To improve our understanding of posttransplant infections, we analyzed bacterial, viral, fungal, parasitic, and other infections in 604 consecutive recipients of kidney (n = 518), kidney-pancreas (n = 82), kidney-liver (n = 3), or kidney-islet (n = 1) allografts (355 cadaveric, 14 living-unrelated, 235 living-related donors) who also received cyclosporine, azathioprine, and prednisone immunosuppression. Recipients of cadaveric grafts received additional induction immunosuppression (antilymphocyte globulin or murine monoclonal antibody OKT3). Rejection episodes were treated with high-dose steroids, and either antilymphocyte globulin or OKT3 was administered when clinically indicated. Perioperative antibiotics and posttransplant prophylactic acyclovir sodium or ganciclovir sodium, trimethoprim-sulfamethoxazole, and clotrimazole or nystatin (Mycostatin) were administered to all recipients. Two hundred thirteen patients (35.3%) were found to have had no identifiable infections, while 391 (64.7%) had either isolated bacterial (97 [16.1%]), viral (53 [8.8%]), or fungal (34 [5.6%]) infections or combination (concurrent or sequential) infections with bacterial plus viral (46 [7.6%]), bacterial plus fungal (66 [10.9%]), viral plus fungal (20 [3.3%]), bacterial plus viral plus fungal (64 [10.6%]), or bacterial plus viral plus fungal plus parasitic (11 [1.8%]) pathogens in the posttransplantation period. Renal allograft survival (percentage, actuarial method) was diminished in patients with infections at both 1 year (91% vs 83%) and 3 years (81% vs 76%) after transplantation, as was actuarial patient survival (1 year, 97% vs 92%; 3 years, 93% vs 88%). We conclude that infection remains a major cause of both patient demise and allograft loss following successful solid-organ transplantation.

Based upon these data and a review of the literature, it can be concluded that the risk of recurrence of HUS in the allograft is confined almost entirely to patients with atypical forms of HUS.

No abstract

Anticoagulation after implantation of a bioprosthetic heart valve has been suggested during a high-risk period of 3 months following surgery. There is little information available concerning the risk of thromboembolism during this period if anticoagulation is not carried out. However, this is of interest since 60-80% of all bleeding complications due to anticoagulation occur during the first year of treatment. Between 1983 and 1993, 57 of our patients did not receive oral anticoagulation after implantation of a bioprothesis in the aortic position (49 Hancock, 7 Mitroflow and one Edwards stentless). All patients were investigated retrospectively. A risk for thromboembolic complications of 1.75% is calculated for the first six months following surgery, being 3.5 per 100 patients/year. There seems to be no advantage in standard anticoagulation (INR 2.5-4) with its risk of serious bleeding complications of about 4% during this period of treatment. Low-dose anticoagulation (INR 2.0-2.3), however, preferably in combination with prothrombin estimation by the patients, seems to offer a relatively safe treatment for these patients.