladder augmentation. J Urol. 2001 Jun. 165 (6 Pt 2):2265-8. [QxMD MEDLINE Link].
McDonald RA, Smith JM, Stablein D, Harmon WE. Pretransplant peritoneal dialysis and graft thrombosis following pediatric kidney transplantation: a NAPRTCS report. Pediatr Transplant. 2003 Jun. 7 (3):204-8. [QxMD MEDLINE Link].
Whitaker RH. Clinical assessment of pelvic and ureteral function. Urology. 1978 Aug. 12 (2):146-50. [QxMD MEDLINE Link].
Kumar A, Verma BS, Srivastava A, Bhandari M, Gupta A, Sharma R. Evaluation of the urological complications of living related renal transplantation at a single center during the last 10 years: impact of the Double-J* stent. J Urol. 2000 Sep. 164 (3 Pt 1):657-60. [QxMD MEDLINE Link].
Renoult E, Buteau C, Lamarre V, Turgeon N, Tapiero B. Infectious risk in pediatric organ transplant recipients: is it increased with the new immunosuppressive agents?. Pediatr Transplant. 2005 Aug. 9 (4):470-9. [QxMD MEDLINE Link].
Silkensen JR. Long-term complications in renal transplantation. J Am Soc Nephrol. 2000 Mar. 11 (3):582-588. [QxMD MEDLINE Link].
Sia IG, Paya CV. Infectious complications following renal transplantation. Surg Clin North Am. 1998 Feb. 78 (1):95-112. [QxMD MEDLINE Link].
Kahwaji J, Bunnapradist S, Hsu JW, Idroos ML, Dudek R. Cause of death with graft function among renal transplant recipients in an integrated healthcare system. Transplantation. 2011 Jan 27. 91 (2):225-30. [QxMD MEDLINE Link].
Bock GH, Sullivan EK, Miller D, Gimon D, Alexander S, Ellis E, et al. Cytomegalovirus infections following renal transplantation--effects on antiviral prophylaxis: a report of the North American Pediatric Renal Transplant Cooperative Study. Pediatr Nephrol. 1997 Dec. 11 (6):665-71. [QxMD MEDLINE Link].
Granger DK, Burd RS, Schmidt WJ, Dunn DL, Matas AJ. Incidence and timing of infections in pediatric renal transplant recipients in the cyclosporine era. Transplant Proc. 1994 Feb. 26 (1):64. [QxMD MEDLINE Link].
Humar A, Michaels M, AST ID Working Group on Infectious Disease Monitoring. American Society of Transplantation recommendations for screening, monitoring and reporting of infectious complications in immunosuppression trials in recipients of organ transplantation. Am J Transplant. 2006 Feb. 6 (2):262-74. [QxMD MEDLINE Link].
Kotton CN, Kumar D, Caliendo AM, Asberg A, Chou S, Danziger-Isakov L, et al. Updated international consensus guidelines on the management of cytomegalovirus in solid-organ transplantation. Transplantation. 2013 Aug 27. 96 (4):333-60. [QxMD MEDLINE Link].
Chapman JR. The KDIGO clinical practice guidelines for the care of kidney transplant recipients. Transplantation. 2010 Mar 27. 89 (6):644-5. [QxMD MEDLINE Link].
Cox KL, Lawrence-Miyasaki LS, Garcia-Kennedy R, Lennette ET, Martinez OM, Krams SM, et al. An increased incidence of Epstein-Barr virus infection and lymphoproliferative disorder in young children on FK506 after liver transplantation. Transplantation. 1995 Feb 27. 59 (4):524-9. [QxMD MEDLINE Link].
Newell KA, Alonso EM, Whitington PF, Bruce DS, Millis JM, Piper JB, et al. Posttransplant lymphoproliferative disease in pediatric liver transplantation. Interplay between primary Epstein-Barr virus infection and immunosuppression. Transplantation. 1996 Aug 15. 62 (3):370-5. [QxMD MEDLINE Link].
Green M, Michaels MG, Webber SA, Rowe D, Reyes J. The management of Epstein-Barr virus associated post-transplant lymphoproliferative disorders in pediatric solid-organ transplant recipients. Pediatr Transplant. 1999 Nov. 3 (4):271-81. [QxMD MEDLINE Link].
Ho M, Jaffe R, Miller G, Breinig MK, Dummer JS, Makowka L, et al. The frequency of Epstein-Barr virus infection and associated lymphoproliferative syndrome after transplantation and its manifestations in children. Transplantation. 1988 Apr. 45 (4):719-27. [QxMD MEDLINE Link].
Dharnidharka VR, Abdulnour HA, Araya CE. The BK virus in renal transplant recipients-review of pathogenesis, diagnosis, and treatment. Pediatr Nephrol. 2011 Oct. 26 (10):1763-74. [QxMD MEDLINE Link].
Smith JM, Dharnidharka VR, Talley L, Martz K, McDonald RA. BK virus nephropathy in pediatric renal transplant recipients: an analysis of the North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) registry. Clin J Am Soc Nephrol. 2007 Sep. 2 (5):1037-42. [QxMD MEDLINE Link].
Broyer M, Tete MJ, Guest G, Gagnadoux MF, Rouzioux C. Varicella and zoster in children after kidney transplantation: long-term results of vaccination. Pediatrics. 1997 Jan. 99 (1):35-9. [QxMD MEDLINE Link].
Furth SL, Sullivan EK, Neu AM, Tejani A, Fivush BA. Varicella in the first year after renal transplantation: a report of the North American Pediatric Renal Transplant Cooperative Study (NAPRTCS). Pediatr Transplant. 1997 Aug. 1 (1):37-42. [QxMD MEDLINE Link].
Broyer M, Tete MJ, Guest G, Gagnadoux MF, Rouzioux C. Varicella and zoster in children after kidney transplantation: long-term results of vaccination. Pediatrics. 1997 Jan. 99 (1):35-9. [QxMD MEDLINE Link].
Broyer M, Boudailliez B. Varicella vaccine in children with chronic renal insufficiency. Postgrad Med J. 1985. 61 Suppl 4:103-6. [QxMD MEDLINE Link].
Hardy I, Gershon AA, Steinberg SP, LaRussa P. The incidence of zoster after immunization with live attenuated varicella vaccine. A study in children with leukemia. Varicella Vaccine Collaborative Study Group. N Engl J Med. 1991 Nov 28. 325 (22):1545-50. [QxMD MEDLINE Link].
Zamora I, Simon JM, Da Silva ME, Piqueras AI. Attenuated varicella virus vaccine in children with renal transplants. Pediatr Nephrol. 1994 Apr. 8 (2):190-2. [QxMD MEDLINE Link].
Chugh KS, Sakhuja V, Jain S, Talwar P, Minz M, Joshi K, et al. High mortality in systemic fungal infections following renal transplantation in third-world countries. Nephrol Dial Transplant. 1993. 8 (2):168-72. [QxMD MEDLINE Link].
Chugh KS, Sakhuja V, Jain S, Singh V, Tarafdar A, Joshi K, et al. Fungal infections in renal allograft recipients. Transplant Proc. 1992 Oct. 24 (5):1940-2. [QxMD MEDLINE Link].
Tolkoff-Rubin NE, Rubin RH. Opportunistic fungal and bacterial infection in the renal transplant recipient. J Am Soc Nephrol. 1992 Jun. 2 (12 Suppl):S264-9. [QxMD MEDLINE Link].
Neu AM, Fivush BA. Recommended immunization practices for pediatric renal transplant recipients. Pediatr Transplant. 1998 Nov. 2 (4):263-9. [QxMD MEDLINE Link].
Esposito S, Mastrolia MV, Prada E, Pietrasanta C, Principi N. Vaccine administration in children with chronic kidney disease. Vaccine. 2014 Nov 20. 32 (49):6601-6. [QxMD MEDLINE Link].
Gangappa S, Kokko KE, Carlson LM, Gourley T, Newell KA, Pearson TC, et al. Immune responsiveness and protective immunity after transplantation. Transpl Int. 2008 Apr. 21 (4):293-303. [QxMD MEDLINE Link].
Rubin LG, Levin MJ, Ljungman P, Davies EG, Avery R, Tomblyn M, et al. 2013 IDSA clinical practice guideline for vaccination of the immunocompromised host. Clin Infect Dis. 2014 Feb. 58 (3):309-18. [QxMD MEDLINE Link].
Enke BU, Bökenkamp A, Offner G, Bartmann P, Brodehl J. Response to diphtheria and tetanus booster vaccination in pediatric renal transplant recipients. Transplantation. 1997 Jul 27. 64 (2):237-41. [QxMD MEDLINE Link].
Mathew JL, El Dib R, Mathew PJ, Boxall EH, Brok J. Hepatitis B immunisation in persons not previously exposed to hepatitis B or with unknown exposure status. Cochrane Database Syst Rev. 2008 Jul 16. CD006481. [QxMD MEDLINE Link].
American Academy of Pediatrics. Report of the committee on infectious diseases. Pickering LK, Baker CJ, McMillan M, Long S (Editors). Red Book. 27th Edition. 2006.
Nuorti JP, Whitney CG, Centers for Disease Control and Prevention (CDC). Prevention of pneumococcal disease among infants and children - use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine - recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2010 Dec 10. 59 (RR-11):1-18. [QxMD MEDLINE Link].
Robinson CL, Romero JR, Kempe A, Pellegrini C, Advisory Committee on Immunization Practices (ACIP) Child/Adolescent Immunization Work Group. Advisory Committee on Immunization Practices Recommended Immunization Schedule for Children and Adolescents Aged 18 Years or Younger - United States, 2017. MMWR Morb Mortal Wkly Rep. 2017 Feb 10. 66 (5):134-135. [QxMD MEDLINE Link].
Penn I. Incidence and treatment of neoplasia after transplantation. J Heart Lung Transplant. 1993 Nov-Dec. 12 (6 Pt 2):S328-36. [QxMD MEDLINE Link].
Foster BJ, Dahhou M, Zhang X, Platt RW, Hanley JA. Change in mortality risk over time in young kidney transplant recipients. Am J Transplant. 2011 Nov. 11 (11):2432-42. [QxMD MEDLINE Link].
Coutinho HM, Groothoff JW, Offringa M, Gruppen MP, Heymans HS. De novo malignancy after paediatric renal replacement therapy. Arch Dis Child. 2001 Dec. 85 (6):478-83. [QxMD MEDLINE Link].
Smith JM, Martz K, Blydt-Hansen TD. Pediatric kidney transplant practice patterns and outcome benchmarks, 1987-2010: a report of the North American Pediatric Renal Trials and Collaborative Studies. Pediatr Transplant. 2013 Mar. 17 (2):149-57. [QxMD MEDLINE Link].
Farrugia D, Mahboob S, Cheshire J, Begaj I, Khosla S, Ray D, et al. Malignancy-related mortality following kidney transplantation is common. Kidney Int. 2014 Jun. 85 (6):1395-403. [QxMD MEDLINE Link].
Wong G, Chapman JR, Craig JC. Death from cancer: a sobering truth for patients with kidney transplants. Kidney Int. 2014 Jun. 85 (6):1262-4. [QxMD MEDLINE Link].
Mynarek M, Hussein K, Kreipe HH, Maecker-Kolhoff B. Malignancies after pediatric kidney transplantation: more than PTLD?. Pediatr Nephrol. 2014 Sep. 29 (9):1517-28. [QxMD MEDLINE Link].
Smith JM, Martz K, Blydt-Hansen TD. Pediatric kidney transplant practice patterns and outcome benchmarks, 1987-2010: a report of the North American Pediatric Renal Trials and Collaborative Studies. Pediatr Transplant. 2013 Mar. 17 (2):149-57. [QxMD MEDLINE Link].
Engels EA, etal. Spectrum of cancer risk among US solid organ transplant recipients. JAMA. 2011 Nov 2. 306 (17):1891-901. [QxMD MEDLINE Link].
Yanik EL, Smith JM, Shiels MS, Clarke CA, Lynch CF, Kahn AR, et al. Cancer Risk After Pediatric Solid Organ Transplantation. Pediatrics. 2017 May. 139 (5):[QxMD MEDLINE Link].
Dharnidharka VR. Comprehensive review of post-organ transplant hematologic cancers. Am J Transplant. 2018 Mar. 18 (3):537-549. [QxMD MEDLINE Link].
Penn I. De novo malignances in pediatric organ transplant recipients. Pediatr Transplant. 1998 Feb. 2 (1):56-63. [QxMD MEDLINE Link].
Haas M et al. The Banff 2017 Kidney Meeting Report: Revised diagnostic criteria for chronic active T cell-mediated rejection, antibody-mediated rejection, and prospects for integrative endpoints for next-generation clinical trials. Am J Transplant. 2018 Feb. 18 (2):293-307. [QxMD MEDLINE Link].
Kidney Disease: Improving Global Outcomes (KDIGO) Transplant Work Group. KDIGO clinical practice guideline for the care of kidney transplant recipients. Am J Transplant. 2009 Nov. 9 Suppl 3:S1-155. [QxMD MEDLINE Link].
Choi J, Aubert O, Vo A, Loupy A, Haas M, Puliyanda D, et al. Assessment of Tocilizumab (Anti-Interleukin-6 Receptor Monoclonal) as a Potential Treatment for Chronic Antibody-Mediated Rejection and Transplant Glomerulopathy in HLA-Sensitized Renal Allograft Recipients. Am J Transplant. 2017 Sep. 17 (9):2381-2389. [QxMD MEDLINE Link].
Mongeau JG, Clermont MJ, Robitaille P, Plante A, Jéquier JC, Godbout C, et al. Study of psychosocial parameters related to the survival rate of renal transplantation in children. Pediatr Nephrol. 1997 Oct. 11 (5):542-6. [QxMD MEDLINE Link].
Birk PE, Matas AJ, Gillingham KJ, Mauer SM, Najarian JS, Chavers BM. Risk factors for chronic rejection in pediatric renal transplant recipients--a single-center experience. Pediatr Nephrol. 1997 Aug. 11 (4):395-8. [QxMD MEDLINE Link].
Crespo M, Collado S, Mir M, Cao H, Barbosa F, Serra C, et al. Efficacy of influenza A H1N1/2009 vaccine in hemodialysis and kidney transplant patients. Clin J Am Soc Nephrol. 2011 Sep. 6 (9):2208-14. [QxMD MEDLINE Link].

Media Gallery

Etiology of end-stage renal disease in North American children. Data from Annual Report North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS), 2007.
Etiology of end-stage renal disease in children aged 0-18 years by age group. Data from North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) Annual Report, 2007.
Management of end-stage renal disease in US children aged 0-19 years by age group. Data from US Renal Data Systems, 2008.
Simplified diagram of the immune response to nonidentical major histocompatability complex (MHC) antigens. Foreign antigens are processed by macrophages or dendritic cells (antigen-presenting cell) and then presented to T-helper lymphocytes. Release of interleukin-1 from macrophages activates T-helper lymphocytes. Thus activated, these T-helper lymphocytes produce cytokines (interleukin-2) that stimulate production of cytotoxic T lymphocytes, antibody-producing B lymphocytes, and natural killer cells. Diagram provided by David A. Hatch, MD, copyright 2001, used with permission.
Simplified diagram illustrating the points of action of immunosuppressive drugs. Corticosteroids inhibit production of interleukin-1. Macrolides (ie, cyclosporine, tacrolimus, sirolimus) inhibit production of or use of interleukin-2, thus inhibiting stimulation of a clone of cytotoxic T lymphocytes directed against specific human lymphocyte antigen types. Antimetabolites (ie, mycophenolate mofetil, azathioprine) inhibit purine production, thus impairing cell proliferation. Antibodies impair normal function of cell surface markers, thus inhibiting stimulation of T-lymphocyte clones directed against foreign antigens. Diagram provided by David A. Hatch, MD, copyright 2001, used with permission.
Comparison of imaging techniques for a living kidney donor. (A) Digital subtraction angiogram showing lower pole artery. (B) Three-dimensional CT scan depicting 2 left renal arteries. Images provided by David A. Hatch, MD, copyright 1999, used with permission.
Incisions used for kidney transplantation. (A) Gibson incision used for large children and adults. (B) Midline abdominal incision used for small children.
Vascular anastomoses used in a kidney transplantation in a 5-year-old patient, renal artery to common iliac artery and renal vein to common iliac vein. Image provided by David A. Hatch, MD, copyright 2001, used with permission.
Anastomosis of kidney transplant ureter to bladder.
Anastomosis of kidney transplantation. Ureter to (A) bladder augmented with a patch of bowel and (B) urinary conduit constructed from a segment of ileum.
Kidney transplantation ultrasonograms. (A) Normal kidney. (B) Color Doppler ultrasonogram documenting normal perfusion to the kidney. (C) Color Doppler ultrasonogram showing absence of perfusion in a patient with thrombosis. (D) Hydronephrosis. (E) Lymphocele. (F) Stone in a kidney transplant. Images provided by David A. Hatch, MD, copyright 1998, used with permission.
Nuclear renograms of kidney transplantations. (A) Normal perfusion. Note that the isotope is observed in the aorta, iliac vessels, and the kidney in the first image (0-5 s). (B) Normal tubular function and drainage. Note that the isotope is rapidly excreted and drained. The highest concentration of isotope (darkest image) is observed in the first image (0-3 min). (C) Delayed perfusion in a patient with acute rejection. Note that the isotope is observed in the aorta and iliac vessels in the first frame (0-5 s), but the kidney first shows uptake of the isotope in the second frame (6-10 s). (D) Decreased tubular function in a cadaver kidney transplant with acute tubular necrosis. Image provided by David A. Hatch, MD, copyright 2001, used with permission.
Digital subtraction angiogram showing renal artery stenosis. Image provided by David A. Hatch, MD, copyright 1998, used with permission.
Histology of percutaneous kidney transplantation biopsy. (A) Normal kidney. (B) Acute rejection. Note the infiltration of lymphocytes. Images provided by David A. Hatch, MD, copyright 1999, used with permission.
Kidney transplantation survival in North American children. Data from US Renal Data Systems, 2008.
Etiology of kidney transplant loss in children. Data from US Renal Data Systems, 2008.
Pediatric patient survival following kidney transplantation. Data from US Renal Data Systems, 2008.
Cause of death among pediatric recipients of kidney transplantation. Data from US Renal Data System, 2008.
Donor source of kidneys transplanted into children. Data from North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) annual report, 2007.
Probability of first rejection at 12 months following transplantation. Data from North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) annual report, 2007.