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      Impact of Different Immunosuppressive Regimens on Antigen-Presenting Blood Cells in Kidney Transplant Patients

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          Background: Alloantigen-specific and unspecific immune processes contribute to chronic renal graft dysfunction. Despite ‘optimized immunosuppressive therapy’ (IS), the role of chronic cell activation still remains open. Methods: 69 kidney transplant recipients (NTX) were assessed for monocyte surface antigens CD14 (LPS receptor) and CD16 (Fc-γ-III receptor) by flow cytometry including the percentage amount of the proinflammatory CD14+CD16+ subset. 14 non-dialysis patients with chronic renal failure (CRF) and 24 healthy persons served as controls. Results: All 14 patients suffering from CRF revealed higher CRP serum levels compared to healthy controls (p = 0.01). NTX patients had a (not significant) tendency to higher CRP concentrations (p > 0.05). The mean expression of CD14 on monocytes (mCD14) was lower in patients with CRF and in NTX patients (p = 0.024 – p = 0.026). NTX patients revealed low expression of monocytic CD14 with no difference between the single IS therapy groups. The proinflammatory monocyte subpopulation positive for CD14 and CD16 was elevated both in uremic and NTX patients (p < 0.002), despite long-lasting IS therapy. Conclusions: Continuing IS therapy, even under ‘optimized’ drug-monitoring conditions, does not sufficiently prevent or suppress a microinflammatory (and potential fibrotic growth-promoting) status in NTX patients.

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          Most cited references 5

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          Strategies to improve long-term outcomes after renal transplantation.

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            Risk of renal allograft loss from recurrent glomerulonephritis.

            Recurrent glomerulonephritis is a known cause of renal allograft loss; however, the incidence of this complication is poorly defined. We determined the incidence, timing, and relative importance of allograft loss due to the recurrence of glomerulonephritis. A total of 1505 patients with biopsy-proved glomerulonephritis received a primary renal transplant in Australia from 1988 through 1997. Recurrence was confirmed by renal biopsy. The Kaplan-Meier method was used to estimate the 10-year incidence of allograft failure due to recurrent glomerulonephritis, and this incidence was compared with the incidence of acute rejection, chronic rejection, and death with a functioning allograft. Characteristics of the recipients and donors were examined as potential predictors of recurrence. Allograft loss due to the recurrence of glomerulonephritis occurred in 52 recipients, with a 10-year incidence of 8.4 percent (95 percent confidence interval, 5.9 to 12.0). The type of glomerulonephritis, the sex of the recipient, and the peak level of panel-reactive antibodies were independent predictors of the risk of recurrence. Recurrence was the third most frequent cause of allograft loss at 10 years, after chronic rejection and death with a functioning allograft. Despite the effect of recurrence, the overall 10-year incidence of allograft loss was similar among transplant recipients with biopsy-proved glomerulonephritis and among those with other causes of renal failure (45.4 percent [95 percent confidence interval, 40.9 to 50.2] vs. 45.8 percent [95 percent confidence interval, 42.3 to 49.3], P=0.09). Recurrence is an important cause of allograft loss for those with renal failure due to glomerulonephritis. No risk factors for recurrence were identified that warrant altering the approach to transplantation. However, accurate estimates of risk can now be provided to potential recipients of renal allografts.
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              Challenges to achieving clinical transplantation tolerance


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                April 2004
                12 August 2004
                : 27
                : 3
                : 177-180
                Städt. Krankenhaus München-Harlaching, 2. Med. Abteilung, Sanatoriumsplatz 2, and KfH-Nierenzentrum München-Süd, München, Deutschland
                79807 Kidney Blood Press Res 2004;27:177–180
                © 2004 S. Karger AG, Basel

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                Figures: 1, Tables: 1, References: 13, Pages: 4
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