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  • Canafax DM
  • Torres A
  • Fryd DS
  • Heil JE
  • Strand MH
  • et al.
Transplantation. 1986 Feb;41(2):177-81 doi: 10.1097/00007890-198602000-00009.

We randomized 158 recipients of cadaver renal allografts to cyclosporine-prednisone (83) or antilymphocyte globulin-azathioprine-prednisone (75) to evaluate: the effects of immunosuppression and pretransplant risk factors on the incidence of delayed graft function, the effects of immunosuppression on the resolution of delayed graft function, and the effects of delayed graft function and pretransplanted risk factors on patient and graft survival. Cyclosporine did not increase the incidence of delayed graft function, compared with ALG-azathioprine-treated patients (33% versus 27%, P = 0.550) but doubled the mean (+/- SD) duration of oliguria (11.8 +/- 11.0 versus 5.9 +/- 3.2 days, P = 0.002) and the number of required dialyses (6.6 +/- 7.6 versus 3.2 +/- 1.3, P = 0.031). Retransplanted patients had a higher incidence of delayed graft function that recipients of primary grafts in both the cyclosporine (82% versus 25%, P = 0.001) and ALG-azathioprine (55% versus 22%, P = 0.025) treatment groups. The presence of delayed function reduced one-year graft survival from 89% in all patients without delayed function to 72% (P = 0.011) in all patients with delayed function. Cyclosporine-treated patients had a slightly, but not significantly better one-year graft survival rate than ALG-azathioprine treated patients both with (73% versus 68%, P = 0.750) and without (92% versus 82%, P = 0.069) delayed graft function. A preservation time longer than 24 hr did not increase the incidence of delayed graft function in cyclosporine-treated patients (34% versus 32%, P = 0.811) or ALG-azathioprine-treated patients (27% versus 27%, P = 0.902). Cyclosporine-treated patients given kidneys with greater than 24 hr of preservation time had reduced graft survival only when delayed graft function occurred (67% versus 92%, P = 0.009). In conclusion, (1) cyclosporine did not increase the incidence of delayed graft function over ALG-azathioprine treatment; (2) cyclosporine did significantly slow recovery of kidneys with delayed function; (3) delayed graft function correlated with poorer graft survival rate in both treatment groups; but (4) prolonged preservation time did not increase the incidence of delayed graft function or reduce graft survival.

  • Raine AEG
  • Mann JI
  • Chapman JR
  • Oliver DO
  • Morris PJ
Nephrol Dial Transplant. 1986;1(2):142.
  • Or,
  • owski T
  • Smogorzewski M
Int Urol Nephrol. 1986;18(2):205-10.
To assess the influence of ranitidine on kidney allograft function a double-blind, placebo-controlled clinical study in 42 cadaver kidney recipients has been performed. Patients received ranitidine or placebo for 1 month. Four years after transplantation 81% of the patients in the control group were alive; 67% in the control and 71% in the ranitidine group with functioning grafts. These differences were statistically not significant. However, a slightly more intensive steroid therapy was given to keep the ranitidine patients adequately immunosuppressed. Ranitidine thus can be safely used in kidney graft recipients. Because of a lack of gastrointestinal complications in both groups, no conclusions can be drawn regarding the prophylactic value of ranitidine.
  • Hirsch RL
  • Goldstein G
Dialysis Transplant. 1986;15(12):659-662.
Several studies have now demonstrated the efficacy of OKT3 in the reversal of acute renal allograft rejection. In a controlled randomized multicenter clinical trial, OKT3 was significantly more effective than high-dose steroids in reversing acute renal allograft rejection. Patients were treated with conventional high-dose steroids or with OKT3 for a mean of 14 days, with a concomitant decrease in the dosage of maintenance immunosuppression. In this study OKT3 reversed 94% of rejections. This was significantly (P = 0.006) greater than the reversal rate achieved in the steroid treatment group (75%). The early success in reversing graft rejection was reflected in the greater one- and two-year graft survival rates in the OKT3-treated population. Furthermore, in contrast to earlier reports, there were no significant differences in the rates of recurrent rejection in patients treated with OKT3 and steroids.
  • De Vecchi A
  • Tarantino A
  • Rivolta E
  • et al.,
Transplant Proc. 1986;18(5):999.
A prospective controlled trial was performed to assess the need for steroids in 51 recipients of first cadaveric kidney grafts who were given either cyclosporine (CsA) alone or associated with methylpredniolone (MP).
  • De Vecchi A
  • Tarantino A
  • Rivolta E
  • Egidi F
  • Montagnino G
  • et al.
Contrib Nephrol. 1986;51:88-90 doi: 10.1159/000413101.
  • Frascà GM
  • Vangelista A
  • Raimondi C
  • Bonomini V
  • Frasca GM
Life Support Syst. 1986 Jul-Sep;4(3):231-7.

Eighty transplanted patients were randomized to receive either a new antithrombotic agent, defibrotide (group A), or dipyridamole (group B) in addition to immunosuppressive therapy, in order to evaluate the effectiveness of these drugs in preventing graft vascular damage. While the incidence of rejection and the occurrence of specific anti-HLA antibodies were similar in the two groups, the peak serum creatinine levels during rejection were significantly lower in patients treated with defibrotide (3.3 +/- 1.8 versus 5.6 +/- 2.4 mg/dl; P less than 0.01), 97.5 per cent of whom had a still-functioning graft after a mean follow-up period of 24 months, compared with 80.5 per cent of the patients treated with dipyridamole (P less than 0.05). Graft biopsy, carried out during rejection, showed less severe vascular lesions in patients from group A than in those from group B. Our results suggest that the prophylactic administration of defibrotide may play a role in improving the long-term results of renal transplantation.

  • Orłowski T
  • Smogorzewski M
  • Orlowski T
Int Urol Nephrol. 1986;18(2):205-10 doi: 10.1007/BF02082609.

To assess the influence of ranitidine on kidney allograft function a double-blind, placebo-controlled clinical study in 42 cadaver kidney recipients has been performed. Patients received ranitidine or placebo for 1 month. Four years after transplantation 81% of the patients in the control group were alive; 67% in the control and 71% in the ranitidine group with functioning grafts. These differences were statistically not significant. However, a slightly more intensive steroid therapy was given to keep the ranitidine patients adequately immunosuppressed. Ranitidine thus can be safely used in kidney graft recipients. Because of a lack of gastrointestinal complications in both groups, no conclusions can be drawn regarding the prophylactic value of ranitidine.

  • Spielberger M
  • Schmid T
  • Aigner F
  • et al.,
Nieren Hochdruckkr. 1986;15(4).
Between Dec. 1st, 1980 and Dec. 31, 1982 a total of 173 cadaveric renal allografts were performed at our institution. Sixty-eight of the recipients were treated with CyA and 105 with conventional immunosuppression (CI). Most, although not all, of the patients were entered in various random trials. However, these groups were comparable as far as age, sex, preoperative blood transfusions, HLA-AB and -DR mismatches are concerned. CyA was given to 18 patients as the sole immunosuppressive agent; all the others received CyA + corticosteroide for various periods of time. Patient survival at 4 years was 94% in the CyA group as compared to 84% (p < 0.005) in the conventionally treated group. Actuarial graft survival at 4 years was found to be 84% in the CyA group in contrast to 42% in the CI group (p < 0.001). After 4 years, mean creatinine levels in the CyA group were 2.31 mg% in comparison to 2.27 mg% in the control group. While transaminases and bilirubin remained normal throughout the whole observation time alkaline phosphatase became abnormal within the first six months but normalized spontaneously thereafter. Interestingly, the same observation was made in the CI group. The mean CyA dose given was 5.61 mg/kg after three and 3.8 mg/kg after four years.
  • Ponticelli C
  • Minetti L
  • Quarto di Palo F
  • et al.,
Transplant Proc. 1986;18(5):1246-1247.