Publications by authors named "Beatrice Coupes"

Post-transplant lymphoproliferative disorder (PTLD) is a rare, serious complication following solid organ transplantation, with an incidence of 2.6 cases per 1000 patient years. Optimal treatment strategies and risk stratifications specific to kidney transplantation are lacking and PTLD mortality remains high.

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Background: Critically ill children and neonates are at high risk of developing acute kidney injury (AKI). AKI is associated with short- and long-term renal impairment and increased mortality. Current methods of diagnosing AKI rely on measurements of serum creatinine, which is a late and insensitive marker.

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Background: Extended criteria donor (ECD) and donation after circulatory death (DCD) kidneys are at increased risk of delayed graft function (DGF). Experimental evidence suggests that erythropoietin (EPO) attenuates renal damage in acute kidney injury. This study piloted the administration of high dose recombinant human EPO-beta at implantation of ECD and DCD kidneys, and evaluated biomarkers of kidney injury post-transplant.

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The kidneys and the interstitial compartment play a vital role in body fluid regulation. The latter may be significantly altered in renal dysfunction, but experimental studies are lacking. To help define this we measured the subcutaneous interstitial pressure, bioimpedance volumes, and edema characteristics in 10 healthy subjects and 21 patients with obvious edema and chronic kidney disease (CKD).

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Background: There is little information in the literature describing the relationship between posttransplantation lymphoproliferative disorder (PTLD) incidence and presentation with both recipient Epstein-Barr virus (EBV) serostatus and EBV status of PTLD histology, particularly in the late posttransplantation period.

Methods: This study reports the largest UK single-center, single-organ analysis of PTLD to date in a retrospective cohort study of 80 cases occurring in 4189 adult renal transplant recipients.

Results: The incidence rate was 2.

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Background: Uremic toxins are typically measured in plasma and little is known of their interstitial concentrations. We undertook experiments to validate a microdialysis technique for simultaneous recovery of small and large uremic toxins in the subcutaneous interstitial fluid (ISF).

Methods: Microdialysis catheters were inserted into the subcutaneous interstitium of 8 subjects (controls and uremic patients) and perfused using two different solutions at incremental flow rates to determine analyte recovery and ISF concentrations of urea and protein.

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Background: Evidence from experimental models and clinical studies supports a major role for transforming growth factor-beta1 (TGF-beta1) in renal fibrosis. The aim of this study was to use repeated measurement of plasma TGF-beta1 as an indicator of persistent expression in a cohort of patients during the first 2 years post-renal transplantation and to correlate the findings with the development of chronic allograft nephropathy (CAN).

Methods: Active plasma TGF-beta1 was quantified in 100 consecutive renal allograft recipients (samples/patient = 35.

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The efficiency of activating latent transforming growth factor (TGF)-beta1 in systemic lupus erythematosus (SLE) may control the balance between inflammation and fibrosis, modulating the disease phenotype. To test this hypothesis we studied the ability to activate TGF-beta1 in SLE patients and control individuals within the context of inflammatory disease activity, cumulative organ damage and early atherosclerosis. An Activation Index (AI) for TGF-beta1 was determined for 32 patients with SLE and 33 age-matched and sex-matched control individuals by quantifying the increase in active TGF-beta1 under controlled standard conditions.

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Background: Changes in renal vasculature, with vascular and interstitial fibrosis, are hallmarks of progression to chronic kidney disease (CKD) stage 5. Vascular endothelial growth factor (VEGF) is a potent angiogenic and vascular permeability factor. Transforming growth factor-beta1 (TGF-beta1) plays a critical role in promoting extracellular matrix (ECM) deposition and fibrosis.

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