Clinical experience with segmental pancreatic allografts.
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Biomedical subjects
Publications and source records attributed to M R First.
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The association of renal vein thrombosis and membranous glomerulopathy in native kidneys has been well documented. However, this association has only occasionally been described following renal transplantation. A review of 693 renal transplant recipients revealed 77 (11%) in whom persistent, heavy proteinuria (greater than 2 g/24 hr) developed. Renal histology was available in all 77 patients. A diagnosis of membranous glomerulopathy was made in 7 patients. Two further cases were added on the basis of biopsy findings--1 patient had a protein excretion of 1.7 g/24 hr, the other had microscopic hematuria and red cell casts in the urine. Renal venography was performed in 4 cases. The decision to perform venography was based on clinical criteria (thrombophlebitis or marked edema of the leg on the side of the allograft), and/or histological criteria (associated interstitial edema and venous congestion). Renal vein thrombosis was present in 2 patients. Three of the 9 patients had membranous glomerulopathy as the cause of their end-stage renal disease; 2 of these patients had received kidneys from living-related donors. Four of the patients were classified as having de novo membranous glomerulopathy on the basis of having a different cause for their end-stage renal disease. Two patients were classified as having unspecified membranous glomerulopathy; both of these patients had had chronic glomerulonephritis, but there was lack of characterization of the original glomerular disease. Seven of the 9 patients continued to have stable allograft function 1-12 months after the diagnosis of membranous glomerulopathy was made in the renal allograft. The remaining 2 patients both had associated renal vein thrombosis; 1 had progressive deterioration of renal function and returned to dialysis 24 months after the diagnosis of membranous glomerulopathy had been made, while the other died of unrelated causes 27 months after the diagnosis had been made.
A review of 693 renal transplant recipients revealed 77 (11%) in whom persistent, heavy proteinuria (greater than 2 g/24 hr) developed. Renal histology was available in all 77 patients. Twenty-one patients had received kidneys from living-related donors, the remaining 56 from cadaveric donors. The cause of proteinuria in these 77 patients was as follows: transplant glomerulopathy (30), allograft glomerulonephritis (22), chronic rejection (21), renal vein thrombosis (2), diabetic glomerulosclerosis (1), and hypertensive nephrosclerosis (1). Of the 22 patients who developed glomerulonephritis in the transplanted kidney, 6 had recurrent disease (3--membranous glomerulopathy, 2--focal sclerosis and hyalinosis, 1--membranoproliferative glomerulonephritis); 6 developed de novo glomerulonephritis; and in 10 the type of glomerulonephritis could not be classified as recurrent or as de novo because of lack of characterization of the original kidney disease. Renal vein thrombosis occurred in association with other lesions in an additional 5 cases (3--chronic rejection; 2--membranous glomerulopathy). In follow-up only 23.4% (18 of 77) of the patients maintained prolonged graft function; the majority of grafts being lost within one year of the development of persistent, heavy proteinuria. Of the 18 patients who retained their grafts, 8 had glomerulonephritis, 5 transplant glomerulopathy, and 5 chronic rejection. This study confirms the poor prognosis that has been reported with the development of nephrotic-range proteinuria in renal allograft recipients.
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Expanded polytetrafluoroethylene (PTFE) graft fistulas are widely used as secondary vascular access for patients receiving long-term hemodialysis treatment. Sixty-seven grafts were implanted in 48 patients and followed for 12 to 51 months. Cumulative patency for all grafts at 12 months was 67% +/- 6%, at 24 months 50% +/- 7%, and at 48 months 43% +/- 9%. Graft survival rates were different when considering graft configuration and location. Forearm straight graft survival at 12 months was 35% +/- 13%, upper arm curved grafts 60% +/- 19%, and forearm looped grafts 78% +/- 7%. Complications that decreased graft survival were related to thrombosis (21%), infection (25%), and intimal hyperplasia at the venous anastomosis (34%). After reviewing our experience, we believe that the challenge of secondary vascular access has not been solved by PTFE grafts. This should stimulate the search for better grafts and techniques.
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Bacterial cultures of graft perfusion fluid were taken on 514 renal perfusions during a ten-year period. A total of 22 positive cultures were found. Two sets of kidneys were discarded because of the bacteriology report. Only two possible wound infections were found that could be attributable to the preoperative contamination even though 19 of 24 patients with "contaminated" kidneys received no antibiotics. No loss of kidneys or life was found. Of the 22 contaminated perfusates, 18 (80%) originated from other institutions although only 144 (28%) of the total kidneys that were perfused came from other institutions. The majority of cultures indicated that the organisms were skin contaminants or organisms of low virulence. Microbial contamination of perfused cadaver kidneys is uncommon (1.2% in local kidneys and 9.3% in shared kidneys). Contaminated kidneys are not a major source of infection in renal transplant recipients. Kidneys that are contaminated with frequently virulent Gram-negative bacteria, such as Escherichia coli, should be discarded. Contamination of kidneys with Gram-positive organisms should not be a contraindication for transplantation, but the patients should probably be given prophylactic antibiotics.
Significant elevation of serum creatinine concentration and reduction in creatinine clearance have been reported following cotrimoxazole therapy in patients with normal and impaired renal function. Both components of co-trimoxazole, trimethoprim and sulfamethoxazole, have been proposed as the causative agent. Ten healthy male volunteers were treated for seven days with either sulfamethoxazole (5 subjects) or co-trimoxazole (5 subjects) in the usual recommended doses. After a one-week recovery period, the subjects were allocated to the alternate treatment regimen for another seven days. Cotrimoxazole caused a mean elevation in the serum creatinine concentration of 0.12 mg/dl over the base-line value (p less than 0.05). Sulfamethoxazole produced an insignificant fall in the serum creatinine level. The increase in the serum creatinine concentration induced by co-trimoxazole was reversed seven days after discontinuation of the drug. From this study, it can be concluded that either trimethoprim alone or an interaction between trimethoprim and sulfamethoxazole is responsible for the increase in serum creatinine observed following co-trimoxazole therapy and that sulfamethoxazole alone is not the causative agent.
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Wegener's granulomatosis was diagnosed in a 42-year-old female 16 years ago. From the outset there was upper respiratory, pulmonary, and renal involvement. Over the years she received varying combinations of glucocorticoids and azathioprine. Renal function deteriorated, and she was treated by hemodialysis and living related donor transplantation 9 and 10 years, respectively, after the onset of the disease. 3 months prior to transplantation, the patient had a right pneumonectomy for bronchial stenosis, bronchiectasis and repeated sepsis. 5 years' posttransplantation, she is well and has no signs of activity of original disease.
Hyperacute and renal allograft failure, whether due to rejection or other mechanisms, such as perfusion injury, is usually associated with extensive intraglomerular fibrin deposition and allograft loss. Defibrination with ancrod was used to treat a patient with hyperacute renal allograft failure and extensive glomerular fibrin deposition and necrosis. The patient's plasma had normal fibrinolytic activity but a complete absence of the ability to generate prostacyclin-like activity from rat aortic endothelium "in vitro". Treatment was associated with complete recovery of renal function, disappearance of glomerular fibrin, and restoration toward normal of glomerular structure.
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Renal transplantation and preservation techniques permit the use of vascular and microvascular surgical procedures for the reconstruction of renal vessels in situations where the size or location of involved renal vessels does not permit the application of standard in situ techniques. Six cases with renal vascular lesions were studied, one each of intimal fibromuscular hyperplasia, medial arterial fibroplasia, renal artery aneurysm, atherosclerosis, iatrogenic arteriovenous fistula, and traumatic venous laceration, that were repaired by ex vivo surgery and autotransplantation under cold storage or continuous hypothermic perfusion protection, which preserved renal tissue. We believe these techniques should be considered before nephrectomy is undertaken, especially in the patient with one kidney.
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Because of the risk of serious pneumococcal infections in patients receiving a renal transplant, a study was undertaken to determine if pneumococcal vaccine could be administered before or after transplantation. Vaccine was given to recipients of transplants and to patients who were undergoing dialysis. Both groups responded to the vaccine, and although the mean antibody levels were lower than those reported for normal populations, the levels were in the range thought to be protective for most pneumococcal types. Antibody levels, both before and after vaccination, were substantially lower in patients with recent transplants than in patients who were undergoing hemodialysis. Patients who are awaiting renal transplantation can be immunized while they are undergoing hemodialysis. Further study is needed to determine how long antibody levels will persist after vaccination in both patients undergoing hemodialysis and those receiving a transplant.
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