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Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Fosinopril and losartan inhibit LDL oxidation and attenuate atherosclerosis in apolipoprotein E-deficient mice. Incidence of subdural haematoma is high in haemodialysis (HD), with data suggesting an increasing incidence over time.
Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Fosinopril and losartan inhibit LDL oxidation and attenuate atherosclerosis in apolipoprotein E-deficient mice. Incidence of subdural haematoma is high in haemodialysis (HD), with data suggesting an increasing incidence over time.
Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Fosinopril and losartan inhibit LDL oxidation and attenuate atherosclerosis in apolipoprotein E-deficient mice. Incidence of subdural haematoma is high in haemodialysis (HD), with data suggesting an increasing incidence over time.
12951302 23. Griendling KK, Minieri CA, Ollerenshaw JD et al. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Circ Res 1994; 74: 11411148 24. Hayek T, Attias J, Coleman R et al. The angiotensin-converting en- zyme inhibitor, fosinopril, and the angiotensin II receptor antagonist, losartan, inhibit LDL oxidation and attenuate atherosclerosis inde- pendent of lowering blood pressure in apolipoprotein E deficient mice. Cardiovasc Res 1999; 44: 579587 25. Daugherty A, Manning MW, Cassis LA. Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E-deficient mice. J Clin Invest 2000; 105: 16051612 Received for publication: 6.11.09; Accepted in revised form: 7.1.10 Nephrol Dial Transplant (2010) 25: 22722275 doi: 10.1093/ndt/gfq013 Advance Access publication 26 January 2010 High but stable incidence of subdural haematoma in haemodialysisa single-centre study Albert Power, Mohamed Hamady, Seema Singh, Damien Ashby, David Taube and Neill Duncan West London Renal and Transplant Centre, Hammersmith Hospital, Imperial College Healthcare NHS Trust, DuCane Road, London W12 0HS, UK Correspondence and offprint requests to: Albert Power; E-mail: albert.power@imperial.nhs.uk Abstract Background. The incidence of subdural haematoma (SDH) is high in haemodialysis (HD), with data suggesting an increasing incidence over time. The prognosis remains poor with 40% mortality at 30 days. The extent of this problem in non-US populations has not been described in the literature. Methods. We conducted a retrospective, single-centre UK study of non-traumatic SDH in patients established on maintenance HD between 1 January 2002 and 1 June 2009. Results. The prevalence of SDH was 0.4% at our centre with an overall annual incidence of 189 per 100 000 pa- tients. SDH was associated with increased patient age (mean 71.3 8.5 years) but not associated with a higher prevalence of major comorbid conditions and antiplatelet or anticoagulant use. Mortality was high (46% at 30 days, 58% at 1 year). We did not observe a trend to increasing prevalence of this condition over time. Conclusions. SDH has a higher (>20 times) incidence in HD patients than in the general population and is associat- ed with high mortality. Although the prevalence in this study was lower than in published US studies, the inci- dence rate is similar. Further studies to validate prognostic criteria that guide decisions regarding surgery are required. Keywords: haemodialysis; haematoma evacuation; subdural haematoma Introduction The incidence of stroke in patients on maintenance haemo- dialysis (HD) is 510 times that of the general population, with a higher prevalence of haemorrhagic events [13]. Studies evaluating stroke in this patient population have traditionally excluded subdural haemorrhage (SDH) from analyses. There are just two studies of SDH in dialysis pa- tients to date in the literature both deriving from US popu- lations [4,5]. The incidence of SDH in dialysis patients is higher than in the general population, with a mortality reaching 40% [5]. One study suggested that the incidence of SDH was stable in patients on peritoneal dialysis but steadily increasing among HD patients [5]. There are no European studies to guide management and no studies have reported exclusively on a HD population during the last decade. We studied the incidence of non-traumatic SDH in maintenance HD patients at our centre and exam- ined the demographics and clinical characteristics of pa- tients who developed SDH. Subjects and methods The West London Renal and Transplant Centre (comprising of the renal units of Hammersmith, St. Marys and Charing Cross Hospitals) provides renal services to a population of over 2 million people and cares for a total of 1200 HD patients who receive their treatment in 10 satellite dialysis units. This retrospective study identified all patients established on mainte- nance HD (defined as receiving >90 days continuous treatment) from 1 January 2002 to 31 May 2009 at St. Marys Hospital (January 2002 September 2005) and the West London Renal and Transplant Centre at Hammersmith Hospital, London (October 2005May 2009). All paper and electronic records from both sites relating to admission, inpatient stay, laboratory tests, radiological investigations and inpatient and outpatient dialysis data were analysed. Non-traumatic SDH was defined in accor- dance with the International Classifications of Diseases, Ninth Revision criteria (Code 432.1). All cases of SDH were reviewed by the neurosurgi- cal team at our centre with regards to surgical treatment. Patients were dialysed three times weekly using low-flux synthetic AM- BIO-1000Wet (Asahi Kasei Medical Europe GmbH, Frankfurt, Germany) and Nipro Sureflux-L (Nipro Europe NV, Zaventem, Belgium) haemodia- The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org 2272 A. Power et al.
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lysers during the periods 2002January 2009 and FebruaryMay 2009, respectively. Unfractionated heparin (Monoparin sodium heparin, CP Pharmaceuticals, Wrexham, UK) was used for dialysis circuit anticoagu- lation apart from the period September 2008January 2009 where tinza- parin (Innohep, Leo Pharma, Princes Riseborough, UK) was at an initial dose of 2500 U at the start of dialysis as previously described [6]. Unfrac- tionated heparin was administered as a 500-IU bolus at the start of dialysis followed by a maintenance dose of 500 IU/h thereafter. Patients weighing in excess of 80 kg received an increase in the bolus and maintenance dose of 50 IU/kg excess weight. Dialysis session length varied from 4 to 5 h. Dialysis adequacy was measured by single-pool Kt/V (spKt/V) using the Daugirdas method on a monthly basis [7]. Dialysis prescription was tai- lored to achieve a spKt/Vof 1.6. Statistics Descriptive statistics are expressed as the mean standard deviation. Continuous and categorical variables were compared using Students t-test and the chi-square or MannWhitney U-test, respectively, as appropriate. Timeline incidence data were analysed using a Poisson model and ex- pressed with 95% confidence intervals (CI). Statistical significance was defined by P < 0.05. STATISTICA 9.0 (StatSoft Inc., Tulsa, OK, USA) was used to perform the statistical analysis. Results During the study period, a total of 2542 patients received maintenance HD. Complete demographic, clinical and therapeutic data was available in 2155 patients comprising the study cohort with a total of 7508 patient-years follow- up. Population demographics are presented in Table 1. Eleven patients (0.4% cohort) experienced non-traumatic SDH (mean patient age of 71.3 8.5 years, mean time on HD of 2.8 2.3 years, mean spKt/Vof 1.72 0.29); 5/11 (45%) patients were diabetic, 6/11 (55%) hypertensive and 1/11 (9%) had established cerebrovascular disease (past transient ischaemic attacks and/or stroke). There was no significant association between SDH occurrence and anti- platelet or anticoagulant use. The presence of diabetes, hy- pertension or cerebrovascular, coronary or peripheral vascular disease was not significantly associated with SDH (Table 2). There was no evidence of derangement of haematological parameters at the time of SDH (Table 3). The overall annual incidence rate of SDH was 188.6 per 100 000 patients per year in our population (95% CI 97.5 329.5). This is similar to the recent (2002) rate of 191 per 100 000 patients per year reported in a recent study based on USRDS data, but in contrast, there was no ev- idence of an increasing incidence rate over time (Figure 1) [5]. Patient mortality was 46% at 30 days and 58% at 1 year. Subdural thickness was >20 mm in 7/11 (64%) cases and there was a significant (>10 mm) associated midline shift in 4/11 (36%) cases. The majority (86%) of patient deaths occurred in patients deemed not fit for operative treatment with SDH thickness >20 mm and/or midline shift >10 mm. All these patients died directly as a result of SDH. Discussion SDH develop from bleeding into the space between the du- ra and the arachnoid membranes and are seen most com- monly following head trauma. Acute SDH occur following traumatic shear force, tearing the bridging veins on the sur- face of the brain in the majority of cases with around 25% attributed to arterial rupture [8]. Traction injury to venous structures from low cerebrospinal fluid (CSF) pressure, Table 1. Demographic characteristics of the study cohort (2002June 2009) Mean age (years) 57.9 16.1 Ethnicity White 905 (42%) Afro-Caribbean 409 (19%) South Asian 733 (34%) Other 108 (5%) Comorbidities Diabetes 829 (38%) Ischaemic heart disease 686 (32%) Hypertension 1202 (56%) Peripheral vascular disease 247 (12%) Cerebrovascular disease 327 (15%) Therapies Aspirin 823 (38%) Clopidogrel 226 (11%) Warfarin 61 (3%) Table 2. Comparative demographic characteristics of patients with and without SDH SDH present No SDH present P-value Mean patient age (years) 71.3 8.5 57.9 16.1 0.006 Mean time on HD (years) 2.8 2.3 3.5 3.5 0.5 Diabetes 5 (46%) 829 (38%) 0.6 Ischaemic heart disease 4 (36%) 686 (32%) 0.7 Hypertension 6 (55%) 1202 (56%) 0.5 Peripheral vascular disease 1 (9%) 247 (12%) 0.9 Cerebrovascular disease 1 (9%) 327 (15%) 0.3 Aspirin 6 (55%) 823 (38%) 0.3 Clopidogrel 0 226 (11%) 0.3 Warfarin 0 61 (3%) 0.7 Data are expressed as mean standard deviation and patient number and percentage in parentheses. Table 3. Haematological parameters at time of SDH Mean haemoglobin (g/dl) 12.0 2.3 Mean platelet count (10 9 /ml) 183 73 Mean PT (s) 11.7 0.9 Mean APTT (s) 30.4 3.5 Mean fibrinogen (g/L) 4.11 0.79 PT, prothrombin time; APTT, activated partial thromboplastin time. 0.0 50.0 100.0 150.0 200.0 250.0 300.0 350.0 400.0 1 2 3 4 5 6 7 8 Year S D H
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y e a r Fig. 1. Annual incidence rate of SDH during the period of study. Subdural haematoma in haemodialysis 2273
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typically as a result of spontaneous or iatrogenic CSF leak- age (such as following diagnostic lumbar puncture), has al- so been implicated in the pathogenesis of SDH. Significant cerebral atrophy, a finding that increases in prevalence with advancing age, and the use of antithrombotic agents are major risk factors for SDH [9]. In addition, SDH has been described in association with subarachnoid haemorrhage, arteriovenous malformations and meningiomas [1012]. HD is associated with fluctuations in cerebral blood flow and an increase in intracranial pressure [13,14]. By contrast, there is a reduction in the pressure within the SDH cavity intradialytically [15]. The bleeding diathesis of uraemia is exacerbated by the use of anticoagulants such as heparins and coumarins in dialysis circuit anticoagula- tion, vascular access patency and management of atrial fi- brillation [16,17]. This is compounded by the use of antiplatelet agents for coronary and peripheral arterial dis- ease in an ageing HD population with a high prevalence of cerebrovascular disease and cerebral atrophy [18,19]. It can be hypothesized that the mechanical forces described above may trigger non-traumatic SDH formation in pa- tients at high risk for this lesion. The incidence of non-traumatic SDH in HD patients in this study is more than 20 times that in the general popu- lation (38/100 000 patients per year) [20,21], with an overall incidence rate that is similar to that in the US. The prevalence of SDH in our HD population was much lower than previously reported (0.4 vs 3%) [4]. This is like- ly to be multifactorial and may reflect differences in patient demographics, dialysis circuit technology and anticoagula- tion and use of oral anticoagulants. We do not use warfarin for vascular access patency and have a low prevalence of arteriovenous graft (AVG) use (1% prevalent population currently). As the authors point out, the increasing inci- dence of SDH in the US may relate to an increase in AVG and consequent warfarin use [5]. In keeping with studies from the general and HD popu- lation, it is associated with increasing age where it carries a poor prognosis [2022]. Patients with SDH in this study were significantly older than controls73% were >65 years old. This is similar to available US data [5]. We did not observe an over-representation of major comorbid conditions in patients with SDH in this study, in contrast to prior published work [5]. This may reflect a different ethnic case mix to that reported in US studies, with a lower per- centage of African-American patients and a greater propor- tion of South Asians in UK studies, but can also be influenced by the considerably smaller number of affected patients in this study. We did not observe an association with antiplatelet agent or warfarin use, although this could be subject to prescription bias (i.e. elderly patients consid- ered at high risk of falls are less likely to be prescribed po- tent anticoagulation) and bias by indication. The recorded absence of preceding head trauma could have been subject to reporting bias from the patient and/or their carers who, in addition, may not have reported minor trauma that has been implicated in SDH pathogenesis [23]. The retrospec- tive nature of this study cannot demonstrate causation. Patient mortality was high (46% at 30 days) and sim- ilar to US data [5]. No recent study in HD patients to date has comprehensively examined clinical outcomes following diagnosis. An initial study by Leonard et al., reporting on 13 patients, found poor survival (15%) and surgical outcomes [4]. There are no rigorous, pub- lished studies on clinical outcomes in HD patients with SDH whether managed conservatively or surgically. Data from the general population suggest a worse prognosis with a lower Glasgow Coma Scale score (GCS) [24], greater haematoma thickness [25] and the degree of mid- line shift [22,26]. These clinical and radiological criteria have not been validated in HD patients. Available surgical guidelines recommend surgical evacuation for patients with an acute SDH and who have a haematoma thickness >10 mm or midline shift >5 mm regardless of the level of the GCS [27]. Our study suggests that similar criteria may be appropriate in this patient population but the results need to be approached with caution. Appraisal of fitness for surgery was potentially influenced by the appreciation of the natural bleeding diathesis [28] and the comorbid burden of HD patients. In total, 3/11 (27%) patients proceeded to surgery as determined by clinical and neuroimaging criteria described above. No patients died in the immediate post- operative period (one patient died after 43 days, the other after 355 days). Tailored and judicious anticoagulation, avoidance of po- tentially pathogenic circulatory volume shifts on HD and blood pressure control may all have a role to play in reduc- ing the incidence of SDH in the HD population. There is a paucity of data on the epidemiology of SDH in Europe. Published data from the US give grounds for concern but describe different populations and HD practices to those in Europe [2933]. We believe that larger global studies are required to determine the incidence, prevalence and prog- nostic impact of SDH. In addition, prospective validation of established criteria for surgical intervention need to be undertaken in this high-risk group with potential to im- prove short-term and long-term outcomes. Conflicts of interest statement. None declared. References 1. Seliger SL, Gillen DL, Longstreth WT Jr et al. Elevated risk of stroke among patients with end-stage renal disease. Kidney Int 2003; 64: 603609 2. Sozio SM, Armstrong PA, Coresh J et al. Cerebrovascular disease incidence, characteristics, and outcomes in patients initiating dialysis: the choices for healthy outcomes in caring for ESRD (CHOICE) study. Am J Kidney Dis 2009; 54: 468477 3. Toyoda K, Fujii K, Fujimi S et al. Stroke in patients on maintenance hemodialysis: a 22-year single-center study. Am J Kidney Dis 2005; 45: 10581066 4. Leonard A, Shapiro FL. Subdural hematoma in regularly hemodia- lyzed patients. Ann Intern Med 1975; 82: 650658 5. Sood P, Sinson GP, Cohen EP. Subdural hematomas in chronic dial- ysis patients: significant and increasing. Clin J Am Soc Nephrol 2007; 2: 956959 6. Davenport A. Low-molecular-weight heparin for routine hemodialy- sis. Hemodial Int 2008; 12: S34S37 7. Daugirdas JT. Second generation logarithmic estimates of single-pool variable volume Kt/V: an analysis of error. J Am Soc Nephrol 1993; 4: 12051213 8. Maxeiner H, Wolff M. Pure subdural hematomas: a postmortem analy- sis of their form and bleeding points. 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Pisoni RL, Young EW, Dykstra DM et al. Vascular access use in Eur- ope and the United States: results from the DOPPS. Kidney Int 2002; 61: 305316 Received for publication: 11.12.09; Accepted in revised form: 7.1.10 Nephrol Dial Transplant (2010) 25: 22752283 doi: 10.1093/ndt/gfp781 Advance Access publication 26 January 2010 Perioperative outcomes among patients with end-stage renal disease following coronary artery bypass surgery in the USA Dipen S. Parikh 1,2,3 , Madhav Swaminathan 4 , Laura E. Archer 5 , Jula K. Inrig 1,2,6 , Lynda A. Szczech 1,2 , Andrew D. Shaw 4 and Uptal D. Patel 1,2 1 Division of Nephrology, Department of Medicine, Duke University Medical Center, Durham, NC, USA, 2 Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, USA, 3 Vascular Access Center of Durham, Durham, NC, USA, 4 Division of Cardiothoracic Anesthesiology, Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA, 5 Division of Biostatistics, Duke Comprehensive Cancer Center, Duke University Medical Center, Durham, NC, USA and 6 Division of Nephrology, Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA Correspondence and offprint requests to: Dipen S. Parikh; E-mail: dipenparikh@yahoo.com Abstract Background. Patients with end-stage renal disease (ESRD) requiring chronic haemodialysis who undergo coronary ar- tery bypass graft surgery (CABG) are at significant risk for perioperative mortality. However, the impact of changes in ESRD patient volume and characteristics over time on op- erative outcomes is unclear. The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org Outcomes among ESRD after CABG 2275
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