Improved graft survival in 100 retransplant recipients following AHG-negative crossmatching.
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Biomedical subjects
Publications and source records attributed to R H Kerman.
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The glomerular ultrastructure was retrospectively reviewed from 45 renal transplant biopsies with the clinical and light microscopic diagnosis of acute rejection (25 cases) and chronic rejection (20 cases). Three grades of morphologic alteration were ultrastructurally defined. In acute rejection, capillary lumenal obliteration with endothelial cell hypertrophy and cellular infiltration were interpreted as the local glomerular expression of the endothelial vascular alterations of acute humoral rejection and were correlated with a poor graft survival. Graft nephrectomy was necessary in 9 of 11 patients with grade III glomerulopathy. In chronic rejection, thickened basement membranes and increased amount of mesangial matrix were considered the result of ischemia. The degree of ultrastructural glomerular alterations in chronic rejection did not correlate with graft survival. Urine protein values were consistently elevated, although poorly correlated with the severity of glomerular alterations. Recurrent glomerulonephritis was not documented in any case. We concluded that the glomerular alteration in acute rejection is a component of acute humoral rejection and that the degree of glomerulopathy in acute rejection is a good predictor of the graft survival.
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)
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)