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Biomedical subjects

D Serón

Publications and source records attributed to D Serón.

65 records · Page 4Linked to original sources
PubMed1991

Quantitative and morphometric analysis of Langerhans cells in non-exposed skin in renal transplant patients.

Renal transplant recipients have a high incidence of cutaneous complications such as neoplasia and viral or fungal infections. Morphologic alterations of epidermal Langerhans cells (LC) have furthermore been described in these patients. Since these changes have been mainly found in sun-exposed skin, a direct effect of immunosuppressive therapy remains a matter of discussion. A quantitative and morphometric study of epidermal LC in non-exposed skin was performed in 28 renal transplant patients (RTP). RTP were divided in two groups according to immunosuppressive treatment: group A; azathioprine + prednisone (14 cases) and group B; cyclosporine + prednisone (14 cases). Twenty sex-age matched non-immunosuppressed patients acted as controls (group C). Epidermal sheets were obtained by incubation in EDTA and stained for ATPase activity and with the monoclonal antibody T6 (CD1) using the avidin-biotin peroxidase method. Langerhans cells were counted using a calibrated graticule (400x) and expressed as the mean number of LC/mm2. The mean area of the LC and the number of primary dendrites (pd) and secondary dendrites (sd) were determined with a morphometer adapted to an Apple II computer. The mean number of positive cells in controls was: ATPase, 677 +/- 157; T6, 695 +/- 164. Patients in group A had the maximum reduction in both ATPase and T6 LC density (ATPase, 339 +/- 142; T6, 402 +/- 194). Patients in group B had an intermediate reduction in the number of LC (ATPase, 494 +/- 121; T6, 529 +/- 112).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1990

Number of interstitial capillary cross-sections assessed by monoclonal antibodies: relation to interstitial damage.

Using thin Plexiglass sections stained with silver, the peritubular capillary area and number of capillary cross-sections can predict both interstitial damage and plasma creatinine concentrations. This technique is both difficult to perform and time-consuming. We have restudied this topic using conventional cryostat sections from 46 biopsies with chronic glomerulonephritis and tubulointerstitial nephritis and two monoclonal antibodies (MoAb) recognising capillary endothelium. Seven pretransplant biopsies acted as controls. The number of capillary cross-sections/mm2 was counted, and the degree of tubular atrophy, interstitial fibrosis and cell infiltration of the interstitium independently assessed on a semiquantitative scale using paraffin sections. These results were correlated with the plasma creatinine or 51Cr-EDTA glomerular filtration rate. Mean number of capillary cross-sections in normal interstitium was 373 +/- 50/mm2, and in the 46 biopsies studied 242 +/- 57/mm2. The number of capillary cross-sections reflected the plasma creatinine (r = 0.82, P less than or equal to 0.0001) and the glomerular filtration rate (r = 0.64, P less than or equal to 0.0001) at the time of biopsy with greater accuracy than any of the conventional gradings of interstitial damage on paraffin sections. We conclude that the use of anti-endothelial cell monoclonal antibodies makes counting capillary cross-sections easy and reliable, and that this technique can be employed to assess the extent of interstitial damage in conventional cryostat sections.

Antibodies, Monoclonal↗
PubMed1989

Diagnosis of rejection in renal allograft biopsies using the presence of activated and proliferating cells.

Forty cyclosporine-treated renal allograft biopsies were stained with anti-Tac, a monoclonal antibody (MoAb) against interleukin 2 receptor (CD25), anti-transferrin receptor MoAb, and Ki67 MoAb (a proliferating cell marker), using a method of gold enhancement of the diaminobenzidine reaction product, in order to study the utility of these markers to differentiate rejection from other causes of graft dysfunction. Biopsies were selected on the basis of availability of sufficient frozen material and optical microscopy diagnosis, and only biopsies that showed acute cellular rejection and biopsies that did not show any sign of rejection (cyclosporine toxicity or a stable graft) were studied. In addition biopsies were stained with a panel of monoclonal antibodies reacting with CD45, CD3, CD4, CD8, EBM11 (a monocyte-macrophage marker), HLA-DR, DP, and DQ, using the usual indirect immunoperoxidase method. The clinical diagnosis (rejection versus no rejection) was made in ignorance of the biopsy findings. In 17 of 18 (94%) episodes of rejection, anti-Tac and anti-transferrin receptor-positive cells, and in 15 of 18 rejection episodes (83%), proliferating cells, were found in the interstitium. Anti-Tac-positive cells were never found in the 11 biopsies diagnosed as no rejection, and only in two a few anti-transferrin receptor-positive cells were present. The proportion of activated and proliferating cells in rejection episodes, expressed as the percentage of CD45-positive cells were: anti-Tac MoAb 4.1 +/- 2.9%, anti-transferrin receptor MoAb 6.9 +/- 3.9%, and Ki-67 MoAb 6.3 +/- 4.8%. There was a positive correlation between the total number of infiltrating cells and the number of cells stained with anti-Tac (r = 0.75, P less than 0.005), anti-transferrin receptor MoAb (r = 0.84, P less than 0.0001), and Ki-67 (r = 0.50, P less than 0.05). The episodes of rejection that took place when cyclosporine levels were high had fewer 1L-2R-bearing cells in the interstitium than those that took place when cyclosporine levels were low (r = 0.47, P less than 0.05). We conclude that during rejection the presence of activated and proliferating cells is a consistent finding, and that these markers could be useful in differentiating between rejection and other causes of graft dysfunction as well as in grading the severity of rejection.

Adolescent↗
PubMedDate not supplied

Prevention and management of late renal allograft dysfunction.

Chronic allograft nephropathy is the leading cause of return to dialysis after transplantation. At present, no efficient therapies are available to modify the natural history of chronic allograft nephropathy, mainly because of difficulties in designing prospective clinical trials to prevent or treat this entity. The main risk factors for chronic allograft nephropathy, the utility of protocol biopsies in the design of trials, and different strategies to prevent or treat this problem are reviewed.

Clinical Trials as Topic↗