肾移植术后“爬行肌酐”患者使用他克莫司替换环孢素A疗效观察

目的观察他克莫司（FK506）替换环孢素A（CsA）逆转肾移植术后“爬行肌酐”的可行性。方法24例肾移植患者术后均采用以CsA为主的三联免疫抑制方案，出现“爬行肌酐”后用FK506替换CsA。观察替换前后的移植肾功能变化，同时监测血压、抗高血压药物分值（AHS值）、血糖和血脂的变化，随访12个月。结果“爬行肌酐”患者采用FK506替换CsA后，移植肾功能较替换前明显好转，血肌酐下降明显（P〈0．05）；同时降低了血脂水平，并减少降脂药物及抗高血压药物的使用。结论肾移植术后“爬行肌酐”患者采用FK506替换CsA的治疗方案可以有效地改善或者稳定移植肾的功能。     

多次肾移植受者的临床病理特征及预后

目的：探讨多次肾移植受者的临床病理表现及预后。方法：回顾性分析国家肾脏疾病临床医学研究中心2013年1月至2022年10月多次肾移植受者临床病理及预后资料。结果：共纳入38例多次肾移植受者,其中二次肾移植35例、三次肾移植3例。二次肾移植受者首次肾移植肾脏平均存活时间83.2月,29例行二次移植后行移植肾肾活检,肾活检距二次肾移植中位时间31月;病理类型中21例与移植排斥相关,8例为非移植肾排斥反应相关,其中7例复发或新发肾小球疾病。患者二次肾移植中位肾脏存活66(49,108)月,1年、3年和5年肾存活率分别为94.3%、88.6%和60.0%。首次移植肾存活时间≤6月患者和≤1年患者二次移植肾脏存活时间明显低于首次移植肾存活时间>6月患者(P=0.016)和>1年患者(P=0.049)。此外,首次移植肾失功至二次移植间的等待时间≤1年患者二次移植肾脏存活时间明显高于等待时间>1年患者(P=0.022)。3例患者三次移植肾存活时间分别为99月、115月、101月,第1例和第3例移植肾失功。结论：多次移植肾脏预后总体良好,再次移植肾存活时间与首次移植肾脏存活时间及再次...     

肾移植2,3,5年患者的免疫抑制用药分析

目的：分析肾移植后免疫抑制剂对长期存活的影响，寻找移植后不同时间合适的免疫抑制用药方案及其用药剂量。 方法：对肾移植一年以上、肾功能正常的４９７例患者进行５年连续随访。根据移植后２、３、５年的不同免疫抑制用药将患者分为三联、二联、传统二联治疗三组。统计各组的排异发生率，排异和无排异患者免疫抑制用药的种类、剂量及ＣｓＡ浓度，对排异患者追踪排异发生前１２个月内的药物更动情况。 结果：肾移植后２、３、５     

他克莫司治疗移植肾慢性排斥的初步临床观察

目的：探讨他克莫司（FK506）、环孢素A（CsA)治疗移植肾慢性排斥（CR)的可行性及安全性。方法：40例同种异体肾移植患者肾功能减退经病理证实为CR，随机分为CsA切我为FK506组20例、继续使用CsA组20例。观察各组移植肾功能、肾小球滤过率、蛋白尿、血压、血脂变化及急性排斥（AR）发生率，治疗后随访12个月。结果：追踪12个月，FK506组16例移植肾功能稳定（80％）；3例行血液透析治疗，1例死亡，人存活率95％。CsA组15例移植肾功能稳定，3例行血液透析治疗，逆转成功率75％；2例死亡，人存活率90％。结论：FK506可以延缓慢性移植物失功。FK506的使用是安全和有效的。     

抗中性粒细胞胞质抗体相关肾炎患者肾移植的转归

目的:回顾性分析抗中性粒细胞胞质抗体(ANCA)相关肾炎(AAGN)患者接受肾移植后的转归。方法:11例AAGN患者[男4例,女7例,中位年龄48(33.5~52.5)岁]接受肾移植。采用激素、吗替麦考酚酯联合他克莫司/环孢素A三联抗排斥治疗。肾移植后排斥反应及其类型均经移植肾活检病理诊断。回顾性分析移植肾预后、血管炎复发及血清ANCA对移植肾预后的影响。结果:11例AAGN均为MPO-ANCA相关血管炎,10例在肾移植前接受肾脏替代治疗,中位时间为30.5(14.8~50.5)个月。肾移植前均无血管炎活动(BVAS 0分),7例血清MPO-ANCA阳性。肾移植术后均未出现移植肾功能延迟恢复,4例(36.4%)发生急性细胞性排斥反应,分别有1例术后18个月和22个月发生血管炎复发和慢性体液性排斥反应。术后中位随访56(46.5~135)个月,随访末8例(72.7%)血清肌酐水平正常,2例血清肌酐升高,1例移植肾失功。5年人、肾生存率分别为100%和90.9%。术前ANCA阳性与阴性患者比较移植肾排斥反应发生率和血管炎复发率均无显著差异。结论:AAGN患者肾脏移植后远期预后好,血管炎复发率低,但术后早期急性排斥反应发生率高,应加强预防抗排斥反应。     

移植肾常规活检肾组织C4d沉积的检测及其意义

目的：观察C4d在肾移植术后常规活检组织中沉积发生情况及临床意义。方法：294例移植肾功能正常者（男211例，女83例）于术后2～4周内接受常规活检，应用间接免疫荧光检测肾组织C4d的沉积。观察CAd阳性患者病理特点、预后以及移植肾功能情况。结果：“无症状”CAd阳性检出率为6．12％（18／294）。其中弥漫分布2．38％（7／294），局灶分布3．74％（11／294）。该组患者除女性多数术前有妊娠史外（6／8），术前皆无高群体反应性抗体（PRA，panel reactive antibodes）、二次移植、输血等排斥高危因素的存在。随访12月，除1例患者因术后肺部感染救治过程中移植肾受损伤，其余17例患者肾功能稳定。该组患者移植肾组织中除1例出现动脉内膜炎外，并未发现动脉纤维素样坏死、动脉血栓、间质出血、透壁性动脉炎等组织形态学改变。术后起始免疫抑制方案11例为他克莫司（FK506）＋霉酚酸酯（MMF）＋激素，7例为环孢素A（CsA）＋MMF＋激素。8例患者行重复移植肾活检，其中6例CAd转阴，1例CAd由弥漫转为局灶阳性。结论：“无症状”CAd阳性患者术前多无发生排斥反应的高危因素，术后移植肾功能稳定，而移植肾组织中无抗体介导体液性排斥反应的特征性组织学改变。在接受免疫抑制治疗后，CAd在肾组织中的沉积可以消失或减弱。     

影响肾移植术后移植肾失功的因素

目的分析影响肾移植手术后移植肾失功的因素。方法接受同种异体肾移植手术的患者共750例,分析移植肾失功率及失功原因。应用Logistic分析影响移植肾失功的独立因素。结果 5年内移植肾失功率为3.87%,存活率为96.13%,肾移植受者的存活率为97.73%;移植肾功能延迟恢复、急性排斥反应、加速性排斥反应、感染,显著影响移植肾的存活率(P0.05)。年龄、免疫抑制方案对移植肾存活的影响无统计学意义(P0.05)。移植肾冷缺血时间、肌酐恢复正常时间、患者1个月内状况(移植肾功能延迟恢复、急性排斥反应、加速性排斥反应、感染)均属影响移植术后移植肾存活的独立因素。结论对肾移植术后患者进行移植肾功能延迟恢复、急性排斥反应、加速性排斥反应、感染的发生进行严格控制,对提高移植肾的存活率具有重要的临床意义。     

移植肾功能延迟恢复的病因学分析与防治

目的探讨移植肾功能延迟恢复（DGF）的病因学与及防治措施。方法分析35例肾移植术后移植肾DGF患者的临床资料。DGF的主要原因为急性肾小管坏死（ATN）20例，急性排斥反应（AR）8例，免疫抑制剂毒性肾损害4例，输尿管梗阻2例，尿漏1例。血液透析治疗24例，外科手术3例。结果34例DGF移植肾功能恢复正常，1例AR所致DGF最终切除移植肾，恢复规律血液透析。结论ATN和AR是引起肾移植术后DGF的主要因素；术前严格配型、合理筛选受者及保证供肾质量等是防治肾移植术后DGF的主要措施。     

移植肾急性肾衰竭的救治

由于肾脏移植手术技巧的改进及新型免疫抑制剂和免疫抑制方案的进展，移植肾的近期生存率与长期生存率均有很大的提高，但肾移植至今仍面临许多亟待解决的困难。肾移植受者因其特殊性，发生急性肾衰竭（ARF）的可能性远高于一般人群。移植后早期的基础肾功能对移植肾长期生存有重要影响，故移植肾ARF的救治成功与否成为影响移植肾长期生存的突出问题。     

雷帕霉素联合环孢素A预防肾移植急性排斥反应

目的 :研究雷帕霉素 (rapamycin ,RPM)预防移植肾早期急性排斥反应 (AR)的临床疗效及其安全性。　 方法 :采用RPM、环孢素A(CsA)和强的松“三联”免疫抑制方案。RPM首次负荷剂量 6mg/d口服 ,第 2天开始改为维持剂量 2mg/d。肾移植术后 4 8h内给予首次剂量 ,在给予CsA后约 4h服用RPM ,并持续使用至 12个月。根据患者的临床情况和血药谷值浓度 (Co) ,调整RPM和CsA剂量。　 结果 :术后 1、3、6个月 ,全血RPMCo分别为 (5 12± 0 2 1) μg/L、(6 39± 0 73) μg/L、(5 18± 0 12 ) μg/L ;CsACo分别为 (2 5 1 6 8± 98 3) μg/L、(2 2 4 92± 88 9) μg/L、(10 1 91± 5 9 31) μg/L 16例患者完成 6～ 12个月的随访 ,提前中止治疗 9例 (中止原因包括 2例进食困难和腹泻 ,1例体重明显减轻 ,3例肝毒性反应 ,1例移植肾功能延迟恢复和 2例并发肺部感染 )。随访期间无一例死亡和移植肾丧失 ,AR 2例 (占 12 5 % ) ,分别发生于术后第 12天和 2 6天 ,经肾活检病理证实均为急性细胞性排斥反应 ,经甲基强的松龙冲击治疗后逆转 ,仍维持RPM 2mg/d治疗。并发症包括消化道症状 (恶心 2 4 % ,呕吐 2 4 % ,胸骨后烧灼样疼痛 12 % ,进食困难 8% ,腹泻 12 % )和高脂血症 (高胆固醇血症 37 5 % ,高甘油三酯血症 31 5 % )     

Anti-CD25 monoclonal antibody against polyclonal antibodies in pediatric renal transplantation

Although usually reversible, acute rejection of kidney graft is a negative factor in long-term graft survival. Commonly used in pediatric renal transplantation, immunosuppresive induction therapy is established to prevent it. New immunosuppressive agents have been developed in recent years and among them anti-CD25 monoclonal antibody appears to be specially interesting. AIM: To evaluate efficacy and safety of anti-CD325 monoclonal antibody (basiliximab) versus polyclonal antibodies as induction therapy in renal transplantation. MATHERIAL Y METHODS: Thirty consecutive kidney transplants performed in children 4-16 years age in Hospital Infantil La Fe through 1997-2000. The first 15 patients received polyclonal antibodies as induction therapy, and 15 consecutive ones received monoclonal anti-CD25 antibodies. Receptor, donor and graft characteristics were similar in both groups. Also, maintenance immunosuppression was the same. RESULTS: The follow-up was over one year in all patients. Four patients in the polyclonal antibody group suffered one acute rejection episode and four other patients had some drug reaction. In the anti-CD25 treatment group there was one episode of acute graft rejection and no collateral effects were observed. Glomerular filtration rate, proteinuria, hypertension, infection episodes, graft and patient survival were similar in both groups. CONCLUSIONES: Induction therapy for pediatric renal transplantation with anti-CD25 antibody has been effective and safe. Compared with polyclonal antibodies as standard treatment, basiliximab reduced acute rejection episodes and had no collateral side effects. Graft and patient one year survival were identical in the two groups.     

Donor‐transmitted adenovirus infection causing kidney allograft nephritis and graft loss

T. Kozlowski, V. Nickeleit, K. Andreoni. Donor‐transmitted adenovirus infection causing kidney allograft nephritis and graft loss.
Transpl Infect Dis 2011: 13: 168–173. All rights reserved Abstract: Adenovirus (AdV) infection can occur early after transplantation, especially with potent immunosuppression for induction or acute rejection treatment. We present the largest case series of adult renal recipients from a single institution with AdV infection, and the first apparent case of transferred AdV infection from 1 deceased donor to 2 kidney recipients. Three patients received kidneys from 2 deceased donors: 2 from a 23‐year‐old donor, and the third from a 4‐year‐old donor. The recipients with the same donor both displayed early rejection. One who eventually lost his graft to AdV nephritis required treatment with plasmapheresis, intravenous immunoglobulin, rituximab, and anti‐thymocyte globulin for severe antibody‐mediated rejection. The second required only steroids for acute cellular rejection and has good renal function at 7 years. The third recipient was discovered to have AdV and microabscesess on renal biopsy and required nephrectomy. In the 2 cases of graft loss, we observed sudden deterioration of graft function with rising creatinine and subsequent necrosis resulting in nephrectomy within 40 days after transplantation. AdV was detected by polymerase chain reaction in urine or serum and/or renal tissue. AdV activation after potent immunosuppression can lead to systemic infection and may trigger rejection and/or early graft loss.     

Microchimerism and Renal Transplantation: Doubt Still Persists

Background: The Presence of donor leukocytes in recipients of organ allograft has been shown even several years after transplantation. However, it remains unclear whether this donor cell microchimerism plays an effective role in allograft acceptance or is simply a consequence of immunosuppressive conditions in recipients. Objective: To study microchimerism in a group of kidney transplant recipients. Methods: In this study, the Peripheral Blood Microchimerism (PBM) after renal transplantation was retrospectively evaluated in 32 male-to-female recipients of living (unrelated) and cadaveric donor renal transplants. Using a Nested Polymerase Chain Reaction (Nested-PCR) amplification specific for SRY region of the Y chromosome, microchimerism was detected with a sensitivity of 1:1000000. Recipients were classified and compared according to the presence of PBM, acute and chronic rejection episodes, type of allotransplant, recipient and donor age at transplantation, previous male labor or blood transfusion, allograft function (serum creatinine level), and body mass index. Results: Among 32 recipients, 7 (21.9) were positive for PBM in multiple testing at different post-transplantation times. All microchimeric recipients had received kidney from living-unrelated donors. No significant difference was observed with regard to other parameters mentioned above. In addition, acute rejection rate in the microchimeric group was 3 (42%) versus 4 (16%) in the nonmicrochimeric recipients (not significant). Conclusion: Our results demonstrate better establishment of microchimerism after living donor kidney transplantation. However, concerning the true effect of microchimerism after renal transplantation doubt still persists; and it seems that microchimerism alone has no major protective role in renal allograft survival.     

Mono-oligoclonal immunoglobulin abnormalities in diabetic patients after kidney transplantation: influence of simultaneous pancreas graft

Summary Monoclonal components (MC) are detected in as high as 30 % of renal transplant recipients. Our aim was to evaluate the incidence, relevance and consequence of monoclonal components in patients with Type I (insulin-dependent) diabetes who received kidney (n = 22), kidney and whole pancreas (n = 41), kidney and segmental pancreas (n = 24) and kidney and islets (n = 12) transplants. Immunosuppression was based on prophylactic anti-lymphocyte globulins, corticosteroids, azathioprine and cyclosporin in all patients; acute rejection was treated with steroids or anti-lymphocyte monoclonal immunoglobulin therapy (OKT3) or both. Serum immunofixation was carried out in all patients before transplantation and then after at 6 months and then yearly. Monoclonal components were detected in 81 of 99 patients (82 %); 52 patients (52 %) developed them within 6 months of transplantation, 15 (15 %) between 6 and 12 months, with a peak prevalence at 1 year post-transplant (58 %) and a decrease thereafter (10 % at 9 years). Kidney recipients showed a lower incidence of monoclonal components when compared with those who received kidneys and segmental pancreases and those who received kidneys and whole pancreases. Monoclonal components were more often detected in patients who had previously experienced an acute renal rejection. Cytomegalovirus infection and acute rejection occurring in the same patient further increased the risk of developing monoclonal components, the development of which did not correlate with OKT3 treatment. A Post-transplant lymphoproliferative disorder was developed by two patients (2 %), one with 5 and the other with 6 monoclonal components. In conclusion, diabetic patients receiving kidney and/or Pancreas transplantation, experiencing both cytomegalovirus infection and acute rejection, are at greatest risk of developing monoclonal components but they appear to be benign and transient; multiple band detection is a marker for the subsequent development of post-transplant lymphoprolifertive disorder. [Diabetologia (1998) 41: 1176–1179] Received: 5 January 1998 and in revised form: 28 April 1998     

Limitations of current liver transplant immunosuppressive regimens: renal considerations

BACKGROUND:The use of calcineurin inhibitor (CNI)-based immunosuppressive regimens following liver transplantation (LTx) has improved the outcomes of the recipients.However,CNI has nephrotoxicity and causes short-and long-term renal complications.The progressive structural changes can be irreversible in the long-term,leading to chronic kidney dysfunction.The present review was to evaluate the different strategies of CNI application to renal function in liver recipients.DATA SOURCES:PubMed database was searched for relevant articles in English on the issue of immunosuppressive regimen and kidney injury that related to early minimization of CNI after LTx.RESULTS:Total avoidance of CNI from post-LTx immunosuppressive regimens has been associated with unacceptable high rates of acute,steroid resistant rejections;late conversion from CNI to non-nephrotoxic immunosuppressant failed to recover renal function.Early CNI minimization and conversion to non-nephrotoxic immunosuppressant,although had no effect on patient survival rates,improved glomerular filtration rate.The combination of everolimus (a mammalian target of rapamycin inhibitor) and tacrolimus not only maintains immunosuppressive efficacy but also minimizes kidney injury.CONCLUSIONS:Up to now,protocols entirely avoiding CNI have not passed the primary safety endpoint of patient and graft survival,as well as the FDA mandated endpoint of biopsy proven acute rejection.Thus,early CNI minimization after LTx is the most rational approach preserving post-transplant renal function.     

Prediction of Rejection in Renal Transplantation by Immune Parameters

Background: Monitoring of phenotypic characteristics of T-lymphocytes in peripheral blood is commonly performed to give the clinical parameters in the management of kidney transplant recipients.   Objective: To predict rejection in renal transplantation by immune parameters. Methods: 16 non-diabetic kidney transplant candidates (4 females and 12 males, age = 20-65 yr, first time transplant) were selected. The transplanted patients were divided into two groups based on the rejection during 3 weeks post transplant: group I (n = 9) without rejection and group II (n = 7) with a rejection episode. Immune parameters including lymphocytes subpopulations (by flowcytometry) and immunoglobulin classes (IgM, IgG, IgA and IgE by nephlometric assay) before and 45 days after transplantation were determined.   Results: The results of this investigation showed that the level of immunoglobulin IgG, IgM, IgA and IgE decreased post transplantation due to immunosuppressive drugs. CD3, CD4, CD8 T cells count, CD56 NK cells count and CD20 B cells count pre- and post-transplantation did not show any significant differences. The amount of IgE (220   vs. 462 IU/ml), CD3 (62% vs. 69.7%) and CD4 (35% vs. 41.3%) cells increased in group II during rejection episode pre-transplantation. In addition, IgA increased pretransplantation in group I those without rejection episode in comparison with group II with a rejection episode. Forty five days post transplantation IgA (209   vs. 152 mg/dl), IgG (1009 vs. 703 mg/dl) and CD20 (15%   vs. 10%) increased in group I patients. Conclusion: It is suggestive that pre-transplantation increases IgE, CD3 and CD4 are predictive of acute rejection.     

Transmission of toxoplasmosis in two renal allograft recipients receiving an organ from the same donor.

Toxoplasma gondii is a ubiquitous protozoan parasite. After acute infection it continues to exist as cysts in the muscles and brain. Recipients of organ allografts are susceptible to the disease as a result of reactivation of quiescent infection either by transmission from the organ donor or by consumption of undercooked meat. We describe 2 cases of fatal toxoplasmosis in renal allograft recipients who received their organs from the same cadaveric donor. Both recipients died 5 weeks after renal transplantation, within days of each other. Multiorgan involvement with toxoplasmosis was demonstrated at autopsy. No evidence of the parasite was found in the transplanted kidney, either at the time of insertion or at autopsy. Neither recipient had serologic evidence of previous exposure to T. gondii. The donor had positive IgG but indeterminate IgM antibodies suggesting acute infection at the time of death; there was no clinical suspicion that the donor died from acute toxoplasmosis. We conclude that toxoplasmosis was transmitted by the donor kidneys. In an attempt to minimize the possibility of future transmission, donors are now tested for anti-toxoplasma IgM antibodies and recipients are treated with trimethoprim/sulfamethoxazole for the first 6 months after renal transplantation.     

Outcomes of transplantation from living renal donor

Living donors represent 30% of our kidneys for renal transplantation. Laparoscopic nephrectomy is the best surgical procedure to obtain them due to its clear advantages such as low morbidity, less blood supply and donor time in hospital. From March 2002 to August 2004 we performed 50 laparoscopic nephrectomies for renal transplantation. Kidneys were transplanted to recipients receiving tacrolimus 0.1 mg/kg/bid, mycophenolate mofetil 1 g/bid and prednisone 0.5-1 mg/kg/day p.o 48 hours before transplantation. Mean time for surgery was 170 minutes (120-260), warm ischaemia time 3.1 minutes (1.5-10) and cold ischaemia time 1.27 hours (0.85-4). Mean bleeding was 270 cc (100-900) and donor time in hospital 5.5 days (3-9). Four cases required conversion of the laparoscopic procedure to open surgery because of bleeding. 72 hours post-transplant mean plasmatic creatinine was 170 micromol/l. None of the patients suffered delayed graft function. 18% presented acute rejection. Survival of donor and recipient was 100% at 1 year and graft survival was 94% at 1 year (kidney losses were due to acute rejection, severe acute pancreatitis and surgical problem).     

Donor Phosphorus Levels and Recipient Outcomes in Living-Donor Kidney Transplantation

Summary

Background and objectives

In living-donor kidney transplantation, various donor factors, including gender, age, and baseline kidney function, predict allograft function and recipient outcomes after transplantation. Because higher phosphorus is predictive of vascular injury in healthy adults, the effect of donor phosphorus levels on recipient renal function after transplantation was investigated.

Design, setting, participants, and measurements

Phosphorus levels in 241 living donors were analyzed from a 7-year period, and recipient renal function and acute rejection at 1 year posttransplantation were examined controlling for other influencing factors, including multiple donor variables, HLA matching, and acute rejection.

Results

Female and African-American donors had significantly higher phosphorus levels predonation. By multivariable analysis, higher donor phosphorus correlated with higher recipient serum creatinine (slope = 0.087, 95% confidence interval [CI]: 0.004 to 0.169, P = 0.041) and lower recipient estimated GFR (slope = −4.321, 95% CI: −8.165 to −0.476, P = 0.028) at 12 months. Higher donor phosphorus also displayed an independent correlation with biopsy-proven acute rejection and delayed or slow graft function after transplantation.

Conclusions

In a cohort of living kidney donors, higher donor phosphorus correlated with female gender and African-American ethnicity and was an independent risk factor for early allograft dysfunction after living-donor kidney transplantation.     

Simultaneous transplantation of the heart and kidney

Background: Multiple organ transplants have become frequent. Combined heart-and-kidney grafting has been reported recently and we have pursued this in selected cases. Aims: To devise a protocol for simultaneous heart-and-kidney transplantation, review our clinical experience with the procedure and the causes of cardiac and renal disease in this group. Methods: Seven patients with advanced cardiac failure (LV ejection fraction < 0.29 units; five with IDCM), and chronic renal failure (serum creatinine > 375 μmol/L) due to a variety of causes, were accepted for combined heart-and-kidney transplantation. Four males, of mean age 33 years, underwent the procedure. Each received his organs from a single cadaveric donor with ABO blood group compatibility and a negative ‘current’ lymphocytotoxic cross-match, but without regard to HLA-antigen matching. Cardiac ischaemic time averaged 3 hours 40 minutes, the renal first warm time was 0 minutes in all cases, and renal cold and second warm ischaemic times averaged 5 hours 17 minutes and 52 minutes respectively. The heart was grafted first and the kidney second in a procedure which averaged seven hours. Immunosuppression was achieved by induction with antithymocyte globulin, thence steroids, azathioprine and cyclosporin A. Results: No patient required post-operative dialysis. One patient had early urological complications requiring operative correction, but no serious opportunistic infections were observed. Early cardiac rejection on biopsy (ISHT grade 3a) was seen in three patients at four-ten weeks and responded promptly to increased steroids, but severe steroid-resistant rejection of both heart and kidney contemporaneously occurred in one of these three at 19 months and required a course of muromonab-CD3. All four patients developed hypertension. Mean creatinine clearance was 1.23 ± 0.22 mL/second (74±13 mL/minute) at last follow-up. All four recipients were alive, well and rehabilitated 5, 20, 28 and 35 months after grafting. Two patients died while waiting for the double procedure and another patient eventually died after being taken off the dual waiting list and receiving a renal transplant only. Conclusions: In experienced hands, combined heart-and-kidney transplantation is feasible and offers a compelling therapeutic solution in the treatment of advanced cardiac and renal failure. IDCM is a frequent cause of the heart failure in this group. (Aust NZ J Med 1994; 24: 554–560.)