Significance of anticardiolipin antibodies on short- and long-term allograft survival and function following kidney transplantation.
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Epoetin treatment of renal anemia has been practiced in Slovenia since 1988. More than 90% of hemodialysis patients and 83% of peritoneal dialysis patients have been treated with epoetin. Epoetin has also been available for patients with renal anemia in the pre-dialysis period and for those with a failing kidney allograft. Although epoetin treatment did not accelerate the worsening of native kidney function or allograft function, intensified antihypertensive treatment was required in kidney graft recipients. In patients on peritoneal dialysis, hypervolemia had a greater effect on hypertension than did epoetin treatment. Epoetin resistance was connected with C-reactive peptide cryptorchidism, intact parathyroid hormone, and treatment with angiotensin-converting enzyme inhibitors. In hemodialysis patients, lower doses of epoetin were required for patients receiving low molecular heparin and those with lower iPTH. Epoetin alpha, epoetin beta and epoetin omega seemed to be effective and safe in the treatment of renal anemia. In the past 2 years, epoetins were administered to hemodialysis patients only intravenously.
The phagocytic capacity of the reticuloendothelial system (R.E.S.) was assessed in patients with chronic renal failure and in renal transplant recipients. R.E.S. phagocytosis was increased in the former group. Soon after transplantation R.E.S. phagocytosis was moderately reduced (through levels were comparable with those of normal controls) but was particularly reduced after high-dose corticosteroid treatment for rejection. In long-term allograft recipients R.E.S. phagocytosis was also depressed though steroid maintenance doses were small.
We present the histological findings of an extensor mechanism allograft which was used in a total knee arthroplasty two years after implantation. Analysis of the graft was undertaken at four distinct anatomical levels and it was found to be incorporated into host tissue at each level. A wedge of fibrinoid necrosis, probably related to impingement of the graft on the tibial polyethylene insert, was seen. Impingement may play a role in the injury and necrosis of an allograft and may be one mode of failure in an extensor mechanism allograft.
We present a case of 29-year-old female who underwent an ABO-incompatible living kidney transplantation from her father. The serum creatinine (s-Cr) level of this patient was stabilized about 1.1-1.2 mg/dl during the first 3 months after the transplantation. Thereafter, the function of allograft was deteriorated gradually. A biopsy performed on post-transplant day (PTD) 520 to evaluate a rise in creatinine revealed an interstitial nephritis and chronic renal allograft nephropathy. The renal function worsened persistently, although we increased the dosage of immunosuppressant subsequently. The following biopsy performed on PTD 630 showed a suspicion of BK virus nephropathy, with a mass of tubular epithelial nuclear inclusions and an interstitial nephritis. The diagnosis of BK virus nephropathy was confirmed on the immunohistochemistry staining using anti-SV40 antibody and PCR analysis. Despite reducing the immunosuppressants, the function of the allograft worsened progressively and was lost on PTD 912.
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To study the effectiveness and nephrotoxic side-effects of cyclosporin A (CsA) in renal transplant recipients, a prospective randomised trial was designed to compare CsA with azathioprine (Aza). Each treatment group consisted of 40 patients; in the CsA group, 18 were randomly selected for conversion to Aza after 3 months. The 1-year graft survival for CsA-treated patients was 87% compared with 66% for the Aza group (P = 0.033). Anti-rejection therapy was administrated to 78% of the patients in the Aza group and 47% of those in the CsA group (P less than 0.01). There was no difference in the incidence of primary non-functioning kidneys, cytomegalovirus infections, hypertension, or degree of proteinuria between the two treatment groups. At 3 months the mean creatinine clearance was 42 +/- 2 ml/min (mean +/- SEM) for the CsA group compared with 56 +/- 4 ml/min for the Aza group (P less than 0.01), whereas the mean creatinine clearances at 6 months for both the converted and the non-converted CsA-treated patients did not differ from that found in the Aza-treated group. At 1 year, the mean creatinine clearance for CsA-treated patients who were converted to Aza was higher than that found for Aza-treated patients (62 +/- 7 vs 50 +/- 6 ml/min; P less than 0.05). Furthermore, the increment in creatinine clearance observed after conversion from CsA to Aza at 3 months showed a linear relationship (r = 0.9061) with the CsA trough levels before discontinuation of the drug. This indicates that CsA treatment induces a dose-dependent, nephrotoxic side-effect which is probably reversible.
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