Hyperfiltration nephropathy as a cause of late graft loss in renal transplantation

Summary Despite improved immunosuppression and early allograft survival, long-term survival of allografts remains unchanged. Late renal allograft loss has traditionally been considered to result from repeated or unresolved episodes of acute rejection that lead to chronic immune-mediated allograft rejection. However, late renal allograft loss is known to occur in the absence of prior episodes of acute rejection. It is therefore proposed that factors other than histocompatibility influence long-term allograft survival. Evidence for nonimmunologic factors contributing to late allograft loss is presented. The central hypothesis is that following renal allograft mass reduction (from any etiology), glomerular hyperperfusion and hyperfiltration develop and lead to progressive renal dysfunction, proteinuria, histopathologic allograft changes, and late allograft failure. Multiple nonimmunologic factors that could contribute to reduced renal mass and ultimately promote chronic allograft loss as a result of hyperfiltration nephropathy are presented along with possible therapeutic strategies for the prevention and treatment of glomerular hyperfiltration.     

Long-term survival and causes of late graft loss after adult-to-adult living donor liver transplantation

The vast amount of experience with deceased donor liver transplantation allows for the evaluation of the causes underlying late graft loss and the adoption of strategies for its prevention. In contrast, the long-term results or causes of late graft loss after adult-to-adult living donor liver transplantation have not been fully examined. Thus, we analyzed 176 adult recipients who survived at least 1 year after living donor liver transplantation. The median follow-up period was 33 months. Of the 176 recipients, eight died and three others underwent retransplantation. The most common cause of graft loss in our series was cholangitis (n = 4), which might be due partly to technical problems. The 3-year and 5-year patient survival rates of the subjects were 95% and 90%, respectively. Long-term survival after living donor liver transplantation was satisfactory in our series. Further improvement of surgical techniques for biliary reconstruction may reduce late graft loss.     

A case of late onset cyclosporine-induced hemolytic uremic syndrome resulting in renal graft loss

A case of late onset hemolytic uremic syndrome (HUS) associated with cyclosporine (CYA) is described in this report. A 50-yr-old man with end-stage renal failure due to immunoglobulin A (IgA) nephropathy received a renal transplant from his wife. Human leucocyte antigen was completely unmatched. Immunosuppressant was a combination of prednisolone, azathioprine, and CYA. He was discharged 1 month after transplantation, with no episode of acute rejection. Twenty-one months after transplantation, his platelet count and hematocrit began to decrease and lactate dehydrogenase began to increase. Graft biopsy showed thrombotic microangiopathy and recurrent IgA nephropathy. Graft function was rapidly deteriorated and methylprednisolone pulse therapy was not effective. Twenty-five months after transplantation, he returned to a regular hemodialysis. Hemolysis was immediately improved after a reduction of the dose of CYA to 50 mg/d. The trough level of CYA was less than 200 ng/mL in most periods of his clinical course. Blood pressure was high throughout the clinical course. Although acute vascular rejection or malignant hypertension could also cause a thrombotic microangiopathy, CYA was most likely a cause of HUS in the present case because of the following reasons: neither anti-acute rejection therapy nor an adequate control of his blood pressure was effective in improving clinical features of HUS; hemolysis and thrombocytopenia disappeared immediately after the reduction of the dose of CYA to 50 mg/d. It has been reported that HUS carried poor prognosis only when occurring shortly after transplantation in cadaver kidney recipients. The present transplant was from a living donor and HUS occurred 21 months after transplantation and was severe enough to result in graft loss. High blood pressure might be one of the predisposing factors of HUS associated with CYA in the present case. CYA should be stopped and other alternative immunosuppressants should be given in cases of acute graft deterioration with hemolysis and thrombocytopenia, irrespective of the interval from transplantation, CYA dose, or CYA trough level.     

Tobramycin-adhesive in preventing and treating PTFE vascular graft infections

The present study was designed to determine the effectiveness of N-butyl-2-cyanoacrylate as a vehicle to deliver antibiotics locally to contaminated vascular graft sites and to grafts with established infections. Phase I--Contaminated wound model: Sixteen dogs had a 1-cm section of infrarenal aorta replaced with a PTFE graft. Prior to placement, the graft was immersed in solutions of Escherichia coli 3 X 10(8) CFU/ml and then Staphylococcus aureus 3 X 10(8) CFU/ml. After anastomosis, 1 cc of each solution was placed directly over the graft. Eleven dogs served as controls and 5 as treatment dogs. Parenteral cefonecid was given preoperatively and daily until sacrifice. Treatment animals had the anastomoses and graft sealed with a suspension of N-butyl-2-cyanoacrylate and 1.2 g tobramycin powder (antibiotic glue, ANGL) after contamination. All dogs were reoperated on the third postoperative day. Results: Eleven of 11 control dogs had positive cultures for S. aureus and 9 of 11 had positive cultures for E. coli. Seven of 11 had pseudoaneurysms, 1 exsanguinated. None of the 4 treatment dogs had positive cultures (P = 0.0002), pseudo-aneurysms (P = 0.017), or local signs of sepsis. Phase II--Infected graft model: The 10 surviving infected control dogs served as the established graft infection model. These dogs were randomized into two groups; Group 1 control (N = 5) had the graft replaced; Group 2 treatment (N = 5) had the graft replaced and ANGL treatment. Dogs were sacrificed after 2 weeks. Results: Graft cultures were positive in all 4 control dogs and negative in the 4 treatment dogs (P = 0.005). One dog in each group was eliminated secondary to failure to obtain graft culture. The data show that ANGL can be effective in the prevention and treatment of prosthetic graft infection.     

The late results of renal transplantation and the importance of chronic rejection as a cause of graft loss

The results of 279 renal transplants performed in a single centre between 1974 and 1986 are reviewed. Improvements in the management of acute rejection and a reduction in mortality have resulted in an improvement in 1-year actuarial graft survival rates from 44% for transplants performed before 1980 to 68% for those performed after 1983. After the second year post-transplant there has been a steady rate of graft failure (6% per annum), mainly due to chronic rejection. In total 52 grafts have developed chronic rejection (19% of the total and 30% of those at risk at 6 months). Chronic rejection is assuming greater relative importance as a cause of graft loss as early results improve.     

晚期移植肝功能不全的原因

总结复习晚期移植肝功能不全各方面的相关文献，综合分析肝移植术后晚期移植肝功能不全的原因。结果显示晚期移植肝功能不全是比较常见的远期并发症，其病因主要包括有排异、胆道或血管并发症、原发病的复发、感染、以及其他原因等，随着肝移植存活率的不断提高，晚期移植肝功能不全将日益受到重视。     

探讨远期移植肾丢失原因

不断提高移植肾长期存活率是移植医生与受者共同迫求的目标。过去的20年,肾移植后急性排斥反应明显减少,但远期移植肾丢失率仍维持在4％-6％。曾经将远期移植肾丢失原因主要归结于肾纤维化、药物毒性或慢性移植肾肾病,针对这些损害因素进行的治疗策略改变并未取得移植肾长期存活率的提高。以计划性移植肾穿刺活检为基础,结合实验室相关检测技术,为我们了解移植。肾丢失病因提供了技术保障。当前,特别要重视抗体介导的排斥反应、肾病复发或新发以及多瘤病毒肾病所引起的移植肾丢失。     

Titanium-coated silicone is not effective for preventing graft infection

AIM: Titanium-coated grafts for breast augmentation are available since 2001 and are used clinically. The titan surface is supposed to improve the tissue compatibility and to lower the infection rate. It was the aim of the present study to validate the antibacterial efficiency of titanium-coated silicone. MATERIAL AND METHODS: C3H/HcN mice were assigned to four different groups (n=6/group). Silicone without (group I and III) or with (group II and IV) titanium were implanted subcutaneously. Following this in groups III and IV a local contamination was induced with 2 x 10 (7) CFU/0.1 ml Staphylococcus aureus ATCC 25923. Groups I and II were not infected. 14 days after primary operation all animals were euthanized and the grafts harvested. Specimens were examined for signs of infections by macroscopy, histology and microbiology. RESULTS: In group I none of the grafts were infected (0/5). In group II (silicone, + titanium, no contamination) one infection was evident due to biting of the animal (1/6). In group III (silicone, no titanium, contamination) an infection was detected in all mice (6/6). The use of titanium, however, did not significantly reduce the infection rate in contaminated animals (group IV, 5/6). Interestingly, tissue integration of titanium-coated grafts was macroscopically reduced compared to non- titanium-coated grafts (group II vs. I). CONCLUSION: The titanium-coated silicone grafts were not effective in protecting infection in vivo. The decreased tissue integration of titanium-coated grafts, however, might reduce the rate of capsular contracture. This potential advantage of titanium needs to be validated in controlled clinical trials.     

Hydronephrosis after aorto bifemoral graft surgery: a marker for late graft complications

Ureteral obstructions are serious late complications after aortoiliac reconstructive vascular surgery, which lead to loss of kidney function if they remain untreated. One case report serves to describe the incidence, aetiology, clinical presentation and treatment options of an obstructive uropathy following graft surgery. Hydronephrosis due to a ureteral obstruction is considered as a "marker" of graft complication. Therefore, ultrasound examination and close follow-up beyond 1 year are recommended in all patients who undergo aortoiliac surgery.     

Analysis of skin-graft loss due to infection: infection-related graft loss

This prospective study was performed to analyze the causes of infection-related skin-graft loss in a general population of plastic and reconstructive surgery patients. One hundred thirty-two patients who received either full- or split-thickness skin grafts to reconstruct soft-tissue defects were included. The tissue defects were grouped according to the cause as follows: vascular ulcers (9.2%), burns (14.5%), traumatic tissue defects (36.6%), and flap donor-site defects (39.7%). In all cases, the preoperative evaluation indicated an adequate wound-bed preparation. However, graft loss secondary to infection was recorded in 31 patients (23.5%). The microbiological cultures revealed Pseudomonas aeruginosa in 58.1% of the cases (P<0.05), followed by Staphylococcus aureus, Enterobacter, enterococci, and Acinetobacter; 58.3% of grafts in vascular ulcers, 47.4% of grafts in burns, 16.7% of grafts in traumatic-tissue defects; and 13.5% of grafts in donor-site defects were lost due to infection. Vascular ulcers and burns were more commonly associated with graft losses due to infection than other tissue defects (P<0.001). No correlation was found between the etiological cause of the defects and the microorganisms cultured. However, Pseudomonas infections were more fulminant and caused an increased reoperation rate 4.2 times (P<0.05). Full-thickness grafts were more resistant to infection than split-thickness grafts (P<0.05). Graft loss due to infection was also more common in grafts applied to the lower extremities or when performed at multiple sites. In conclusion, 23.7% of skin grafts were lost due to infection in a group of general plastic surgery patients. Infection-related graft loss was more commonly encountered in vascular ulcers and burn wounds, and the most common cause was Pseudomonas aeruginosa.