Up to now one of the major problems for successful organ transplantation has been the reaction of the immune system of the recipient against the donor organ. This could lead to acute and chronic rejection, and in cases of unsuccessful treatment to the loss of the transplant. In organ graft recipients, immunosuppressive agents are used to prevent or treat rejection episodes and to maintain graft function. Although there is an increasing number of immunosuppressive substances, the immunosuppressive therapy currently in use is relatively unspecific and targets many immunological functions. The net state of immunosuppression is a complex function determined by the interaction of a number of factors, the most important of these are the dose, duration and temporal sequence in which immunosuppressive drugs are employed. Any kind of immunosuppressive protocol is thus associated with an increased infection rate. This has an important socioecological impact, because frequent hospitalizations resulting from infectious complications are necessary, having an overall mortality rate of 3.5% within 2 weeks of admission. The most common cause of septicaemia is urinary tract infection. Frequent urinary tract infections are associated with the early onset of chronic rejection, suggesting a pathogenetic relationship between these two features. The occurrence of chronic rejection has led to reduced transplant survival. The prevention of urinary tract infections, or the early diagnosis and accurate treatment of urinary tract infections is important in renal transplant recipients.

Rapamycin is a new immunosuppressive agent approved for maintenance therapy after kidney transplantation. It may allow calcineurin-inhibitor-free, non-nephrotoxic immunosuppression. We report, however, on four kidney-transplant recipients who developed post-transplantation glomerulonephritis after conversion from a calcineurin-inhibitor-based immunosuppression to rapamycin. In all four patients nephrotic-range proteinuria occurred 2-9 months after conversion to rapamycin. Renal biopsy confirmed membrano-proliferative glomerulonephritis type 1 in one case, membranous glomerulonephritis in another and IgA-nephropathy in two cases, respectively. Calcineurin-inhibitor-based immunosuppression was reintroduced and resulted in complete remission of proteinuria and in stabilised renal function in all patients. We conclude that in the case of rapamycin-associated post-transplantation glomerulonephritis an attempt should be made to replace rapamycin by a calcineurin inhibitor.

Administration of iopromide did not lead to a persistent decline of residual renal function in CAPD patients. Nevertheless, non-ionic hypo-osmolar CM should be given to these patients with the lowest possible dose and only if there is a real clinical indication.

Rapamycin is a new immunosuppressive agent approved for maintenance therapy after kidney transplantation. It may allow calcineurin-inhibitor-free, nonnephrotoxic immunosuppression. We report, however, on four kidneytransplant recipients who developed post-transplantation glomerulonephritis after conversion from a calcineurin-inhibitor-based immunosuppression to rapamycin. In all four patients nephrotic-range proteinuria occurred 2-9 months after conversion to rapamycin. Renal biopsy confirmed membrano-proliferative glomerulonephritis type 1 in one case, membranous glomerulonephritis in another and IgA-nephropathy in two cases, respectively. Calcineurin-inhibitorbased immunosuppression was reintroduced and resulted in complete remission of proteinuria and in stabilised renal function in all patients. We conclude that in the case of rapamycin-associated post-transplantation glomerulonephritis an attempt should be made to replace rapamycin by a calcineurin inhibitor.

Background: During pregnancy, familial hyperlipidemia or systemic lupus erythematosus (SLE) can exacerbate having devastating consequences for both mother and fetus. Immunoadsorption is established for removal of pathogenic proteins lipoproteins or autoantibodies, but this procedure has only rarely been used in pregnancy. Methods: We evaluated retrospectively 126 extracorporeal treatments during six pregnancies. Forty low-density lipoprotein immunoadsorptions, 6 sole plasma exchanges and 36 combined procedures (plasma exchange followed by immunoadsorption) were performed for severe hypertriglyceridemia, complicated by acute pancreatitis. Forty-four IgG immunoadsorptions were executed in 2 pregnant women suffering from SLE with a disastrous course during prior pregnancies. Results: In hyperlipidemic pregnant women, mean triglyceride levels prior to treatment were 3,841 ± 2,076 mg/dl (mean ± SD) and total cholesterol was 617 ± 354 mg/dl. Until delivery, a 27% reduction of triglycerides could be achieved. Clinical and serological signs of pancreatitis disappeared after initiation of extracorporeal therapy. Four healthy babies were delivered (birthweights between 2,250 and 3,360 g). In 1 woman suffering from SLE, intrauterine fetal death occurred in the 22nd week of gestation despite a reduction of cardiolipin antibodies by 69%. The second case (a twin pregnancy) was complicated by steroid-resistant antibody-mediated anemia. Due to frequent immunoadsorptions, red blood cell count improved (reduction of antierythrocyte antibodies by 66.6%) and 2 healthy babies (birthweights 2,120 and 2,350 g) were delivered by cesarean section. Conclusion: Long-term antibody-based immunoadsorption has been demonstrated to be safe and well tolerated in pregnant women and enables normal intrauterine/fetal development. Although rarely indicated during pregnancy, this treatment modality might be a promising new technique for removal of autoantibodies and lipoproteins in patients with serious gestational complications without sufficient response to conventional therapy.