Spontaneous kidney allograft rupture

Spontaneous renal allograft rupture is one of the most dangerous complications of kidney transplantation, which can result in graft loss. This condition needs immediate surgical intervention. Conservative management has dismal results. Its prevalence varies from 0.3% to 3%. Rupture occurs in first few weeks after transplantation. Predisposing factors for graft rupture are acute rejection, acute tubular necrosis, and renal vein thrombosis. There are growing reports about successful results of repairing these ruptured kidneys. In this study, we reviewed the medical records of 1682 patients who received kidney allografts from living donors from 1986 through 2003. There were six (0.35%) cases of renal allograft rupture. All were preceded by acute graft rejection. They were treated with antirejection medications. In first three cases, the kidney allografts were removed because the procedure of choice in this situation is graft nephrectomy; but in three next cases we repaired the ruptured grafts with good results in two of them. In conclusion, the procedure of choice for kidney allograft rupture is graft repair.     

Renal allograft rupture caused by acute tubular necrosis

Renal allograft rupture is a rare but potentially lethal complication of kidney transplantation. A renal allograft recipient receiving quadruple immunosuppressive therapy developed a spontaneous allograft rupture 13 days after kidney transplantation. Warm ischaemia time during the transplant was 80 minutes. The ruptured kidney graft could not be salvaged because of the patient's haemodynamic instability. The histopathological examination showed interstitial oedema with severe acute tubular necrosis with no signs of acute rejection. The most common causes of renal graft rupture are acute rejection and vein thrombosis, while acute tubular necrosis may only rarely be responsible for this complication. Renal graft rupture may be the result of interstitial damage attributed both to the prolonged warm ischaemia time during the transplant and to post-transplant acute tubular necrosis in the absence of graft rejection. In those patients whose haemodynamic status cannot be stabilized by appropriate aggressive haemodynamic support therapy, graft nephrectomy should be considered the only definitive treatment.     

Surgical repair of spontaneous renal allograft rupture: a new procedure

Background: The purpose of the present paper is to introduce a new surgical procedure using the external oblique aponeurosis (EOA) for repair of spontaneous renal allograft rupture. Methods: Thirty‐eight cases with spontaneous renal allograft rupture were encountered in 1000 consecutive kidney transplants between April 1991 and August 2000. Thirty‐three cases underwent surgical exploration with two grafts undergoing nephrectomy, while a further 31 were repaired using the new surgical procedure. The external oblique aponeurosis (EOA) from the incision was trimmed into 1 cm × 1 cm square pieces. A 2/0 Dexon suture was placed through each piece of the EOA, then through the parenchyma of the kidney perpendicular to the rupture. Each suture was then placed through another piece of EOA and tied. Results: Two repaired grafts were removed on day 7 and day 10, one due to graft re‐rupture and another with ischaemia secondary to irreversible acute rejection. The graft function of 29 cases had recovered completely at 30 days following surgical repair with one graft improving rapidly. Thirteen grafts were diagnosed as undergoing mild to moderate acute rejection, whereas a further 20 cases were considered to have acute tubular necrosis on histopathology. The allograft survival rate at 1 year and 5 years post grafting was 86% and 64%, respectively. No patients died from postoperative complications following repair using this procedure. Conclusions: Spontaneous renal allograft rupture is a relatively common post‐transplant complication secondary to either acute tubular necrosis or acute rejection. This new surgical procedure is proposed as a reliable and practical method of repair following graft rupture. Preservation of graft function and viability following rupture appears achievable both in the medium and long‐term.     

Renal allograft rupture: diagnostic role of ultrasound.

To evaluate the diagnostic role of ultrasound in spontaneous renal allograft rupture we reviewed 18 cases observed in our centre in 10 years. Ultrasound studies were performed immediately before surgery in 15 cases. Renal allograft rupture occurred during the first 3 weeks after transplantation in 17 cases (94%). Clinical findings were consistent with previous reports. The diagnosis was confirmed by surgical exploration in 17 cases, and by necropsy in the remaining one. Nine patients were treated by corsetage and eight by graft nephrectomy, while one patient died before surgery. Acute rejection was present in nine cases, and severe acute tubular necrosis in five; no renal tissue was available for histological study in four patients. On ultrasound examination, perirenal haematoma was the most frequent finding, while subcapsular/intrarenal haematoma or findings suggesting rejection or urinary tract obstruction were less frequently observed. In six cases, disruption of the white linear echoes of the capsule of the graft could be seen; this finding has not been described previously. Ultrasound has a definite role in presurgical evaluation of suspected renal transplant rupture.     

Conservative surgery of spontaneous rupture of renal grafts]

17 cases of spontaneous rupture of renal allografts were noted after 285 renal transplantations performed during the years 1967-1978. All ruptures occurred within the first two weeks after transplantation. Acute rejection, combined with hypertension, dialysis and/or anticoagulation seem to be the main etiological factors of graft rupture. Due to severe hemorrhage surgical exploration had to be performed in 15 patients. While removal of the graft was necessary in 4 patients the kidney could be preserved by tamponade and suture in 11 patients. 5 patients later lost their graft, due to chronic rejection, while 8 patients (6 of the 15 patients who needed surgical exploration) currently have satisfactory graft function.     

Higher graft salvage rate in renal allograft rupture associated with acute tubular necrosis

BACKGROUND: Renal allograft rupture is an early postoperative complication threatening graft and patient survival. We reviewed the etiology and prognostic factors for renal allograft rupture. MATERIAL AND METHODS: Among 657 renal transplants performed between 1990 and 2001, renal allograft rupture was diagnosed in 10 cases. Statistical analysis by Student t test, ANOVA, and chi-square was performed to assess donor and recipient characteristics. Multivariate logistic regression to predict renal allograft rupture used variables with P <.15 in the univariate analysis. RESULTS: Patients with renal allograft rupture were mainly men and young. Renal allograft rupture incidence was higher among allografts from non-heart-beating donors, kidneys with delayed graft function, or patients with a high antibody titer. Histopathological findings revealed that six renal allograft ruptures were secondary to acute rejection, three to acute tubular rejection and one to allograft infarction. Only one of six renal allograft ruptures (17.7%) secondary to rejection was resolved by surgery; two of the three patients (66.7%) with acute tubular necrosis were successfully operated and a nephrectomy was performed for the patient with allograft infarction. By multivariate logistic regression analysis, factors shown to be predictive for renal allograft rupture were: delayed graft function, age of recipient, peak panel-reactive antibody >25%, and initial immunosuppressive treatment without antithymocyte globulin. CONCLUSIONS: Higher graft salvage rates are possible in cases of graft rupture associated with acute tubular necrosis.     

Late spontaneous kidney graft decapsulation after administration of sirolimus in a recipient with chronic hepatitis B and C infection: a case report

Late spontaneous kidney graft decapsulation with fluid collection is a rare condition with only a few cases reported in the literature. Common causes of renal allograft rupture include acute rejection, acute tubular necrosis, renal vein thrombosis, and trauma. Sirolimus related late spontaneous decapsulation has not been reported in the past. Interestingly, sirolimus may promote lymphocele formation in renal transplant recipients, including those presenting with chronic hepatitis B or C. Herein, we report a case of late spontaneous decapsulation with subcapsular hematoma formation developing 12 years after receipt of a cadaveric allograft. The patient was infected with both hepatitis B and C viruses. Cyclosporine was replaced by sirolimus for maintenance therapy because of chronic rejection and acute deterioration of renal function. He presented to the hospital at 9 months after sirolimus inception because of a sudden onset of pain and swelling over the kidney graft. Magnetic resonance imaging found the capsule to be stripped from the kidney by a collection of liquefied hematomas. A laparoscopic fenestration was performed by creation of a peritoneal window adjacent to the renal allograft. When patients have chronic hepatitis, tacrolimus might be a better choice than sirolimus.     

Liver-kidney recipients with chronic viral hepatitis C treated with interferon-alpha

Antiviral therapy with interferon-alpha (IFN-alpha) and pegylated IFN-alpha (PEG-IFN-alpha) for chronic hepatitis C (HCV)-infected kidney recipients remains controversial. IFN-alpha is not recommended in most cases because it induces severe acute graft rejection. However, IFN-alpha, as PEG-IFN-alpha, is associated with a more pronounced immune response, and is well tolerated in HCV-infected liver recipients without causing graft rejection. In combined liver-kidney transplant (LKT) recipients, IFN-alpha has been occasionally used and appears to be well tolerated. All LKT recipients with a functioning kidney and liver having a HCV replication and who needed IFN-alpha therapy have been included in the study. The occurrence of liver and/or renal acute rejection as well as the HCV replication has been collected. A total of 12 LKT patients treated with PEG-IFN-alpha plus ribavirin have been studied. No acute rejection was observed. Renal function remained stable during and after discontinuing treatment, without any graft dysfunction. Two patients had a partial viral response and four had a sustained viral response. All patients, whatever their viral response, had decreased liver-enzyme levels. Response to PEG-IFN-alpha therapy was correlated with steroid dose and transaminase level when PEG-IFN-alpha was started. These data suggest that the combination therapy of PEG-IFN-alpha plus ribavirin did not have a higher risk of acute kidney-graft rejection after liver-kidney transplantation.     

Successful retransplantation of the human heart.

Cardiac retransplantation has been performed in five patients at Stanford University Medical Center. Long-term survival and rehabilitation have been achieved in two cases. In the first case retransplantation was performed 57 days after the initial procedure because of persistent acute graft rejection. The second patient underwent retransplantation 27 months postoperatively because of documented accelerated graft atherosclerosis. The major indications for cardiac retransplantation consist of intractable acute rejection and late postoperative graft atherosclerosis. These complications should prompt consideration of cardiac retransplantation in carefully selected cases.     

Ruptured human renal allograft. Pathogenesis and management.

From January, 1963, to January, 1977, 4 cases of acute allograft rupture occurred in 474 renal transplants performed at the Cleveland Clinic, an incidence of 0.8 per cent. Rupture developed between the fifth and sixteenth day after transplantation during a period when the patients required dialysis because of poor allograft function. All patients had surgical exploration and successful repair of the laceration. Biopsies in each case at the site of laceration revealed findings consistent with acute allograft rejection. The rejections were mild in 2 cases, moderate in one, and severe in another. Two kidneys failed to sustain function, and the patients were returned to chronic hemodialysis two to five months later. None required a nephrectomy. The other two kidneys are functioning well, with serum creatinine values of 1.3 and 1.5 mg./100 ml. one year after allograft rupture. Since rupture of a renal allograft does not appear to increase the intensity of rejection nor does it represent a severe type of rejection, transplant nephrectomy can be avoided unless hemorrhage is uncontrollable from the site of laceration.     

Renal allograft rupture and its management

Renal allograft rupture, although a rare complication, was encountered in 11 of our 137 cases of live kidney donor transplants. The commonest finding was an associated acute rejection. Our cases were mainly given conservative treatment with repair of the rupture and antirejection therapy. Eight of our kidneys were saved in this way, thus eight of the 11 patients survived. None of the deaths were related to the graft rupture or its effects.     

Nontraumatic rupture of renal allografts.

Eight cases of nontraumatic renal allograft rupture were identified in 237 renal transplants performed at UCLA Medical Center. Careful clinicopathologic studies in these patients suggest three principal underlying causes: major graft vessel occlusion, hyperacute or accelerated rejection, and acute rejection. The clinical and pathologic features of these various categories are compared and contrasted.     

Living donor liver transplantation for fulminant hepatic failure

BACKGROUND: Living donor liver transplantation (LDLT) was originally indicated only for elective cases of pediatric patients with end-stage liver disease. In Japan, however, where liver transplantation from brain-dead donor is performed very rarely, this indication has been expanded to emergency cases such as fulminant hepatic failure (FHF). METHODS: Thirty-eight patients with FHF were treated between May 1992 and April 1999. Causes of acute liver failure were non-A, non-B hepatitis in 27 patients, hepatitis B virus in seven, and hepatitis A virus, Epstein-Barr virus, herpes simplex virus, and chrome poisoning in one each. RESULTS: Four patients did not undergo LDLT because of severe brain damage or combined multiple organ failure. The remaining 34 patients underwent a total of 36 LDLTs, including two retransplantations; 16 children received transplants of 17 lateral segments, three children and eight adults transplants of 11 left lobes, and seven adults transplants of eight right lobes. A total of 15 recipients died, four of primary graft dysfunction, three of refractory acute rejection, two of pneumonia, and one each of ductopenic rejection, sepsis, aplastic anemis, recurrence of Epstein-Barr virus hepatitis, multiple organ failure by chrome poisoning, and unknown hepatic failure. Primary graft dysfunction developed in adult recipients with small-for-size graft transplants, whereas refractory acute rejection and ductopenic rejection occurred in six grafts each of children with non-A, non-B FHF. CONCLUSIONS: LDLT can be safely expanded to cases of FHF in adult patients. Primary graft dysfunction in adult recipients with small-for-size left lobe grafts can be overcome by using right lobes. However, refractory acute rejection and ductopenic rejection in children remain a major problem.     

Case study of paired cadaver renal allografts from the same donor: influence of local DIC kidney and concomitant acute rejection on early graft outcome

We report the clinical course of 2 recipients whose renal allografts were obtained from the same cadaver donor after cardiac arrest. The recipients showed different outcomes after transplantation. Graft biopsy after reperfusion revealed disseminated intravascular coagulation (so-called DIC kidney) and severe acute tubular necrosis (ATN) in both recipients. While one graft showed primary nonfunction, the other graft became functional after a post-operative anuric period. Serial graft biopsies performed during the oligo-anuric period revealed recovery of ATN and no intra-glomerular fibrin thrombi, but development of acute rejection was detected in both recipients. The left kidney graft showed more severe local DIC kidney than the right kidney, as well as more severe acute rejection in the oligo-anuric period. Despite aggressive anti-rejection therapy, the left kidney graft showed primary nonfunction. Therefore, severe acute rejection leading to primary nonfunction might have been related to more severe ischemic injury and more extensive local DIC kidney in the left kidney.     

The efficacy of OKT3 in vascular rejection

Sixty-six consecutive biopsies of renal allograft recipients treated with OKT3 monoclonal antibody were reviewed and placed into one of two groups. Group I (29 patients) had evidence of acute vascular and cellular rejection, while group II (32 patients) had cellular rejection but no vascular rejection. In 5 cases, the sample was inadequate to determine if vascular rejection was present or not. The severity of the cellular rejection was graded histologically as mild, moderate, or severe. The severity was equivalent when comparing group I with group II (mild, 17% vs. 10%; moderate, 52% vs. 59%; and severe, 31% vs. 31%). There was no difference in the rejection reversal rate between the two groups (86% vs. 91%). However, at 6 and 12 months there was a higher graft loss in the group with vascular rejection (graft survival 64% vs. 81%, P = 0.13, and 58% vs. 75%, P = 0.08, respectively). The poorest outcome was in those patients with both severe acute cellular rejection and acute vascular rejection (4/9, or 44%). The serum creatinine level was higher both pre- and post-OKT3 therapy and at 1, 6, and 12 months in the group with vascular rejection. In conclusion, OKT3 was equally successful in reversing acute cellular rejection and acute vascular rejection. However, increased graft loss occurred at 6 and 12 months in the group with vascular rejection.     

排斥反应时血清可溶性白细胞相关免疫球蛋白样受体1的水平及意义

目的 探讨可溶性白细胞相关免疫球蛋白样受体1(sLAIR-1)与移植物排斥反应的相关性.方法 采用双抗体夹心酶联免疫吸附试验测定23例肝移植、139例肾移植患者的血清sLAIR-1水平,并以健康志愿者为对照.结果 健康志愿者的血清sLAIR-1水平为(4.3±2.3)μg/L,移植器官功能正常者(肝移植11例,肾移植87例)的sLAIR-1为(6.3±3.7)μg/L,二者比较,差异无统计学意义(P>0.05).肝移植后发生急性排斥反应的6例患者,其血清sLAIR-1水平为(47.2±25.9)μg/L;肾移植后后发生急性排斥反应的20例患者,其血清sLAIR-1水平(36.3±14.7)μg/L;移植肾功能丧失的5例患者,其血清sLAIR-1水平为(28.8±9.4)μg/L,上述三者的血清sLAIR-1水平均明显高于移植物功能正常者和健康志愿者(P<0.01).移植肝重度排斥反应的1例,其血清sLAIR-1高达117.3μg/L,为正常人的27倍.移植肝慢性排斥反应者(5例)和移植肾慢性排斥反应者(27例)的血清sLAIR-1水平分别为(16.1±6.4)μg/L和(13.1±5.5)μg/L,也明显高于移植物功能正常者和健康志愿者(P<0.05).结论 发生排斥反应者的血清sLAIR-1水平升高,其水平的升高可能是发生排斥反应的重要风险因素.     

Pretransplant monitoring of donor-recipient compatibility.

In these studies, pretransplant testing of donor-recipient compatibility was performed in 10 related donor and 26 cadaveric renal transplants using a variety of cell-mediated immunity tests. Mixed lymphocyte culture results did not correlate with acute rejection (AR), acute irreversible rejection, or chronic rejection (CR). Lymphocyte-mediated cytolysis also did not correlate with AR, acute irreversible rejection, or CR. Cell-mediated lympholysis correlated with AR but not with acute irreversible rejection or CR. Antibody-dependent cell-mediated cytolysis (ADCMC) was positive pretransplant in 13 (36%) of the recipients. Of the positive patients, 4 had early severe AR and 9 developed typical CR. Of these 13 patients, 9 or 69% lost graft function to rejection whereas only 3 of 20 (15%) of ADCMC-negative patients lost graft function because of rejection (P less than 0.05). In summary, cell-mediated lympholysis testing demonstrated a capability to predict AR episodes. The most useful pretransplant monitoring assay in this patient series was the ADCMC assay. A positive ADCMC against donor cells pretransplant indicates a relatively poor prognosis for long-term graft survival.     

Severe Late-Onset Acute Cellular Rejection in a Pediatric Patient With Isolated Small Intestinal Transplant Rescued With Aggressive Immunosuppressive Approach: A Case Report

Small intestinal transplantation is performed for patients with intestinal failure who failed other surgical and medical treatment. It carries notable risks, including, but not limited to, acute and chronic cellular rejection and graft malfunction. Late severe acute intestinal allograft rejection is associated with increased risk of morbidity and mortality and, in the majority of cases, ends with total enterectomy. It usually results from subtherapeutic immunosuppression or nonadherence to medical treatment. We present the case of a 20-year-old patient who underwent isolated small bowel transplant for total intestinal Hirschsprung disease at age 7. Due to medication nonadherence, she developed severe late-onset acute cellular rejection manifested by high, bloody ostomy output and weight loss. Ileoscopy showed complete loss of normal intestinal anatomic landmarks and ulcerated mucosa. Graft biopsies showed ulceration and granulation tissue with severe architectural distortion consistent with severe intestinal graft rejection. She initially received intravenous corticosteroids and increased tacrolimus dose without significant improvement. Her immunosuppression was escalated to include infliximab and finally antithymocyte globulin. Graft enterectomy was considered repeatedly; however, clinical improvement was noted eventually with evidence of histologic improvement and salvage of the graft. The aggressive antirejection treatment was complicated by development of post-transplant lymphoproliferative disorder that resolved with reducing immunosuppression. Her graft function is currently maintained on tacrolimus, oral prednisone, and a periodic infliximab infusion. We conclude that a prompt and aggressive immunosuppressive approach significantly increases the chance of rescuing small bowel transplant rejection.     

Long-term result of conservative surgical management of the ruptured renal transplant

Seven instances of spontaneous allograft rupture have been identified in a series of 585 renal transplants. Edema from acute rejection was the only common feature found. Prompt diagnosis and intervention were required to control hemorrhage. Criteria for conservative therapy are presented. The use of mattress sutures buttressed with Teflon pledgets and topical hemostatic agent proved successful in two-thirds of the cases. Nephrectomy was performed in one instance where the graft was grossly infected and in another case where hemorrhage could not be controlled. Five of seven patients have enjoyed long-term normal renal function.     

Severe acute-hybrid rejection occurring nine months after kidney transplantation: a report of rescue by orchestration of antirejection therapies

Abstract:  Although a majority of acute rejection (AR) in non-sensitized recipients is T-cell-mediated by primed T cells, recent studies have shown that antibody-mediated acute rejection occurs in 20–30% of AR, and that it is often refractory to conventional antirejection therapy; possibly leading to graft loss. We report a case of severe acute-hybrid rejection consisting of both features in a non-sensitized kidney recipient, which was rescued by the orchestration of antirejection therapies. A 33-yr-old Japanese male, with advanced-stage chronic kidney disease with an unknown etiology, underwent a HLA 3/6 mismatch and ABO-compatible living-related kidney transplantation preemptively. He had an excellent clinical course, except for initial cytomegalovirus infection, with good graft function [serum creatinine (sCr) 1.1 mg/dL]. Nine months later, his creatinine abruptly increased to 2.1 mg/dL, when graft biopsy revealed acute T cell-mediated rejection (ATMR) grade IA, and simultaneous acute antibody-mediated rejection (AAMR) grade I. Antirejeciton therapy, comprising methyl-prednisolone pulse and 15-deoxyspergualin, and second line rituximab and plasmapheresis, was ineffective. Moreover, histologically and clinically, the rejection status deteriorated (ATMR grade III and AAMR grade III, max sCr 4.0 mg/dL). Next, we administered muromonab CD3 and basiliximab, which could eradicate the complicated severe AR without opportunistic infection, even under the strong immunosuppression. The present case implies that high-grade combined rejection can respond to anti-CD 20 and anti-CD25 mAbs, without serious complication; however, post-operative, thorough appropriate monitoring of immunosuppression is important because its effects are limited.