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Vollmer C.M.,Renal and Transplant Unit
Urologic nursing | Year: 2010

Unrecognized delirium may lead to negative outcomes, such as increased morbidity, longer hospital stays, and increased health care costs. A prospective cohort design study was used to determine the incidence and prevalence of delirium and percentage of patients with unrecognized delirium in a hospital inpatient unit. The sample consisted of 141 patients admitted to a urology/nephrology unit over a six-week period. Data were collected using the Confusion Assessment Method (CAM) and the Charlson Comorbidity Index (CCI). Results showed the incidence of delirium was 6%, and the prevalence was 12% in this sample. Out of 17 patients with delirium, 6 patient records (35%) had no documentation of delirium by physicians. In the nursing assessment, 1 of 17 (6%) had no documentation of any signs/symptoms of delirium. This study provided baseline data for the development, implementation, and evaluation of a delirium recognition program using the CAM. The CAM may represent an easy-to-use, valid, and reliable instrument to detect delirium as part of a routine nursing assessment. Source


Gardner D.S.,University of Nottingham | Welham S.J.M.,University of Nottingham | Dunford L.J.,University of Nottingham | Dunford L.J.,Renal and Transplant Unit | And 5 more authors.
American Journal of Physiology - Renal Physiology | Year: 2014

Acute kidney injury is common, serious with no specific treatment. Ischemia-reperfusion is a common cause of acute kidney injury (AKI). Clinical trials suggest that preoperative erythropoietin (EPO) or remote ischemic preconditioning may have a renoprotective effect. Using a porcine model of warm ischemia-reperfusion-induced AKI (40-min bilateral crossclamping of renal arteries, 48-h reperfusion), we examined the renoprotective efficacy of EPO (1,000 iu/kg iv.) or remote ischemic preconditioning (3 cycles, 5-min inflation/deflation to 200 mmHg of a hindlimb sphygmomanometer cuff). Ischemia-reperfusion induced significant kidney injury at 24 and 48 h (χ2, 1 degree of freedom, > 10 for 6/7 histopathological features). At 2 h, a panel of biomarkers including plasma creatinine, neutrophil gelatinase-associated lipocalin, and IL-1β, and urinary albumin:creatinine could be used to predict histopathological injury. Ischemia-reperfusion increased cell proliferation and apoptosis in the renal cortex but, for pretreated groups, the apoptotic cells were predominantly intratubular rather than interstitial. At 48-h reperfusion, plasma IL-1β and the number of subcapsular cells in G2-M arrest were reduced after preoperative EPO, but not after remote ischemic preconditioning. These data suggest an intrarenal mechanism acting within cortical cells that may underpin a renoprotective function for preoperative EPO and, to a limited extent, remote ischemic preconditioning. Despite equivocal longer-term outcomes in clinical studies investigating EPO as a renoprotective agent in AKI, optimal clinical dosing and administration have not been established. Our data suggest further clinical studies on the potential renoprotective effect of EPO and remote ischemic preconditioning are justified. © 2014 the American Physiological Society. Source


Caplin B.,University College London | Veighey K.,University College London | Mahenderan A.,Renal and Transplant Unit | Manook M.,Renal and Transplant Unit | And 9 more authors.
Clinical Transplantation | Year: 2013

The amount of irreversible injury on renal allograft biopsy predicts function, but little is known about the early evolution of this damage. In a single-center cohort, we examined the relationship between donor-, recipient-, and transplantation-associated factors and change in a morphometric index of chronic damage (ICD) between protocol biopsies performed at implantation and at 2-3 months. We then investigated whether early delta ICD predicted subsequent biochemical outcomes. We found little evidence to support differences between the study group, who had undergone serial biopsies, and a contemporaneous control group, who had not. In allografts with serial biopsies (n = 162), there was an increase in ICD between implantation (median: 2%, IQR:0-8) and 2-3 months post-transplant (median 8% IQR:4-15; p < 0.0001). Donation from younger or live donors was independently associated with smaller early post-transplant increases in ICD. There was no evidence for a difference in delta ICD between donation after cardiac death vs. donation after brain death, nor association with length of cold ischemia. After adjustment for GFR at the time of the second biopsy, delta ICD after three months did not predict allograft function at one yr. These findings suggest that graft damage develops shortly after transplantation and reflects donor factors, but does not predict future biochemical outcomes. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. Source

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