Can acute cellular rejection occur 27 years after a successful renal transplant?
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R B Baltzan.
Explore the source record for details and available documents.
Forty patients with end-stage chronic renal failure received living donor renal grafts, matched at more than 1 HLA haplotype, over the last 25 years. Of these grafts, 33 were first and 7 were second grafts. All recipients received prophylactic corticosteroids. Thirty-four also received prophylactic azathioprine, and 6, prophylactic cyclosporine. Acute rejection occurred in 65% (11/17) of non-cyclosporine treated grafts when the recipient was given 5 or fewer units of blood preoperatively, but in only 18% (3/17) when more than 5 units were given. High-dose steroid therapy reversed the acute rejection each time. Chronic rejection occurred in 2 grafts. Irreversible rejection did not occur in any second graft. Chronic glomerulonephritis, possibly due to recurrent disease, occurred in 1 graft. Five grafts have been lost, 1 each from technical and immunosuppressive complications, and 3 from incidental death. The 1-year actuarial graft survival rate is 95% and the 10-year rate 84%. All surviving patients lead normal lives without significant health restriction, and employ minimal medication. It is postulated that: 1) acute cellular rejection is HLA-independent, and chronic rejection is HLA-dependent, and 2) hyperacute and chronic rejection are related and are parts of a spectrum of humoral immunity.
A case of bilateral traumatic renal artery thrombosis involving three renal arteries is presented. Four other cases of this entity are summarized for comparison. The recommended course of investigation is outlined, and the urgency of immediate surgical intervention is emphasized.
Seven of 74 patients with early functioning cadaveric renal homografts developed acute oliguric renal failure after the second but before the ninth day post-transplantation. The syndrome characteristically begins with an abrupt and simultaneous decrease in creatinine clearance, urine volume and urine sodium concentration. After a variable period and despite a reduction in immunosuppressive therapy, a diuretic phase ensues and renal function is restored. Complications associated with the syndrome include groin hematoma, pulmonary edema and renal rupture with shock. Renal rupture does not require nephrectomy: if the hemorrhage is controlled, the transplanted organ will resume function. Angiographic studies show normal nephrograms, stretched arterial vasculature and filling defects in the veins. Percutaneous renal biopsy shows interstitial edema and hemorrhage, venous congestion and tubular necrosis. Evidence is presented to support the hypothesis that this is a form of rejection occurring as the result of injury to the renal venous system.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cadaveric renal transplantation was found to be potentially applicable to 80% of a uremic population as observed over a six-year period. Death prior to presentation of a donor kidney occurred in 25%, 40% have received transplants and 15% are awaiting transplantation. Transplantation resulted in restoration of near normal renal function and homograft survival rates of 45% at one year, 40% at two years and 17% at four years. Failure of the therapeutic procedure resulted more often from death of the patient than from failure of the donor organ. Patient death was most frequently ascribed to complications of the immunosuppressive therapy, but cardiovascular accidents were also a significant cause. Early renal failure was due to hyperacute or acute rejection, while the cause of late renal failure remains unproved. Re-transplantation was effective treatment for late failure and, as a result, the four-year patient survival is nearly 40% compared to four-year initial kidney survival of 17%.
Six cases of edema, three due to the nephrotic syndrome, one to congestive heart failure and two to chronic renal failure, are reported in which furosemide was administered in oral doses higher than those usually prescribed (up to 720 mg. a day), in order to obtain a satisfactory diuresis. In one case of severe prerenal failure secondary to cardiogenic shock and in one case of acute tubular necrosis secondary to hypotension at the time of operation, intravenous doses up to 990 and 1400 mg. per day respectively were able to reverse the oliguria. In eight additional patients who were on chronic hemodialysis, furosemide was administered to the amount of 1000 mg. per day orally in divided doses for two weeks, and produced a moderate diuretic response.The use of high doses of furosemide in edema and renal failure resistant to the usual therapeutic measures appears to be safe and effective.
Explore the source record for details and available documents.
Sixteen patients with renal cadaveric allografts who have survived for one year or longer are reported. The patients were analyzed from the standpoint of incidence, quantity and course of proteinuria in relation to renal function and the nature of the original disease.This analysis shows that proteinuria is progressive and is accompanied by a decline in renal function when the original disease is of an immune nature. This was not so in patients with non-immune original disease. These findings suggest that recurrence of original disease plays an important role in late failure of cadaveric renal allografts.
Explore the source record for details and available documents.