Necrotizing fasciitis in a renal transplant patient

We have described a 28-year-old diabetic woman who had necrotizing fasciitis of the perineum three years after receiving a living related renal transplant. The diagnosis of necrotizing fasciitis was made early and she was referred to a tertiary care center where she received radical perineal debridement and aggressive medical and surgical follow-up. Necrotizing fasciitis in a transplant patient is rare; review of the literature shows few cases and no survivors. Our patient has returned to a normal life despite continuation of all immunosuppressive therapy throughout the entire hospital course. In addition, she had a good cosmetic result despite the large necrotic perineal infection. Her survival can be attributed to early diagnosis and referral, immediate and extensive debridement, and aggressive protein replacement.     

Anti-D in a D-positive renal transplant patient

BACKGROUND: The detection of anti-D in a D-positive renal transplant recipient is unusual and may arise by several potential mechanisms. These include passive transfer of alloantibody and the presence of autoanti-D or alloanti-D that is due to microchimerism when the allograft is from a D-negative donor. In the latter case, overt hemolysis has been seen or suspected. The occurrence of anti-D in a D- positive renal transplant recipient without hemolysis, which is most likely attributable to microchimerism, is reported. CASE REPORT: A 51- year-old group O, D-positive woman, who was serologically HLA type A1, A2; B8, B44; DR3, DR6, DR52; DQ1, DQ2, underwent the transplantation of a kidney from a cadaveric donor who was serologically HLA type A1, A2; B8, B44; DR13, DR17, DR52; DQ1, DQ2. The donor was known to be D- negative and immunized to D. No blood components or derivatives were administered at the time of organ graft. Ten weeks after the transplant, the direct antiglobulin test was positive in the recipient, and anti-D was eluted. Polymerase chain reaction amplification using primers to distinguish DR13 (donor) from DR14 alleles (recipient split of DR6) in the peripheral blood showed the recipient to be DR14. No DR13 could be detected, and thus microchimerism could not be confirmed. However, in the peripheral blood, GM and KM allotyping of the serum (GM A,F,X B,G and KM 1,3) and eluate (G1M F, KM 3) showed a pattern of allotypes most consistent with an alloantibody. Eleven months after transplantation, the graft continued to function; the direct antiglobulin test was still positive, and elution of anti-D persisted. CONCLUSION: This case of anti-D in a D-positive renal transplant recipient is attributed to microchimerism, despite the lack of confirmation by genotypic analysis of the peripheral blood. It raises the possibility that microchimerism may be a more common phenomenon in solid allograft recipients than is realized.     

Sirolimus-induced interstitial pneumonitis in a renal transplant patient

We report interstitial pneumonitis caused by sirolimus (Rapamune, an immunosuppressive agent) in a renal transplant patient. This rare manifestation was recently recognized as a troublesome adverse effect of sirolimus in many solid-organ transplant recipients, the majority of whom are kidney transplant recipients. While on sirolimus our patient developed cough, fever, and patchy infiltrates, which failed to respond to multiple courses of antibiotic therapy. Biopsy showed findings characteristic of drug-induced hypersensitivity pneumonitis, and excluded other entities, such as opportunistic infection. Improvement occurred only upon discontinuation of the sirolimus.     

Sublingual administration of tacrolimus in a renal transplant patient

Tacrolimus is used in renal and other organ transplantations for immunossupression therapy. Bioavailability of enterally administered tacrolimus is poor, and further reduced by gastrointestinal failure or enteral nutrition. In these situations, intravenous administration is necessary to prevent treatment failure. However, intravenous administration should be done in a continuous manner and it has been implicated in anaphylaxis, torsades de pointes, cardiac arrhythmia and other serious adverse events. Also it is more expensive than other routes of administration. Sublingual administration of tacrolimus has been used in some cases, and literature reports show that it provides therapeutic tacrolimus levels in lung and liver transplant recipients. Here, we report a first case of sublingual administration of tacrolimus in kidney transplantation.     

血清半胱氨酸蛋白酶抑制剂C在肾移植功能监测中的应用价值

目的探讨血清半胱氨酸蛋白酶抑制剂C（Cys C）在肾移植术后，尤其是感染和排斥时，监测肾功能的临床应用价值。方法同时检测65例肾移植患者术前、术后1个月内、感染或排斥发生时及次日血清中Cys C和血清肌酐（Scr）的浓度，并测定30名健康人和30例非移植感染患者的Cys C和Scr作为对照。结果健康人与非肾移植感染患者的Cys C浓度差异无统计学意义（P=0．32）。移植后肾功能稳定组（n=36）术后前3d内Cys C分别较术前下降了69．2％、74．7％、75．8％（P〈0．01），Scr相应的下降了38．4％、74．5％、81．4％（P〈0．01）。移植术后感染组（n=13）肾功能异常时，Cys C比Scr早（4．4±1．5）d升高，升高幅度分别为39．4％和35．3％（P=0．43）；排斥组（n=16）Cys C比Scr早（2．7±1．8）d升高，升高幅度分别为148．9％和43．9％（P=0．0069）。与肾功能稳定组作横向比较，术后感染组和排斥组的Cys C分别升高了38．7％和108．5％（P〈0．001），Scr分别升高了34．2％和89．5％（P〈0．001）。所有肾移植患者术后3～28d之间，Cys C与Scr呈线性正相关（r=0．785，P〈0．0001）。根据ROC曲线确定Cys C和Scr在术后排斥时的临界值分别为1．79mg／L和122μmol／L。排斥组Cys C的敏感度、特异度、阳性预测值、阴性预测值、符合率以及曲线下面积（AUC）均优于Scr（均P〈0．05）。结论Cys C优于Scr，是一个能早期、灵敏、准确判断移植肾功能变化的血清标志物。     

Serum cystatin C concentration as a marker of acute renal dysfunction in critically ill patients

The second part of this review addresses the treatment and prognosis of the vasculitides Wegener's granulomatosis, microscopic polyangiitis, Churg–Strauss syndrome and polyarteritis nodosa. Treatment regimens consist of an initial remission phase with aggressive immunosuppression, followed by a more prolonged maintenance phase using less toxic agents and doses. This review focuses on the initial treatment of fulminant vasculitis, the mainstay of which remains immunosuppression with steroids and cyclophosphamide. For Wegener's granulomatosis and microscopic polyangiitis plasma exchange can be considered for first-line therapy in patients with acute renal failure and/or pulmonary haemorrhage. Refractory disease is rare and is usually due to inadequate treatment. The vasculitides provide a particular challenge for the critical care team. Particular aspects of major organ support related to these conditions are discussed. Effective treatment has revolutionized the prognosis of these conditions. However, mortality is still approximately 50% for those requiring admission to intensive care unit. Furthermore, there is a high morbidity associated with both the diseases themselves and the treatment.     

Oral care for the renal transplant patient

Renal transplant patients require immunosuppressive therapy, including a combination of prednisone, methylprednisone, azathioprine, antilymphocyte globulins, cyclosporine, and/or OKT 3. Consequently, they are vulnerable to opportunistic infections, especially in the oral cavity. The infections often seen are candida albicans and herpes simplex virus. Routine oral assessments and oral care need to be performed to provide maximum patient comfort and to prevent or minimize painful complications.     

The African variant of BKV in a Turkish renal transplant patient

In renal transplant recipients, BK polyomavirus (BKV) is linked to nephropathy. BK virus genotypes have a strong geographic component. This paper presents the African variant of BKV in a Turkish renal transplant patient, which is a rare cause of infection in the Northern Hemisphere and, to our knowledge, the first case from Turkey.     

Aminoaciduria is an earlier index of renal tubular damage than conventional renal disease markers in the gentamicin-rat model of acute renal failure

There are currently no reliable early markers of renal tubular damage. Since aminoaciduria is an accompanying feature of this condition, the usefulness of increased urinary amino acid excretion as a marker was investigated by inducing renal tubular necrosis in male Wistar rats by the administration of gentamicin (40 mg/kg/d) for 14 d. Plasma amino acids, urea, creatinine, protein and electrolytes, and urine amino acids, protein and N-acetylglucosaminidase (a lysosomal enzyme) were measured over a 20 d period. Amino acid excretion increased dramatically within 24 h of the initial dose for 14 of the 16 amino acids measured. The conventional renal disease markers listed above did not increase until after day 7. Glomerular damage caused by puromycin aminonucleoside did not induce aminoaciduria until marked proteinuria occurred (day 9), and even then amino acid excretion was much less than that caused by gentamicin. To distinguish whether the gentamicin-induced aminoaciduria was a consequence of tubular damage or inhibition of amino acid transport, isolated rat kidneys were perfused with a Krebs-Henseleit albumin buffer with and without gentamicin for 20 min, during which time urinary amino acids were quantitated. Gentamicin did not inhibit amino acid reabsorption. Thus, it appears that in the rat-gentamicin model of acute renal failure, urinary amino acids are early markers of renal tubular damage.     

供者特异性抗体对肾移植术后患者急性排斥和肾功能的影响研究

目的研究抗供者特异性抗体(DSA)对移植肾急性排斥反应和近期肾功能的影响。方法采用MicroAMS HLA-III供者特异性抗体检测试剂盒检测96例肾移植患者术后排斥及恢复期2个时间点的DSA,同时检测移植肾功能。结果①96例肾移植患者有8例肾移植术后出现DSA,占8.33%(8/96)。②8例DSA阳性患者6例发生急性排斥反应,其中5例为抗HLA-I类抗体,1例为抗HLA-II类抗体;未发生急性排斥反应的2例为抗HLA-II类抗体。移植肾功能恢复时,仍有2例DSA-I类弱阳性。③DSA阳性对肾移植术后排斥和肾功能均有影响。结论 DSA是预测肾移植术后发生急性排斥反应的有效方法之一。     

Colchicine-induced toxicity in a heart transplant patient with chronic renal failure

Introduction. Therapeutic doses of colchicine in patients with renal compromise and cyclosporine therapy may result in increased plasma concentrations of colchicine and colchicine toxicity. Case Report. A 60-year-old heart transplant patient with chronic renal failure and cyclosporine-induced immunosuppression was started on colchicine for suspected gout. Four days later, he developed multi-organ failure with rhabdomyolysis, liver damage, polyneuropathy, and cardiotoxicity. Colchicine intoxication was suspected and plasma levels were 7 ng/mL 36 hours after the sixth dose. Neutropenia with an absolute neutrophil count of 700 cells/mm3 was observed five days after colchicine discontinuation. Drug discontinuation, supportive care, antibiotic therapy for a concurrent infection, and G-CSF administration resulted in recovery and he was discharged from the hospital 3 weeks later. Discussion. Cyclosporine co-administration increases colchicine toxicity by a dual mechanism: cyclosporine inhibits P-glycoprotein resulting in increased intracellular colchicine concentrations and decreased hepatic and renal excretion of the drug and cyclosporine interacts with CYP3A4 to decreases the hepatic elimination of colchicine. On the other hand, colchicine may increase cyclosporine neurotoxicity by an addictive mechanism. Conclusions. Shortterm administration of therapeutic colchicine doses may cause life-threatening side effects in cyclosporine-treated patients with renal failure.