***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: BASIS Hyperlipidemia associated to nephrotic syndrome has been involved in the deterioration of the renal function in these patients . The reduction in the synthesis of cholesterol with pravastatin , an hydrophilic inhibitor of such synthesis , may improve both the dyslipemia , the renal function and the proteinuria . METHODS We conducted a controlled open r and omized study in 16 patients with proteinuria greater than 2 g/day , creatinine clearance greater than 0.5 ml/s ( 30 ml/min ) and hypercholesterolemia with LDL cholesterol greater than 4.9 mmol/l ( 190 mg/dl ) distributed in two groups . One of these groups received hypolipemiant dietetic treatment and 20 - 40 mg of pravastatin and the other group , only the dietetic treatment . RESULTS The patients receiving pravastatin showed a 27 % decrease in total plasmatic cholesterol , compared to a 6.7 % in the control group ( p < 0.01 ) . This decrease was more evident in the LDL cholesterol fraction ( 44 vs 9 % ; p < 0.01 ) . No significant modifications were observed in the HDL cholesterol fraction , triglycerides , renal function or proteinuria . Neither clinical nor enzymatiz adverse effects from hepatic or muscular origin were observed Background : Little is known about statins in the prevention of  dyslipidaemia induced renal function decline . The secondary coronary heart disease ( CHD ) prevention GREACE study suggested that dose titration with atorvastatin ( 10–80 mg/day , mean dose 24 mg/day ) achieves the national cholesterol educational programme treatment goals and significantly reduces morbidity and mortality , compared with usual care . Aims : To report the effect of statin on renal function compared with untreated dyslipidaemia in both treatment groups . Methods / Results : All patients had plasma creatinine values within the reference range < 115 µmol/litre ( 13 mg/litre ) .  The on study creatinine clearance ( CrCl ) , as estimated ( for up to 48 months ) by the Cockroft-Gault formula , was compared within and between treatment groups using analysis of variance to assess differences over time . Patients from both groups not treated with statins ( 704 ) showed a 5.2 % decrease in CrCl ( p < 0.0001 ) . Usual care patients on various statins ( 97 ) had a 4.9 % increase in CrCl ( p = 0.003 ) . Structured care patients on atorvastatin ( 783 ) had a 12 % increase in CrCl ( p < 0.0001 ) . This effect was more prominent in the lower two quartiles of baseline CrCl and with higher atorvastatin doses . After adjustment for 25 predictors of all CHD related events , multivariate analysis revealed a hazards ratio of 0.84 ( confidence interval 0.73 to 0.95 ; p = 0.003 ) with every 5 % increase in CrCl . Conclusions : In untreated dyslipidaemic patients with CHD and normal renal function at baseline , CrCl declines over a period of three years . Statin treatment prevents this decline and significantly improves renal function , potentially off setting an additional factor associated with CHD risk Proteinuria is an important risk factor for cardiovascular and renal morbidity and mortality . The effects of 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitor ( statin ) therapy on proteinuria in normolipidemic patients with well-controlled hypertension have not been studied . A total of 63 normolipidemic ( total cholesterol < 240 mg/dL ) and proteinuric ( 300 to 3000 mg/d ) patients with well-controlled blood pressure ( < 140/90 mm Hg ) were r and omized to receive either placebo ( n=32 ) or pravastatin ( 10 mg/d ; n=31 ) after a 3-month placebo period . Pravastatin lowered proteinuria after 6 months by 54 % ( P < 0.0001 ) . Creatinine clearance was stable throughout the study in the 2 groups . Despite unchanged plasma endothelin-1 levels throughout the study , urinary excretion of the peptide was decreased and significantly correlated with improvement in urinary protein excretion in pravastatin-treated patients ( r = 0.64 , P = 0.001 ) . The urinary excretion of retinol-binding protein decreased after pravastatin administration , probably reflecting an improvement in tubular function . In contrast , the urinary excretion of IgG did not change significantly throughout the study in either group . Multivariate analysis revealed that proteinuria was only significantly correlated with statin use ( P < 0.0001 , R2= 0.66 ) . Linear regression analysis in the statin-treated group did not show any correlation between changes in lipid profiles and proteinuria regression . Thus , in addition to their primary function of antilipidemia , the addition of pravastatin to treatment for well-controlled hypertension may have an additive effect on reducing proteinuria independent of hemodynamics and lipid-lowering effects , possibly through inhibiting renal endothelin-1 synthesis and improving tubular function 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 Summary The effect of simvastatin ( 10–20 mg/day ) on kidney function , urinary albumin excretion rate and insulin sensitivity was evaluated in 18 Type 2 ( non-insulin-dependent ) diabetic patients with microalbuminuria and moderate hypercholesterolaemia ( total cholesterol ≥5.5 mmol·l−1 ) . In a double-blind , r and omized and placebo-controlled design treatment with simvastatin ( n=8 ) for 36 weeks significantly reduced total cholesterol ( 6.7±0.3 vs 5.1 mmol·l−1 ( p<0.01 ) ) , LDL-cholesterol ( 4.4±0.3 vs 2.9±0.2 mmol·l−1 ( p<0.001 ) ) and apolipoprotein B ( 1.05±0.04 vs 0.77±0.02 mmol·l−1 ( p<0.01 ) ) levels as compared to placebo ( n=10 ) . Both glomerular filtration rate ( mean±SEM ) ( simvastatin : 96.6±8.0 vs 96.0±5.7 ml·min−1·1.73 m−2 , placebo : 97.1±6.7 vs 88.8±6.0 ml·min−1·1.73 m−2 ) ( NS ) and urinary albumin excretion rate ( geometric mean x/÷ antilog SEM ) ( simvastatin : 18.4x/÷1.3vs 16.2 x/÷1.2 μg·min−1 , placebo 33.1 x/÷ 1.3 vs 42.7 x/÷ 1.3 μg·min−1)(NS ) were unchanged during the study . A euglycaemic hyperinsulinaemic clamp was performed at baseline and after 18 weeks in seven simvastatin- and nine placebo-treated patients . Isotopically determined basal and insulin-stimulated glucose disposal was similarly reduced before and during therapy in both the simvastatin ( 2.0±0.1 vs 1.9±0.1 ( NS ) and 3.1±0.6 vs 3.1±0.7 mg·kg−1·min−1 ( NS ) ) and the placebo group ( 1.9±0.1 vs 1.8±0.1 ( NS ) and 4.1±0.6 vs 3.8±0.2 mg·kg−1·min−1 ( NS ) ) . No different was observed in glucose storage or glucose and lipid oxidation before and after treatment . Further , the suppression of hepatic glucose production during hyperinsulinaemia was not influenced by simvastatin ( −0.7±0.8 vs −0.7±0.5 mg·kg−1·min−1 ( NS ) ) . In conclusion , despite marked improvement in the dyslipidaemia simvastatin had no impact on kidney function or urinary albumin excretion rate and did not reduce insulin resistance in these microalbuminuric and moderately hypercholesterolaemic Type 2 diabetic patients BACKGROUND In animal models , HMG-CoA reductase inhibitors were able to improve renal function and endothelium-dependent vascular reactivity . In various experimental renal diseases , including autosomal dominant polycystic kidney disease ( ADPKD ) , HMG-CoA reductase inhibitors improved the rate of decline in renal function . We studied the effect of simvastatin on ADPKD patients . METHODS In a double-blind cross-over study , 10 normocholesterolaemic ADPKD patients were treated in r and om order for 4 weeks with 40 mg simvastatin or placebo daily . After each treatment period , we investigated the effect of simvastatin on renal blood flow and endothelium-dependent vascular reactivity . These periods were separated by a 4-week wash-out period . RESULTS After treatment with simvastatin , glomerular filtration rate ( GFR ) significantly increased from 124+/-4 ml/min to 132+/-6 ml/min ( P<0.05 ) . Simultaneously , effective renal plasma flow ( ERPF ) increased significantly from 494+/-30 ml/min to 619+/-67 ml/min after simvastatin treatment ( P<0.05 ) . These renal effects were accompanied by a significantly enhanced vasodilator response to acetylcholine in the forearm after simvastatin treatment . Total serum cholesterol levels were significantly reduced after treatment with simvastatin , from 4.24+/-0.32 to 3.17+/-0.22 mmol/l ( P<0.001 ) . CONCLUSION We concluded that simvastatin treatment can ameliorate renal function in ADPKD patients , by increasing renal plasma flow , possibly via improvement of endothelial function . Long-term clinical trials with HMG-CoA reductase inhibitors are needed to confirm these results and to establish a chronic inhibiting effect of HMG-CoA reductase inhibitors on the progression towards end-stage renal disease in ADPKD patients BACKGROUND Chronic kidney diseases , particularly if presenting with significant proteinuria , are commonly associated with substantial alteration of serum lipid levels . Experimental evidence suggests that lipid abnormalities may contribute to the progression of kidney disease . However , studies in humans on the subject are scarce . METHODS In a prospect i ve , controlled open-label study , the authors have evaluated the effects of one-year treatment with atorvastatin , a 3-hydroxy-3-methyglutaryl coenzyme A ( HMG-CoA ) reductase inhibitor , versus no treatment on proteinuria and progression of kidney disease in 56 patients with chronic kidney disease . Before r and omization , all patients had already been treated for one year with angiotensin-converting enzyme ( ACE ) inhibitors or angiotensin AT1 receptor antagonists ( ARBs ) and other 
    Output:
    
Statin therapy seems to reduce proteinuria modestly and results in a small reduction in the rate of kidney function loss , especially in population s with cardiovascular disease