Improved graft survival in 100 retransplant recipients following AHG-negative crossmatching.
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Biomedical subjects
Publications and source records attributed to R M Lewis.
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Until late in gestation, fetal spontaneously hypertensive rat (SHR) is growth retarded. Fetal growth rate increases after placental hypertrophy occurs between fetal days 18 and 20. The increase in placental mass may result in improved transfer of macro nutrients to the fetus and thus stimulate growth. In this study, fetal and placental uptake of the glucose analog 3-O-methyl glucose (3MG) and the amino acid analog amino-isobutyric acid (AIB) from the maternal circulation were compared in the SHR and Wistar-Kyoto (WKY) on days 16, 20 and 22 of gestation. Placental 3MG uptake (d/min/g tissue wet weight) was decreased in the SHR on days 20 and 22 but no differences were observed in fetal 3MG uptake. Increased placental mass in the SHR meant that total placental 3MG uptake was greater in the SHR. Placental uptake of AIB (d/min/g tissue wet weight) was much lower in the SHR (on days 16, 20 and 22) and the decrease was not compensated for by increased placental mass. Fetal uptake of AIB was decreased on days 20 and 22 (P<0.05). AIB uptake (d/min/g tissue wet weight) by the carcass and the internal organs (brain, heart, kidney, liver and lung) was also lower in the SHR. These findings indicate that although fetal growth in the SHR increases rapidly in late gestation following placental hypertrophy, it does so despite a pronounced deficit in amino acid uptake.
Monocytes play a central role in protection against many viruses. In some infections they are target cells for viral replication. There is increasing evidence that these cells may also be important in regulation of hemostasis. The part played by monocytic cells in the pathogenesis of hemorrhage in the viral hemorrhagic fevers is presently uncertain. Monocytes and monocytic cell lines have been used to investigate the ability of viruses to infect these cells in vitro. Several factors may affect the ability of a particular virus to infect monocytic cells, including specific antiserum to virus and the degree of cellular maturation. The effect of cellular maturation on the replication of Rift Valley fever virus in the U937 cell line is discussed in light of studies on the infectivity of other viruses for monocytic cells. Data supporting the ability of specific antibody to enhance the infectivity of Pichinde virus and Lassa fever virus for U937 cells are presented.
The effect of experimentally induced cystitis and iatrogenic blood contamination on the urine protein/creatinine ratio (U P/C) was evaluated in 17 dogs. Before they were included in the study, all dogs were judged to be healthy on the basis of physical examination, serum concentrations of urea nitrogen and creatinine, complete urinalysis, and a U P/C less than 0.4. A single urine sample was contaminated with increasing quantities of canine fresh whole blood (PCV = 42%; total protein = 6.2 g/dl). When added blood was equal to or greater than 25% of the total urine sample volume, the U P/C exceeded 3.5, a finding consistent with nephrotic range proteinuria. When added blood was 10% of the total urine sample volume, the U P/C was less than 1.8. Eleven Beagles underwent routine laparotomy during which a cystotomy was done. The median U P/Cs on postoperative days 1 and 2 were significantly increased compared with preoperative values (P less than 0.05); no U P/C exceeded 2.0. Renal biopsies performed on postoperative day 3 eliminated renal proteinuria as a source of urine protein. Five dogs had bacterial cystitis experimentally induced. At 72 and 96 hours after bacterial inoculation, the median U P/Cs were significantly increased (P less than 0.05); individual values ranged from 1.5 to 40.8. Renal biopsies performed between 5 and 6 days after inoculation eliminated renal proteinuria as a source of urine protein. Cytologic evaluation of urine sediment in each group did not correlate with the magnitude of the increase in the U P/C. The U P/C significantly increased in each model of lower urinary tract inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)
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Aggregate analyses of the impact of long-term cyclosporine administration in kidney transplant recipients have reported generally impaired but stable allograft function. In contrast, experience in extrarenal transplantation has suggested that treatment with cyclosporine for periods in excess of 12 months causes a progressive native nephropathy often leading to dialysis dependence. The extent of this apparent discrepancy between native kidneys and renal allografts is the subject of this study, which examines the evolution of renal function in 119 kidney and 100 heart transplant recipients receiving 12 or more months of cyclosporine immunosuppressive therapy administered in uniform protocols by affiliated clinical transplantation programs. The evolution of renal function in both study cohorts was analyzed retrospectively on the basis of serial serum creatinine (Crs) determinations. Assessment of group mean Crs, reciprocal Crs (1/Crs), and slopes of the curves obtained by plotting 1/Crs versus time in individual patients revealed a significant decline of native kidney function over the first 6 posttransplant months in the cardiac allograft group. Thereafter, however, native kidney function stabilized in these patients, and the aggregate trend was suggestive of no further decline in function over a 3- to 4-year follow-up period. Kidney transplant recipients had an aggregate trend of slowly declining allograft function consistent with the effects of chronic immunologic injury. The data were not consistent with a uniform pattern of a progressive, cyclosporine-induced loss of renal function in either cohort. Long-term use of cyclosporine was found to be associated with impaired but generally stable aggregate renal function in both the heart and the kidney transplant cohorts.(ABSTRACT TRUNCATED AT 250 WORDS)
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Although long-term use of cyclosporine has been implicated in the pathogenesis of arteriolar hyalinosis, interstitial fibrosis, and glomerulosclerosis observed in the native kidneys of heart transplant recipients, it is not clear that these histologic abnormalities are entirely specific for a drug-induced toxic nephropathy. The purpose of this study was to determine whether long-standing congestive heart failure, particularly when complicated by disease processes such as atherosclerosis and hypertension, may independently predispose to the development of similar renal histopathology. Records and specimens were selected from autopsy files for evaluation of clinical profiles and kidney histology in 16 patients who died of end-stage cardiomyopathy of varying causes without having recourse to heart transplantation. The study cohort consisted of 12 men and four women. Cardiomyopathies were the result of coronary artery disease in six patients and nonischemic causes in the other 10 patients. The mean age at the time of death was 53 +/- 3 years (range 28 to 74 years). Thirteen (81%) of 16 patients had a history of hypertension. Nadir serum creatinine concentrations during the month before death were 1.7 +/- 0.2 mg/dl (range 1.2 to 3.5 mg/dl). Interstitial fibrosis, tubular atrophy, and glomerulosclerosis were present in 15 (94%) of 16 patients. Arteriosclerosis and arteriolosclerosis were found in 13 (81%) of 16 and 14 (88%) of 16 patients, respectively. A nodular pattern of arteriolar hyalinosis was observed in two patients with ischemic disease.(ABSTRACT TRUNCATED AT 250 WORDS)