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Centralization of histocompatibility laboratories: impact on organ allocation efficiency and outcomes of cadaveric renal transplantation.

This project was undertaken to determine whether centralization of histocompatibility laboratory services for renal transplants performed within eastern Pennsylvania could improve the efficiency of allograft allocation and short-term allograft function. A nonconcurrent cohort study was performed comparing renal allografts transplanted between September 15, 1993, and September 14, 1994, to those transplanted between September 15, 1994, and September 14, 1995. All allografts were procured and allocated by the Delaware Valley Transplant Program, the organ procurement agency in eastern Pennsylvania. Cold preservation time and delayed allograft function were used to measure efficiency of allograft allocation and short term allograft function, respectively. The mean cold preservation time was reduced from 25.08 hours to 20.68 hours (P < 0.001). The percentage of delayed allograft function was 19.9 and 17.4 for the pre- and postcentralization groups, respectively (P = 0.5). Therefore, centralization of histocompatibility tissue typing was a regionally effective process intervention for reducing cold preservation time without adversely impacting short-term graft function. The magnitude of this reduction varied between individual centers. Further investigation is required to determine the effect on long-term allograft function and system wide costs.

Adult↗

Immunogenicity of decellularized cryopreserved allografts in pediatric cardiac surgery: comparison with standard cryopreserved allografts.

BACKGROUND: Recognition of the immunogenicity of standard cryopreserved allografts has led to the development of new decellularized allografts (CryoValve SG; CryoLife, Inc, Kennesaw, Ga). This preliminary study examined the HLA antibody response to these decellularized allografts and compared it with the response to standard allograft material. METHODS: We prospectively measured the frequency of panel-reactive HLA class I (HLA-A, HLA-B, and HLA-C) and class II (HLA-DR/DQ) alloantibodies in 14 children (age 8.5 +/- 7.9 years) receiving decellularized, cryopreserved allografts, including 6 undergoing allograft patch insertion and 8 with a valved pulmonary allograft. We compared them with 20 historical control subjects (age 1.7 +/- 2.4 years) undergoing implantation of standard cryopreserved allografts, 8 with valves and 12 with allograft patch. All patients had panel-reactive antibody levels measured before and at 1, 3, and 12 months after the operation. HLA class I and class II panel-reactive antibody levels were determined with a sensitive flow cytometry technique. RESULTS: We found panel-reactive antibody levels in decellularized allografts to be elevated slightly from preoperative levels for both class I and class II antibodies at 1, 3, and 12 months (P >.05). The panel-reactive antibody level for both class I and class II antibodies were significantly lower for decellularized allografts as compared to standard allografts. Functionally, the allografts were similar with decellularized valved grafts showing a peak echo-determined systolic gradient of 13 +/- 15 mm Hg at 8 +/- 2.6 months postoperatively as compared to a gradient of 24 +/- 18 mm Hg measured 12 +/- 6 months postoperatively in standard allografts (P =.11). CONCLUSIONS: Decellularized grafts elicited significantly lower levels of class I and class II HLA antibody formation at 1, 3, and 12 months after implantation than did standard cryopreserved allografts. Early hemodynamic function of decellularized grafts was similar to that of standard cryopreserved allograft valves. Further experience is necessary to determine whether the reduced immunogenicity of decellularized allografts will truly allow tissue ingrowth and improved long-term durability in patients.

Adolescent↗

Evidence for a limited contribution of immune regulation to cardiac allograft acceptance.

We have used donor-reactive DTH responses to study the immune regulation that is displayed by C57BL/6 mice after they accept DBA/2 cardiac or renal allografts. This regulation is expressed by splenocytes from the allograft acceptors, and involves their alloantigen-induced production of the anti-inflammatory cytokines transforming growth factor beta (TGFbeta) and/or interleukin-10 (IL-10) at DTH challenge sites, and presumably within accepted allografts. In cardiac allograft acceptors the production of these cytokines depends on a population of CD25(+) splenocytes. During these studies, we have encountered several situations in which allograft acceptance does not correlate with DTH-detectable immune regulation: (1) splenocytes from cardiac or kidney allograft acceptors lose TGFbeta-mediated inhibition of donor-reactive DTH responses by 150 days post-transplant, although they retain ongoing allograft function; (2) cardiac allograft acceptors rapidly reject donor-matched skin allografts, retain good cardiac allograft function, but lose DTH-detectable immune regulation; (3) Balb/c mice accept C57BL/6 cardiac allografts when treated with anti-CD40L mAb (MR1), but fail to express DTH-detectable immune regulation; and (4) infusion of C57BL/6 mice with peritoneal exudate cells (PEC) that were educated ex vivo to DBA/2 alloantigens in the presence of IL-10 and TGFbeta, causes them to exhibit DTH-detectable immune regulation mediated by both TGFbeta and IL-10, but they fail to accept DBA/2 cardiac allografts. These observations suggest that the process of allograft acceptance, as it is studied in murine transplant models, is metastable, and does not necessarily reflect the achievement of allograft tolerance. Further, the development of allograft tolerance probably requires more than regulatory T cells, representing a coordinated evolution of multiple immune processes over a prolonged period of time.

Animals↗

Hypertension after renal transplantation in children.

Hypertension persisted for longer than 6 mo or developed de novo after the first month following transplantation in seven of 77 pediatric recipients of renal allografts; concomitantly there were an elevation of PRA and renal angiographic abnormalities. In two of the four patients who developed RAS there was evidence of diminished allograft function. Successful correction of the stenotic lesion in these two recipients resulted in a return of the blood pressure, PRA, and biochemical function of the allograft to normal. Unsuccessful attempts at surgical repair led to loss of the allograft in the other two patients with RAS. Intrarenal vascular and/or parenchymal lesions were evident in the other three recipients with hypertension. Although an explanation was not apparent, subclinical rejection was hypothesized. Treatment effected reduction of the hypertension in these three patients and no deterioration of allograft function was observed for periods of 5, 34, and 38 mo, respectively. Renal angiographic studies and determinations of PRA are recommended in any pediatric recipient of an allograft who develops hypertension after the first month following transplantation or has hypertension which persists for longer than 6 mo after transplantation.

Acute Disease↗

Terminal loop cutaneous ureterostomy in renal transplantation: an under utilized urinary diversion technique.

PURPOSE: We evaluated the effectiveness of terminal loop cutaneous ureterostomy as a means of urinary drainage in kidney transplant recipients during a 20-year period. MATERIALS AND METHODS: Five cadaveric and 2 living related patients underwent kidney transplantation with terminal loop cutaneous ureterostomy between 1984 and 2004. These patients had no usable bladder or they were not suitable candidates for intermittent catheterization. RESULTS: Followup was 20 months to 17 years. One patient underwent stomal revision 5 months after renal transplantation. Current serum creatinine 4 years later was 166 mumol/l. The remaining 6 patients had no evidence of ureteral obstruction and rarely had bacteriuria or urinary tract infections. Four patients had a functioning allograft with normal serum creatinine. One patient died with a normally functioning allograft and the remaining patient lost his graft due to chronic rejection. No patient in this series lost the graft due to a urological cause. Overall outcomes included excellent allograft function with minimal infection or stomal stenotic complications. CONCLUSIONS: Terminal loop cutaneous ureterostomy is a simple, safe and alternative means of urinary diversion in patients with renal transplant and a defunctionalized lower urinary tract.

Adult↗

Peritoneal dialysis catheter infections in children after renal transplantation: choosing the time of removal.

As a foreign body, the peritoneal dialysis (PD) catheter represents a potential source of infection, particularly for immunosuppressed renal transplant patients. A retrospective study was therefore undertaken to compare the risks and benefits of our policy of removing PD catheters at 3 months following renal transplant, which was established to allow for early re-initiation of dialysis. Between 1984 and 1990, 43 renal transplants were performed in 35 children who had been receiving maintenance PD. During the 1st month post transplantation, the PD catheter was used in 25 patients (58%) because of acute rejection or primary allograft non-function. Thirty-one patients were eventually discharged with functioning allografts and a PD catheter in place. Of them, 43% developed a catheter-related infection within the next 2 months, a period during which PD was not performed. Potential contributing factors included a history of catheter-related infection prior to transplantation, use of high-dose methylprednisolone to treat acute rejection, and the type of maintenance immunosuppression prescribed; conversely, the use of prophylactic antibiotics appeared to decrease this risk. This study established the potential need for the catheter during the first few weeks, but because of the infection risk of 43% by 3 months post transplantation, our protocol was revised to include catheter removal at the time of hospital discharge. From 1990 until the end of 1992, an additional 19 PD recipients underwent transplantation. In this group, catheters were used during the 1st month in 6 children (32%). Fifteen patients were discharged with a functioning allograft and only 1 patient returned to PD at 12 months post transplant. It is concluded that PD catheters represent an additional source of infection following transplantation and should be removed at the time of hospital discharge, after which the likelihood of use is low.

Anti-Infective Agents↗

Effects of candesartan and perindopril on renal function, TGF-beta1 plasma levels and excretion of prostaglandins in stable renal allograft recipients.

AIMS: Although on account of their nephroprotective effects, ACE inhibitors and angiotensin receptor antagonists appear to be advantageous for patients after renal transplantation, their use in these patients has been limited up to now. This is in part due to the risk of inducing a decrease in the glomerular filtration pressure gradient with subsequent impairment of allograft function. The aim of the present study was to investigate the effects of ACE inhibitors and angiotensin receptor antagonists on renal function, excretion of prostaglandins as a parameter of glomerular hemodynamics and TGF-beta1 plasma levels during an 8-week withdrawal phase in pretreated patients. PATIENTS AND METHODS: Sixteen patients with stable long-term allograft function undergoing therapy with candesartan (group 1) and 16 patients with stable long-term allograft function undergoing therapy with perindopril (group 2) were included in the study. Any signs of chronic allograft dysfunction were defined as exclusion criteria. Renal function, albuminuria, TGF-beta1 plasma levels as well as the excretion of thromboxane B2 and 6-keto-prostaglandin-F-1alpha were monitored during an 8-week withdrawal phase of the angiotensin receptor antagonist or ACE inhibitor, respectively. Normotension was maintained throughout the study period through adjustment of other anti-hypertensive drugs. RESULTS: Creatinine clearance as well as TGF-beta1 plasma levels and the excretion of prostaglandins remained unchanged after discontinuation of candesartan or perindopril. However, after withdrawal of the substances a significant increase in albuminuria was noted in both patient groups throughout the observation period. After 8 weeks, median albuminuria had increased by 63% in group 1 and by 163% in group 2. CONCLUSIONS: We were able to demonstrate that the use of ACE inhibitors and angiotensin receptor antagonists in patients after renal transplantation is safe. Favorable effects of both substances on albuminuria were detectable in patients who showed no signs of chronic allograft dysfunction according to the usual criteria. Therefore, a nephroprotective effect of candesartan as well as of perindopril, is highly probable in patients after renal transplantation. Further investigations regarding routine use in these patients are therefore mandatory.

Adult↗

Distinguishing the causes of post-transplantation hypertension.

The purpose of this article is to elucidate the causes of hypertension following kidney transplantation. In the months and years that follow their operation, most recipients of renal transplants develop or maintain blood pressures that are high. This complication has become more prominent since the widespread use of cyclosporine for immunosuppression. Children seem especially prone to hypertension after kidney transplantation. Absence of hypertension is a favorable long-term prognostic sign. It's presence suggests that allograft function is impaired. Impaired allograft function may be due to either lesions intrinsic to the allograft, or lesions that are extrinsic to the allograft but alter its function. Many transplant patients have more than one possible explanation for hypertension. This multifactorial nature of hypertension after transplantation complicates the management of patients.

Cyclosporins↗

Morbidity and mortality of cardiac surgery following renal transplantation.

BACKGROUND: With improved survival following renal transplantation, the number of patients undergoing cardiac surgery has increased. The purpose of this study was to review the morbidity, mortality, and allograft function in renal transplant patients undergoing major cardiac surgery. METHODS: Retrospective database review of consecutive renal transplant patients undergoing cardiac surgery from 1987 to 2002. Patients requiring dialysis (D) before cardiac surgery versus those with stable renal transplants (ND) were compared. RESULTS: Cardiac surgery was performed in 46 patients during the study period. Twenty patients (42%) required dialysis (D) before surgery while 26 (58%) had stable allograft function (ND). Among patients who had stable allograft function prior to surgery, there was no allograft loss. In the ND group, preoperative and discharge creatinine levels were 2.17 +/- 1.0 and 2.4 +/- 1.5 mg/dL, respectively. All operative deaths occurred in the dialysis dependent group. The 30-day and 3-year survival, respectively was 80% and 20% in the D group compared to 100% and 69% amongst the ND group (p </= 0.01). Infectious complications consisted of pneumonia and sepsis each in 8.5% and of deep sternal wound infection in 4.3% of the entire group. CONCLUSIONS: (1) Morbidity and mortality of cardiac surgery in renal transplant patients with stable allograft function is low and stable allograft function can be maintained without allograft loss. (2) Mortality following cardiac surgery is significantly higher among renal transplant patients who become dialysis dependent and intermediate-term survival is poor.

Cardiac Surgical Procedures↗

Renal allograft compartment syndrome: an underappreciated postoperative complication.

PURPOSE: Renal allograft compartment syndrome (RACS) is early graft dysfunction secondary to retroperitoneal hypertension and resultant ischemia. Our purpose was to identify the incidence, therapies and outcomes of patients with RACS. METHODS: All patients who underwent a renal transplant between 2000 and 2005 were reviewed. Patients with signs of acute allograft dysfunction were identified. RACS was diagnosed via visual allograft hypoperfusion and/or with preoperative Doppler ultrasound. RESULTS: Among 458 patients, 11 (2%) were diagnosed with RACS. Characteristics between patient groups were similar. Five (45%) patients displayed adequate initial allograft function after transplantation. Doppler ultrasound was diagnostic. Six (55%) patients displayed poor initial allograft function and were classified as early presenters of RACS. Allograft function improved dramatically upon decompression. CONCLUSIONS: Clinicians must remain aware of RACS as a potential diagnosis when patients display rapid deterioration in kidney performance after good initial allograft function. Doppler ultrasound is useful in diagnosing late presenters.

Adolescent↗

Effects of oral phosphorus supplementation on mineral metabolism of renal transplant recipients.

BACKGROUND: Persistent hyperparathyroidism (HPT) is frequently observed in kidney transplant recipients. Hypophosphataemia is a common biochemical consequence of HPT. Theoretically, oral phosphorus administration may induce negative effects on the control of HPT, though this point has never been demonstrated in kidney-transplant recipients. This study was designed to evaluate the effects of oral phosphorus supplementation on the mineral metabolism of successful kidney transplant recipients. METHODS: Thirty-two kidney transplant recipients with serum creatinine < 2 mg/dl and serum phosphate levels <3.5 mg/dl were included in the study. After a washout period in which oral phosphorus supplementation was discontinued, the following parameters were determined (F0 period): serum calcium, phosphate, alkaline phosphatase, uric acid, bicarbonate, PTH, 1,25-dihydroxyvitamin D3 (1,25 (OH)(2)D) and 25-hydroxyvitamin D3 (25OHD). Creatinine clearance, calcium, and phosphate excretion were determined from a 24-h urine sample. The same determinations were repeated (F1 period) after all patients received 1.5 g of oral phosphorus for 15 days. For data analysis, patients were divided into two subgroups (optimal and suboptimal) according to allograft function (Ccr>or < 70 ml/min/1.73 m2). RESULTS: In the F0 period, only nine of 32 patients had PTH levels within the normal range (<65 pg/ml). The mean concentrations of PTH, 1,25(OH)(2)D and 25OHD were 132+/-97pg/ml, 40.5+16pg/ml and 12.5+/-8.2 ng/ml respectively. Phosphorus supplementation led to significant reductions in serum calcium and 1,25(OH)(2)D concentrations, as well as in urinary calcium excretion in the whole group. On the contrary, serum phosphate, PTH, and urinary phosphate excretion increased significantly. The percentage increase in PTH concentrations after phosphorus supplementation were similar in patients with optimal and suboptimal allograft function (33 vs 36%). The reduction of 1,25 (OH)(2)D concentrations after phosphorus supplementation was observed mainly in the subgroup with optimal allograft function (21% reduction with respect to baseline values), while the mean 1,25(OH)(2)D concentrations in patients with suboptimal allograft function scarcely changed (1.4% increase). Changes in 1,25(OH)(2)D concentrations after phosphorus supplementation, expressed as a percentage of the initial concentrations, correlated positively with the percentage changes in PTH concentrations for the whole group, as well as for each subgroup. The best determinants for the percentage and the absolute increase in PTH concentration after phosphorus supplementation was the final serum phosphate concentration (F=4.84, r=0.37, P=0.035) and the increase in serum phosphate (F=7.69, r=0.45, P= 0.009) respectively. CONCLUSIONS: Oral phosphorus supplementation led to a significant increase in the PTH concentration of kidney transplant recipients. The mean 1,25(OH)(2)D concentration decreased mainly in recipients with optimal allograft function. The counterbalance effect of PTH on 1,25(OH)(2)D production may account for the relative preservation of 1,25(OH)2D levels in recipients with suboptimal allograft function.

Administration, Oral↗

Peripheral blood microchimerism in human liver and renal transplant recipients: rejection despite donor-specific chimerism.

BACKGROUND: Development of donor-specific microchimerism (DSM) has been proposed as one of the possible mechanisms for induction and maintenance of allograft tolerance. The aim of this study was to determine: (1) the state of DSM in liver transplant (LTx) and renal transplant (RTx) recipients, (2) whether the persistent presence of an allograft is a requirement for maintenance of chimerism, and (3) whether donor-specific blood transfusions (DST) facilitate chimerism development in RTx recipients and whether this correlates with allograft function. METHODS: Qualitative and quantitative analysis of DSM in peripheral blood of LTx and RTx recipients was assessed by polymerase chain reaction and competitive polymerase chain reaction using HLA-DR probes for mismatched antigens between the donor and recipient. RESULTS: LTx recipients (11 of 12) who had or were having rejection were positive for DSM in circulation compared with 4 of 11 with normal allograft function (P<0.01). The number of donor cells did not correlate with allograft function. LTx recipients (4 of 4) who lost their first allograft and underwent retransplantation retained DSM for the first donors. RTx recipients who received DST (8 of 8) were positive for DSM compared with 6 of 12 of nontransfused recipients (P<0.045). CONCLUSIONS: The results suggest that LTx and RTx recipients undergo rejection despite DSM. The development of DSM may not be a prerequisite for normal allograft function. Once DSM is established, the presence of the allograft is not required for maintenance of chimerism. DST facilitated the development of DSM in RTx recipients. Direct correlation was not observed between the development of DSM and allograft function in either DST or nontransfused RTx recipients.

Alleles↗

Determination of blood flow to the transplanted kidney. A novel application of phase-contrast, cine magnetic resonance imaging.

There is at present no noninvasive method that reliably measures blood flow in the poorly functioning renal allograft. The present study was designed to evaluate phase-contrast cine magnetic resonance imaging (PC-cine-MRI) for this purpose. We recruited for study 18 patients who had received kidney transplants 13-66 months earlier from closely related living donors. As judged by the glomerular filtration rate, which was elevated for a single kidney (76 +/- 4 ml/min 1.73 m2), allograft function was excellent, permitting the assumption of unimpaired renal extraction of paminohippuric acid (PAH). Allograft blood flow was determined consecutively on the same day, first by the standard PAH clearance technique and they by the product of the velocity of protons and renal vein cross-sectional area using PC-cine-MRI. MRI determinations could not be completed because of claustrophobia in two patients and failure to image the terminus of the allograft vein another two. Comparison of blood flow in the remaining 14 subjects revealed the two techniques to be strongly related (r = 0.91, P < 0.001). On the average, the renal blood flow rate was similar by each method; 732 +/- 62 by PAH clearance and 703 +/- 69 ml/min by PC-cine-MRI, but the agreement among individuals between the two methods was only modest, with a 95% confidence interval of agreement from -214 to +254 ml/min. We conclude that PC-cine-MRI provides a fairly accurate and noninvasive method for determining the rate of blood flow in the transplanted kidney. With further refinement it should permit the role of depressed blood flow in a variety of acute and chronic forms of human allograft dysfunction to be elucidated in humans for the first time.

Glomerular Filtration Rate↗

Causes of late renal allograft loss: chronic allograft dysfunction, death, and other factors.

CAN and patient death with allograft function are the 2 major causes of renal allograft loss after the first year, accounting for 80% or more of cases. According to current estimates from the United Network for Organ Sharing (UNOS), the half-lives for renal allografts performed in 1995 and 1996 from living and cadaveric donors are 15.3 and 10.4 years, respectively (2). Consequently, much attention has been focused on better understanding the causes of CAN and patient death with a functioning allograft in an attempt to improve long-term renal allograft outcomes. Although the pathogenesis of CAN is not completely understood, we know that CAN involves alloantigen-dependent and alloantigen-independent factors that combine to produce chronic deterioration of renal allograft function. CVD is the most frequent cause of death in renal transplant recipients, and we need to address its well-established risk factors in that population. Among other improvements, changes in current immunosuppressive protocols may increase long-term renal allograft survival and function by decreasing both the risk of CAN and the risk of CVD.

Chronic Disease↗

The influence of warm and cold ischemic time on the outcome of cadaveric renal transplantation.

The influence of warm and cold ischemic time (WIT and CIT) on renal allograft function and allograft survival rates was analyzed from the Eurotransplant data. From 1977 through 1980 renal allograft recipients were divided into three groups, according to the length of the WIT of their graft: group I, 0-10 min (n = 2,636); group II, 11-20 min (n = 108); group III, 21-35 min (n = 17). Differences in graft function or graft survival have not been observed between these groups. It is concluded that donor kidneys with a WIT up to 20 min are acceptable for transplantation. The transplantation results in group III suggest that 35 min is a safe limit for acceptance, but the small number of transplantations in this group does not justify a firm conclusion. A combined analysis of warm and cold ischemia shows that simple cold storage up to 50 h is safe and acceptable, provided that warm ischemia is kept minimal (less than 10 min). It seems advisable to keep hypothermic preservation within the limit of 30 h, when WIT exceeds 10 min.

Cold Temperature↗

Nephron mass modulates the hemodynamic, cellular, and molecular response of the rat renal allograft.

Functioning nephron mass has recently been implicated as a risk factor for development of chronic "rejection" of kidney allografts. Reductions in nephron number below 50% may induce glomerular hypertension and hyperfiltration in surviving units, which in turn lead to graft injury. In the present study, which extends and amplifies our previous investigations, cellular and molecular characteristics of single allografts from F344 donors in bilaterally nephrectomized LEW recipients, our standard experimental model of chronic renal allograft dysfunction, were compared with allografts from recipients where total renal mass was reduced (by ligating branches of the graft renal artery) or restored to normal levels by transplanting or retaining a second kidney. Our findings in this study confirm that progressive proteinuria and structural injury in recipients of single allografts were accentuated in grafts with reduced mass but virtually absent in rats with increased kidney mass. A striking observation was that patterns of cell surface molecule expression, cellular infiltration, and expression of all T cell- and macrophage-associated products studied were all markedly modulated by changes in renal mass. Moreover, several molecules that are up-regulated before evidence of graft injury are down-regulated by providing increased renal mass. These data show that the quantity of functioning renal mass is not only an important independent determinant of the tempo and intensity of chronic renal allograft failure, but also a potent modulator of fundamental cellular and molecular components of a complex process. This phenomenon involves antigen-dependent and antigen-independent elements that ultimately result in chronic allograft failure.

Animals↗

Characteristics of long-term live-donor pediatric renal transplant survivors: a single-center experience.

OBJECTIVES: To study the characteristics and the predictors of survival observed in our pediatric live-donor renal transplant recipients with an allograft that functioned for more than 10 yr. METHODS: One hundred fifteen children underwent renal transplantation between 1976 and 1995. Of these, 30 had functioning allografts for more than 10 yr (range, 11-18). The patients included 18 males and 12 females, with a mean age at transplantation of 13 yr (range, 5-18). Characteristics of the patients, data on graft survival, and determinants of outcome were obtained by reviewing all medical charts. RESULTS: At most recent follow-up (January 2005), the mean daily dose of azathioprine was 1.2 mg/kg (range, 1-2) and that of prednisone was 0.16 mg/kg (range, 0.1-0.2). Mean creatinine clearance was 72 mL/min per 1.73 m(2) (range, 45-112). Acute rejection occurred in 14 (47%) patients. Seven patients had one episode, five had two episodes, and two had three episodes of acute rejection. Three patients (10%) developed malignancy. A substantial proportion of patients (44%) were short, with a height standard deviation score (SDS) less than -1.88, which is below the third percentile for age and gender. One quarter of the patients, more commonly the females, were obese. Other complications included osteoporosis in 16 (53%) patients, avascular bone necrosis in four (13%), post-transplantation diabetes mellitus in three (10%), and hypertension in 18 (60%). Twelve (40%) patients were married and 27% had children post-transplantation. The independent determinants of long-term graft survival were acute rejection and post-transplant hypertension. CONCLUSION: Despite good renal function, long-term pediatric renal transplant survivors are at risk of significant morbidity. The determinants of long-term graft survival are acute rejection and post-transplant hypertension.

Adolescent↗

Simultaneous cadaver renal and pancreas transplantation in type I diabetes.

Between February 1985 and April 1986, we performed 11 simultaneous cadaver kidney and segmental pancreatic transplants in patients with type I diabetes. There were nine men and two women ranging in age from 25 to 47 years (mean, 38.5 years). All pancreatic grafts were extraperitoneal, and the pancreatic duct was managed by pancreaticocystostomy utilizing an internal stent. Three patients died from two to six weeks postoperatively of septic complications. Four pancreatic grafts were functioning at 2, 5, 11, and 14 months after operation, and eight patients had had functioning renal allografts from two to 14 months (mean, 6.8 months) with a mean serum creatinine level of 2.4 mg/dL (210 mumol/L). Graft failure occurred in the other four patients from vascular thrombosis (three patients) or hemorrhagic pancreatitis (one patient). Significant morbidity included an infected arterial anastomosis (two patients), pancreatic fistulas (four patients), and bladder leak (four patients). In conclusion, this procedure is an effective option for selective diabetics with end-stage renal disease. Although technical complications were frequent, no adverse effect on renal allograft function was evident. With technical refinements, this procedure should be applicable to most type I diabetics with renal failure.

Adult↗