Fifty-four patients who received a renal allograft between October 1971 and October 1974 were followed prospectively to correlate pretransplant serum antibody to cytomegalovirus (CMV) with shedding of CMV following transplantation. Twenty-five of 54 patients had antibody demonstrable to CMV using immunofluorescent techniques, but only 20 of 54 using complement-fixing techniques. All 24 who had antibody and survived one month or longer, and seven of nine without antibody but who received a kidney from a seropositive donor shed virus after transplantation, whereas none of 12 individuals without antibody and who received a kidney from a seronegative donor (P less than 0.005) shed virus. Three of eight other seronegative patients for whom donor sera were not available for analysis shed virus. Viremia occurred in eight of ten individuals who developed new antibody after transplantation, versus seven of 24 with antibody prior to transplant (P less than 0.02), and virus shedding in seroconverters from other sites was significantly more persistent than in pretransplant antibody-positive patients. Thus, CMV infection was due either to reactivation of latent infection or was transmitted along with the renal allograft and manifested as a primary infection.
To investigate whether hypoxia extends into the post-hemodialysis period, nine clinically stable-end stage renal disease patients were dialyzed against bicarbonate and one against an acetate batch, all with bioincompatible dialyzers. None had clinical evidence of cardiopulmonary overload on the day of the study. Using an oximeter with internal memory, oxygen saturation was monitored continuously at the beginning, during, and for four hours after hemodialysis. Hypoxia was defined as oxygen saturation less than 85%. Three patients had no hypoxia during or after dialysis. Hypoxia occurred in five patients both during and after dialysis, and in two patients only in the post-dialysis period. Episodes of hypoxia were of longer duration and severity in post-dialysis period. We conclude that significant hypoxia can occur in the post-hemodialysis period.
From May 1977 to June 1983, 198 patients were accepted as candidates for renal transplantation at our university. We review our experience with 14 consecutive patients who underwent selective pre-transplant nephrectomy during this interval. Indications for this procedure included recurrent or chronic pyelonephritis, structural abnormalities of the urinary tract predisposing the patient to infection, malignant or renin-dependent hypertension, Goodpasture's disease, certain cases of rapidly progressive glomerulonephritis and selected patients with polycystic kidneys. All patients underwent dialysis 1 day preoperatively. Perioperative fluid losses were measured carefully with prompt and vigorous replacement therapy. Patients received an average of 5,890 cc fluid replacement before postoperative dialysis. All patients underwent dialysis within 29 hours postoperatively. There were no postoperative deaths and 8 complications. Selective pre-transplant nephrectomy has spared 93 per cent of potential renal transplant candidates from a major surgical procedure. No patient has required removal of the original kidneys during the post-transplant period. Our experience has shown that the reluctance to hydrate these patients is unwarranted and that prompt postoperative dialysis, if required, is safe. Since some end stage kidneys are physiologically active and the associated surgical risk is high, pre-transplant nephrectomy should be performed only in carefully selected patients. In contrast to previous reports, which advocated minimal fluid administration and delayed postoperative dialysis, our recent experience indicates that vigorous fluid replacement therapy, carefully monitored with serial vital signs, weights, serum electrolytes and central venous pressure readings, will avert many of the complications encountered previously.
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