***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Objective To determine the prevalence and the prognostic significance of microalbuminuria in patients after aneurysmal subarachnoid hemorrhage ( SAH ) . Design Prospect i ve and observational clinical study . Setting Multidisciplinary intensive care unit . Patients Fifty-one consecutive patients who underwent aneurysm clipping or endovascular surgery after SAH ; 8 patients who underwent surgical clipping for unruptured intracerebral aneurysm served as control . InterventionNone . Measurements and Results General clinical and neurological data were recorded on admission . Urine was collected preoperatively and daily for up to 7 days postoperatively for measuring the urinary microalbumin/creatinine ratio . The Glasgow Coma Scale ( GCS ) score was also determined on admission and daily for up to 7 days after operation . Neurological outcome was assessed using the Glasgow Outcome Scale ( GOS ) at 3 months after stroke . The prevalence rates of microalbuminuria were 74.5 % in SAH and 37.5 % in the control . Among the 51 patients , 25 had unfavorable neurological outcome ( GOS 1–3 ) . The areas under the receiver operator characteristic curves showed that the highest urinary microalbumin/creatinine ratio and the lowest GCS score during the first 8 days were the significant predictors of unfavorable neurological outcome . The threshold value , sensitivity , specificity , and likelihood ratio for the highest urinary microalbumin/creatinine ratio were 200 mg/g , 60 % [ 95 % confidence interval ( CI ) 41–79 ] , 96 % ( 95 % CI 88–100 ) , and 15.6 ( 95 % CI 9.1–26.7 ) , respectively . Conclusions This study confirms a high prevalence of microalbuminuria in the SAH patients , and it suggests that the highest urinary microalbumin/creatinine ratio > 200 mg/g during the first 8 days is a significant predictor of unfavorable neurological outcome Background —Elevated urine albumin excretion ( UAER ) is a modifiable risk factor for renal and cardiovascular disease in type 2 diabetes . Blockade of the renin-angiotensin system lowers UAER , but whether this effect is independent of blood pressure ( BP ) reduction remains controversial . The MicroAlbuminuria Reduction With VALsartan ( MARVAL ) study was design ed to evaluate the BP-independent effect of valsartan on UAER in type 2 diabetic patients with microalbuminuria . Methods and Results —Three hundred thirty-two patients with type 2 diabetes and microalbuminuria , with or without hypertension , were r and omly assigned to 80 mg/d valsartan or 5 mg/d amlodipine for 24 weeks . A target BP of 135/85 mm Hg was aim ed for by dose-doubling followed by addition of bendrofluazide and doxazosin whenever needed . The primary end point was the percent change in UAER from baseline to 24 weeks . The UAER at 24 weeks was 56 % ( 95 % CI , 49.6 to 63.0 ) of baseline with valsartan and 92 % ( 95 % CI , 81.7 to 103.7 ) of baseline with amlodipine , a highly significant between-group effect ( P < 0.001 ) . Valsartan lowered UAER similarly in both the hypertensive and normotensive subgroups . More patients reversed to normoalbuminuria with valsartan ( 29.9 % versus 14.5%;P = 0.001 ) . Over the study period , BP reductions were similar between the two treatments ( systolic/diastolic 11.2/6.6 mm Hg for valsartan , 11.6/6.5 mm Hg for amlodipine ) and at no time point was there a between-group significant difference in BP values in either the hypertensive or the normotensive subgroup . Conclusions —For the same level of attained BP and the same degree of BP reduction , valsartan lowered UAER more effectively than amlodipine in patients with type 2 diabetes and microalbuminuria , including the subgroup with baseline normotension . This indicates a BP-independent antiproteinuric effect of valsartan Microalbuminuria is a strong and independent indicator of increased cardiovascular risk among individuals with and without diabetes . Therefore , microalbuminuria can be used for stratification of risk for cardiovascular disease . Once microalbuminuria is present , cardiovascular risk factor reduction should be more " aggressive . " The nature of the link between microalbuminuria and cardiovascular risk , however , remains poorly understood . There is no strong evidence that microalbuminuria causes atherothrombosis or that atherothrombosis causes microalbuminuria . Many studies have tested the hypothesis that a common risk factor underlies the association between microalbuminuria and cardiovascular disease but , again , have found no strong evidence in favor of this contention . At present , the most likely possibility is that a common pathophysiologic process , such as endothelial dysfunction , chronic low- grade inflammation , or increased transvascular leakage of macromolecules , underlies the association between microalbuminuria and cardiovascular disease , but more and prospect i ve studies of these hypotheses are needed Background —Microalbuminuria is associated with increased risk of cardiovascular events . We assessed whether therapeutic intervention aim ed at lowering urinary albumin excretion would reduce cardiovascular events in microalbuminuric subjects ( 15 to 300 mg/24 hours ) . Methods and Results —From the Prevention of Renal and Vascular Endstage Disease ( PREVEND ) cohort ( n=8592 ) , 1439 subjects fulfilled the inclusion criteria of the PREVEND Intervention Trial ( PREVEND IT ) . Of these subjects , 864 were r and omized to fosinopril 20 mg or matching placebo and to pravastatin 40 mg or matching placebo . The mean follow-up was 46 months , and the primary end point was cardiovascular mortality and hospitalization for cardiovascular morbidity . Mean age was 51±12 years ; 65 % of subjects were male , and 3.4 % had a previous cardiovascular event . Mean cholesterol level was 5.8±1.0 mmol/L , mean systolic/diastolic blood pressure was 130±18/76±10 mm Hg , and median urinary albumin excretion was 22.8 ( 15.8 to 41.3 ) mg/24 hours . The primary end point occurred in 45 subjects ( 5.2 % ) . Fosinopril  reduced urinary albumin excretion by 26 % ( P<0.001 ) . Subjects treated with fosinopril showed a 40 % lower incidence of the primary end point ( hazard ratio 0.60 [ 95 % CI 0.33 to 1.10 ] , P=0.098 , log-rank ) . Pravastatin did not reduce urinary albumin excretion , and subjects treated with pravastatin showed a 13 % lower incidence of the primary end point than subjects in the placebo group ( 0.87 [ 0.49 to 1.57 ] , P=0.649 , log-rank ) . Conclusions —In microalbuminuric subjects , treatment with fosinopril had a significant effect on urinary albumin excretion . In addition , fosinopril treatment was associated with a trend in reducing cardiovascular events  . Treatment with pravastatin did not result in a significant reduction in urinary albumin excretion or cardiovascular events Urinary albumin excretion is a predictor for cardiovascular mortality and morbidity . We investigated which parameters determine baseline urinary albumin excretion in nondiabetic subjects , without renal disease . In addition , we evaluated the parameters that predict the albuminuria-lowering efficacy of an angiotensin-converting enzyme inhibitor . In this sub study of the Prevention of Renal and Vascular Endstage Disease Intervention Trial , 384 microalbuminuric patients were included . Patient and biochemical characteristics were obtained at baseline and after 3 months of double-blinded , r and omized treatment ( fosinopril 20 mg or placebo ) . Mean age was 51.1±11.5 years , and 65.6 % were male .  Median urinary albumin excretion was 22.2 mg per 24 hours . At baseline , mean arterial pressure ( & bgr;st and ardized=0.161 ; P=0.006 ) , urinary sodium excretion ( & bgr;st and ardized=0.154 ; P=0.011 ) , and estimated renal function were independently associated with albumin excretion . In these predominantly normotensive to prehypertensive subjects  , fosinopril  reduced albumin excretion by 18.5 % versus a 6.1 % increase on placebo after 3 months ( P<0.001 ) . Fosinopril use and blood pressure reduction independently predicted the change in urinary albumin excretion . Baseline urinary albumin excretion independently predicted the antialbuminuric effect  of fosinopril ( & bgr;st and ardized=−0.303 ; P<0.001 ) . In conclusion , at baseline , sodium intake and blood pressure were positively associated with urinary albumin excretion . Fosinopril  reduced albuminuria more than might be expected from its blood pressure – lowering effect alone , and this effect was more outspoken in subjects with higher baseline albumin excretion . Based on our data , we hypothesize that angiotensin-converting enzyme inhibition may result in superior cardiovascular protection when compared with other blood pressure – lowering agents in subjects with higher baseline levels of albuminuria BACKGROUND Silent brain infa rcts are frequently seen on magnetic resonance imaging ( MRI ) in healthy elderly people and may be associated with dementia and cognitive decline . METHODS We studied the association between silent brain infa rcts and the risk of dementia and cognitive decline in 1015 participants of the prospect i ve , population -based Rotterdam Scan Study , who were 60 to 90 years of age and free of dementia and stroke at base line . Participants underwent neuropsychological testing and cerebral MRI at base line in 1995 to 1996 and again in 1999 to 2000 and were monitored for dementia throughout the study period . We performed Cox proportional-hazards and multiple linear-regression analyses , adjusted for age , sex , and level of education and for the presence or absence of subcortical atrophy and white-matter lesions . RESULTS During 3697 person-years of follow-up ( mean per person , 3.6 years ) , dementia developed in 30 of the 1015 participants . The presence of silent brain infa rcts at base line more than doubled the risk of dementia ( hazard ratio , 2.26 ; 95 percent confidence interval , 1.09 to 4.70 ) . The presence of silent brain infa rcts on the base-line MRI was associated with worse performance on neuropsychological tests and a steeper decline in global cognitive function . Silent thalamic infa rcts were associated with a decline in memory performance , and nonthalamic infa rcts with a decline in psychomotor speed . When participants with silent brain infa rcts at base line were subdivided into those with and those without additional infa rcts at follow-up , the decline in cognitive function was restricted to those with additional silent infa rcts . CONCLUSIONS Elderly people with silent brain infa rcts have an increased risk of dementia and a steeper decline in cognitive function than those without such lesions Few data are available to clarify whether changes in albuminuria over time translate to changes in cardiovascular risk . The aim of the present study was to examine whether changes in albuminuria during 4.8 years of antihypertensive treatment were related to changes in risk in 8206 patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension ( LIFE ) study .  Urinary albumin/creatinine ratio ( UACR ) was measured at baseline and annually . Time-varying albuminuria was closely related to risk for the primary composite end point ( ie , when UACR decreased during treatment , risk was reduced accordingly ) . When the population was divided according to median baseline value ( 1.21 mg/mmol ) and median year 1 UACR ( 0.67 mg/mmol ) , risk increased stepwise and significantly for the primary composite end point from those with low baseline/low year 1 ( 5.5 % ) , to low baseline/high year 1 ( 8.6 % ) , to high baseline/low year 1 ( 9.4 % ) , and to high baseline/high year 1 ( 13.5 % ) values . Similar significant , stepwise increases in risk were seen for the components of the primary composite end point ( cardiovascular mortality , stroke , and myocardial infa rct ion ) . The observation that changes in UACR during antihypertensive treatment over time translated to changes in risk for cardiovascular morbidity and mortality was not explained by in-treatment level of blood pressure . We propose that monitoring of albuminuria should be an integrated part of the management of hypertension . If albuminuria is not decreased by the patient ’s current antihypertensive and other treatment , further intervention directed toward blood pressure control and other modifiable risks should be considered Background and Purpose — The prevalence 
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In the meantime , with several recent systematic review s of published evidence supporting a robust and independent association of  CKD  with subsequent cerebrovascular disease risk , optimal implementation of established stroke risk reduction strategies in individuals with CKD  might improve stroke outcomes .