Secondary vascular access for hemodialysis.
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Biomedical subjects
Publications and source records attributed to M R First.
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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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Because of the recent licensing of pneumococcal vaccine, the risk of pneumococcal infections on a renal transplant service was determined. The overall risk of infection was 7% (14 of 197 patients) over a six-year period, or 1% per year. In patients with functioning allografts, this represented a risk of 28 infections per 1,000 patient-years of follow-up. Clinically, the major presentations of pneumococcal infection were pneumonia in the patient who was rejecting his kidney and pneumococcemia of sudden onset that was often fatal. Five of the pneumococci isolated from bacteremic patients were typed; three of the isolates were types that are in the vaccine. The frequency and seriousness of pneumococcal infections in renal transplant patients suggest that pneumococcal vaccine should be given to these patients, probably before transplantation.
After renal transplantation low urinary sodium concentration (UNa) has been used to diagnose acute rejection (AR), for the early phase of AR is often associated with reduced renal perfusion. Early postoperative graft failure without low UNa favors the diagnosis of ischemic tubular damage (ATN). As fractional excretion of filtered sodium (FENa) better reflects glomerulotubular balance in renal sodium handling, FENa was analyzed during the first 2 weeks in 118 renal allografts. From data on 41 transplants with good early renal function (GEF), a temporal profile of FENa was obtained and used to evaluate the behavior of FENa by means of standardized FENa (Z score). Individual subjects followed their own profile with a small deviation (delta Z less than 1.4 for 2 days). In 31 instances, acute rejection was diagnosed. In 14 with AR, the Z score deviated little; 2 responded to methylprednisolone given intravenously. In 17 with AR, the Z score fell significantly (delta Z greater than 1.5 for 2 days), an average of 2.6 days before the first rise in serum creatinine concentration; 15 responded to treatment. The difference between these two groups was significant (P less than 0.001). This functional heterogeneity and different responses to treatment may indicate different immunologic mechanisms which damage different target cells in the graft in AR. In 46 patients with acute tubular necrosis after cadaver kidney transplantation FENa was significantly higher than it was in the GEF group as early as the first posttransplantation day and approached normal as the renal function recovered. This behavior of FENa was clearly different from that in AR.
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Heavy proteinuria and/or the nephrotic syndrome rarely occur late in pregnancy. We report the clinical and renal biopsy findings on 11 patients with the nephrotic syndrome occurring during pregnancy in whom light and electron microscopic findings were characteristic of pre-eclampsia. Immunofluorescent microscopy revealed deposits of IgG, IgM, IgA, beta 1C globulin, and fibrinogen, predominantly in the subendothelial position. Only two patients were primigravid; three were in their second or third pregnancy; in six, pre-eclampsia first occurred in the fourth to eighth pregnancy. Clinical abnormalities appeared first between the 23rd and 39th week of gestation. All patients had marked elevation of blood pressure and of serum uric acid levels. Of the 12 infants, eight were alive and well, including one set of twins; four were stillborn. Following delivery, clinical resolution was similar to that in less severe pre-eclampsia. The findings suggest the possible importance of the role of intravascular coagulation in the genesis of pre-eclampsia.
Forty-six episodes of pulmonary infection occurred in 41 patients during a seven year period in which 187 renal transplants were performed in 168 patients. Thirty-seven episodes followed 152 cadaveric transplants (24.39%), and four episodes followed 35 living related donor transplants (11.4%). Five patients had two episodes of pulmonary infection. Twenty-four patients recovered, and 17 died (41.5%). Pulmonary infections appeared from two days to three years after transplantation, but predominated in the first four months (32/46). They were caused primarily by bacterial agents (74%) with protozoa, fungi, and viruses appearing less frequently. In 35 episodes, a single etiologic agent was found, but 11 were caused by two or more agents. When compared with noninfected recipients, there was no significant difference with regard to number of rejection crises, maintenance prednisone dosage, or blood glucose. However, subnormal renal function was significantly associated with the development of infection. Azathioprine dosages were actually higher for the noninfected patients, reflecting a tendency to lower the dose of azathioprine in the presence of decreased renal function. Fever was the most common presenting symptom. Transtracheal aspiration with Gram stain and direct sensitivity plating routinely provided early and accurate identification of the organism and a guide for therapy in bacterial infections. Pulmonary infection in renal transplant recipients is associated with a high mortality rate. Early diagnosis and specific treatment are essential to successful management.
A prospective study of 15 patients who received renal transplants defined the effect of renal transplantation on the cellular immune response to cytomegalovirus infection. Of 15 patients, 14 developed cytomegalovirus infection, usually in the first 2 months after transplantation, and all infections were accompanied by a normal humoral immune response. After the initiation of immunosuppressive therapy and transplantation, there was a general depression of lymphocyte transformation, as reflected in the response to phytohemagglutinin, accompanied by a specific defect in cellular immunity, as indicated by lymphocyte transformation to cytomegalovirus antigen. Eleven patients had cellular immunity to cytomegalovirus before transplantation, and all of these became negative in the first month after transplantation. In subsequent months, only 6 of the 14 study patients with cytomegalovirus infection developed specific cellular immune responses to cytomegalovirus. This occurred most often in patients who had severe febrile illnesses in association with infection. The specific cellular immune response which developed in the posttransplant period did not persist in three of the patients. This study demonstrates the dissociation of the humoral and cellular immune response to cytomegalovirus infection in renal transplant patients and indicates the importance of the loss of cellular immunity in the appearance of infection. Previously infected patients lost their cell-mediated immunity and had reactivation infections despite the presence of serum antibody.