Biomedical subjects
Publications and source records attributed to B Hartley.
With current medical treatment, juvenile dermatomyositis (JDMS) is rarely fatal. However, for most families, it is a chronic illness that interrupts life for both the affected child and the rest of the family. This article provides an overview of the disease, presents a case history of a 9-year-old affected girl, and discusses nursing care using the Roy Adaptation Model and nursing diagnoses.
Human renal epithelial and mesangial cells have been shown to synthesise complement C3 in culture, but the relevance of this finding to the development of complement-mediated nephritis is uncertain. We investigated C3 gene expression in tissue biopsies that showed three main categories of renal injury. By semiquantitative polymerase chain reaction, biopsies from patients with immune-complex glomerulonephritis and those with cell-mediated interstitial nephritis showed increased C3 expression (p < 0.05), but biopsies from patients with non-immune glomerular injury did not. These findings suggest that local C3 production is enhanced in immune-mediated nephritis and are consistent with the hypothesis that locally synthesised complement components are involved in the pathogenesis of tissue injury.
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Although red cell morphology has been used to localise the site of haematuria in the urinary tract, the cause of red cell deformity is still speculative. We have conducted experiments in vitro using venous red cells which indicate that hypochromia depends mainly upon sodium concentration and occurs when this falls below 75 mmol/l. We simulated the passage of red cells through the renal tubule by sequentially treating them with fluids of composition similar to those in different tubular segments, and produced anisocytosis and hypochromia but not the typical "bizarre deformity"--the hallmark of glomerular haematuria. We conclude that dual injury is required to produce the "typical" dysmorphic red cells in glomerular haematuria. First, mechanical damage caused by passage of red blood cells through the glomerular basement membrane followed by a second, osmotic, injury sustained by red cells during passage through the hypotonic tubular segment.
The production and release of cytokines and their receptors are of critical importance in mediating graft injury. In order to evaluate the expression of cytokines in renal allograft biopsies, we performed immunocytochemical studies to detect activated cells positive for TNF-alpha, IFN-gamma, and IL-2R, using an alkaline phosphatase anti-alkaline phosphatase technique (APAAP). Sixty-one biopsy specimens from renal transplant patients were analyzed and were classified according to both clinical and conventional morphological criteria. There was a significant correlation between the number of positive cells reactive with monoclonal antibodies directed against TNF-alpha, IFN-gamma, and IL-2R and the presence of acute cellular rejection. The mean number of infiltrating cells (cells/mm2) positive for TNF-alpha (9.2 +/- 1.1), IFN-gamma (6.7 +/- 1.7), and IL-2R (31.2 +/- 4.8) was significantly greater in acute cellular rejection episodes compared with nonrejecting kidneys (0.9 +/- 0.2, 1.2 +/- 0.4, and 8.8 +/- 2.9 positive cells/mm2 for TNF-alpha, IFN-gamma, and IL-2R, respectively). No significant expression of these cytokines was found in the majority of biopsies with chronic rejection. In two cases, in which acute cellular rejection was not sustained on clinical grounds but was diagnosed on histology, the expression of TNF-alpha, IFN-gamma, and IL-2R was similar to that observed in typical cellular rejection. We conclude that TNF-alpha, IFN-gamma, and IL-2R are markedly expressed by activated mononuclear infiltrating cells in acute cellular rejection, and that these cytokines play an important role in allograft rejection. The immunocytochemical evaluation of cytokine expression is a simple and rapid method that is helpful in differentiating acute cellular rejection from other causes of graft disfunction.
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Many users consider telemedicine a partial solution to problems of delivering health care to remote areas or areas underserved by clinicians. Current telemedical technology benefits from recent developments such as the decreased cost and improved quality of the coder-decoder (codec) equipment used in interactive digital video systems and the expansion of fiber-optic cable networks. The authors outline some pioneering telemedicine programs of the 1960s and 1970s and describe two recently activated systems in Texas. One network, serving the western two-fifths of the state, links faculty members from four campuses of Texas Tech University Health Sciences Center with almost 40 rural communities. The other connects the state hospital and three other facilities in Austin with four health care sites in the town of Giddings, 65 miles away. Besides serving patients, the systems provide continuing medical education and support to reduce the isolation of rural health care professionals. Primary goals include evaluation and certification of telemedical training and analysis of the cost feasibility of telemedical services.
Red cell morphology was examined by light microscopy in 122 urine specimens from 99 patients with haematuria in an attempt to define the site of origin. Altogether 84% of glomerular bleeding and 91% of non-glomerular bleeding was correctly assigned according to diagnoses determined by renal biopsy in 51 patients and clinically in 48. The test should be interpreted with caution as both false positive and false negative results were observed, some in the same individual with unchanged pathology at different times. No advantage of phase contrast over bright field microscopy was apparent even when examining uncentrifuged urines.
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Once considered a rare, fatal illness in children and adolescents, systemic lupus erythematosus (SLE), or lupus, is now understood to be a relatively common chronic disorder in these age groups. This article provides a brief overview of the disease, describing its etiology, pathology, clinical manifestations, diagnosis, and treatment. A case history of an adolescent girl with lupus is presented, and the role of the nurse is discussed in relation to promoting four developmental tasks of adolescents: developing a positive body image, establishing a sexual identity, achieving independence, and acquiring formal thought processes. Since lupus interferes to some degree in the accomplishment of these tasks, we suggest methods of assessment and intervention that the nurse can use in each area to overcome these interferences.
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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.
Repeated low-dose injections of mercuric chloride (HgCl2) in the brown Norway (BN) rat result in polyclonal activation which includes the induction of anti-glomerular basement membrane (GBM) autoantibodies. We examined the kinetics of various autoantibodies produced in vivo, general features of polyclonal activation such as total IgG levels and immune complex formation, and the relationship between organ specific autoimmunity and tissue injury in the kidney and thyroid. The production of immune complexes and autoantibodies to GBM and thyroglobulin was short lived, and the increase in levels of total IgG and antibodies to ssDNA and dsDNA was prolonged; the antibody response to collagen types I and II was intermediate in duration. Autoantibodies induced by HgCl2 caused only mild and variable tissue injury in the kidneys and did not induce abnormalities in the thyroid. These studies demonstrate that immunostimulation by mercury may result in the formation of a range of autoantibodies, with variable kinetics and pathogenicity.
1. Intraortic suprarenal infusion in vivo of New Zealand White rabbits with plasma from patients with the nephrotic syndrome reduced the number of anionic sites labelled by the cationic polymer polyethyleneimine in the lamina rara iterna to 14.0 +/- 2.7 per 1000 nm of lamina rara interna (mean +/- SD) compared with 18.7 +/- 2.1 (P less than 0.005) after infusion of plasma from normal subjects. 2. Proteinuria increased in all nine animals infused with nephrotic plasma and in two of seven infused with control plasma (P less than 0.01). The mean increase in proteinuria in the animals infused with nephrotic plasma was 246 mg/l (P less than 0.05), whereas in those infused with control plasma there was no increase. 3. We conclude that nephrotic plasma contains a factor(s) capable of neutralizing the charge of these anionic sites and concomitantly increasing proteinuria.
Renal tubular display of HLA-DR was estimated semi-quantitatively in 28 biopsies from 27 patients with various forms of tubulointerstitial nephritis (10 following use of non-steroidal anti-inflammatory drugs) using a monoclonal anti-MHC class II non-polymorphic antibody (DK-22). Normal donor kidneys and biopsies from patients with minimal-change nephrotic syndrome were examined as controls. The phenotype of infiltrating cells was also studied quantitatively, using monoclonal antibodies on frozen biopsy tissue; the number of cells infiltrating the interstitium was counted per tubular cross-section. Display of HLA-DR was seen in up to 5% of control tubular cells, but up to 100% expressed HLA-DR in tubulointerstitial nephritis biopsies. There was a correlation between the expression of HLA-DR and the severity of both tubular atrophy and tubulointerstitial fibrosis judged semi-quantitatively by optical microscopy. In controls up to 50 leucocytes per tubular cross-section were evident, but in patients with tubulointerstitial nephritis up to 1500 were observed, approximately 50% being T-lymphocytes, the majority expressing the helper phenotype except in early, active drug-induced tubulointerstitial nephritis; the remainder were mostly monocytes. There were no qualitative differences between the different causes of tubulointerstitial nephritis. Tubular DR expression correlated with the number of DR-positive cells in the interstitium, but not with total leucocytes or T-lymphocytes. HLA-DR tubular expression was greater in the early stages than late stages of NSAID-induced tubulointerstitial nephritis, but this relationship was not present in the group as whole. HLA-DR expression by renal tubular epithelial cells may play a role in localising or amplifying tubular injury in tubulointerstitial nephritis.
Using a panel of monoclonal antibodies, immunohistological analysis was performed on frozen sections taken from 14 peritransplant renal biopsies and 42 biopsies taken 6 +/- 2 days posttransplantation. The following parameters were examined: tubular expression of HLA-DR, DP, and DQ and infiltration with T lymphocytes and macrophages. Of the 42 posttransplant biopsies, 26 were diagnosed as rejecting and 16 as nonrejecting according to clinical and histopathological criteria. HLA-DR antigens were strongly expressed on 8 of 14 peritransplant biopsies, 23 of 26 rejecting biopsies and 13 of 16 nonrejecting biopsies. Tubular expression of HLA-DP and DQ was weak or absent. In the rejecting biopsies there was a significantly increased infiltrate of T lymphocytes of all phenotypes and of macrophages when compared with the nonrejecting biopsies. Graft outcome was invariably favorable in the nonrejecting group, with no graft losses in the first posttransplant year. There were 4 graft losses in the rejecting group, all due to rejection, and further analysis revealed that all 4 had macrophage-dominated infiltrates in their early allograft biopsies. We conclude that immunohistological analysis of early allograft biopsies provides an accurate prognosis of subsequent graft acceptance or rejection and that early macrophage infiltration is a poor prognostic sign.