***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: BACKGROUND We previously reported urinary podocytes to be a marker of glomerular injury . The aim of the present study was to determine whether cerivastatin , a newly developed , potent synthetic statin , affects proteinuria and urinary podocyte excretion in patients with chronic glomerulonephritis ( CGN ) . METHODS We r and omly assigned 40 normotensive hypercholesterolemic patients with CGN to receive either cerivastatin 0.15 mg/day ( n=20 ) or placebo ( n=20 ) . Subjects comprised 24 men and 16 women , with a mean age of 40.8+/-14.4 years ; 27 had IgA nephropathy and 13 had non-IgA proliferative glomerulonephritis . Treatment was continued for 6 months . Plasma total cholesterol , HDL-cholesterol , LDL-cholesterol and triglycerides , urinary protein excretion and the number of podocytes were measured before treatment and at 3 and 6 months after treatment . RESULTS After 6 months , a significant reduction in total cholesterol ( P<0.001 ) , LDL-cholesterol ( P<0.001 ) and triglycerides ( P<0.05 ) , and a significant increase in HDL-cholesterol ( P<0.001 ) were observed in the group treated with cerivastatin .  Urinary protein excretion decreased from 1.8+/-0.6 to 0.8+/-0.4 g/day , ( P<0.01 ) in this group , and urinary podocyte excretion decreased from 1.6+/-0.6 to 0.9+/-0.4 cells/ml ( P<0.01 ) . However , placebo showed little effect on these lipid levels , urinary protein excretion and urinary podocyte excretion . The differences between the cerivastatin group and the placebo group were significant ( cholesterol , P<0.001 ; LDL-cholesterol , P<0.001 ; triglycerides , P<0.05 ; HDL-cholesterol , P<0.001 ; urinary protein , P<0.01 ; and urinary podocytes , P<0.01 ) . CONCLUSION Statins such as cerivastatin may be beneficial for restoration of injured podocytes in patients with CGN and hypercholesterolaemia BACKGROUND Serum creatinine-based estimates of glomerular filtration rate ( eGFR ) are frequently used to identify patients with chronic kidney disease and assess cardiovascular risk both in clinical trials and in clinical practice . Although change in eGFR may be useful to assess change in renal function in patients with chronic kidney disease , the utility of serum creatinine-based eGFR is uncertain , particularly among individuals with normal or only mildly impaired renal function . OBJECTIVE The goal of this study was to examine the relationship between baseline serum creatinine and eGFR , as well as changes in these parameters , in apparently healthy adults in a post hoc analysis of data obtained in participants in the JUPITER study ( Justification for the Use of Statins in Prevention : An Intervention Trial Evaluating Rosuvastatin ) . METHODS JUPITER was a r and omized study of rosuvastatin 20 mg versus placebo in apparently healthy adults with high-sensitivity C-reactive protein levels ≥ 2.0 mg/L , LDL-C < 130 mg/dL , and serum creatinine ≤ 2.0 mg/dL. Changes from baseline in serum creatinine and eGFR , based on the Modification of Diet in Renal Disease ( MDRD ) and Chronic Kidney Disease Epidemiology Collaboration ( CKD-EPI ) equations , were assessed in the entire population and in subsets classified according to baseline eGFR status . RESULTS Baseline characteristics of the 16,279 JUPITER study participants ( mean age , 66 years ; 62 % men ; 72 % white ; and 58 % with a history of hypertension ) who had both a baseline and ≥ 1 postbaseline serum creatinine measurement were similar to the entire population of 17,802 patients who entered the trial . The mean age of the study population was 66 years , 62 % were men , 72 % were white , and 58 % had a history of hypertension . Mean ( SD ) serum creatinine increased from baseline by 0.08 ( 0.16 ) mg/dL and 0.09 ( 0.14 ) mg/dL in the rosuvastatin and placebo groups , respectively ( P = 0.001 ) at year 1 and by 0.09 ( 0.18 ) and 0.10 ( 0.16 ) mg/dL ( P = 0.0045 ) at the final visit . Reductions in MDRD and CKD-EPI eGFR were ∼ 0.5 mL/min/1.73 m(2 ) greater with placebo than with rosuvastatin ( P < 0.004 ) at year 1 and the final visit . The magnitude of eGFR change was closely related to baseline eGFR , with greater reductions among subjects with eGFR ≥ 60 mL/min/1.73 m(2 ) in both the rosuvastatin and placebo groups . Among those with an eGFR ≥ 90 mL/min/1.73 m(2 ) , mean changes at year 1 and final visit ranged from -16 to -23 mL/min/1.73 m(2 ) with MDRD and CKD-EPI , respectively ; in contrast , mean changes were < 1 mL/min/1.73 m(2 ) in subjects with eGFR < 60 mL/min/1.73 m(2 ) . CONCLUSIONS In JUPITER , reductions in MDRD or CKD-EPI eGFR levels were greater in study participants with higher baseline eGFR levels but less in the rosuvastatin than in the placebo group . Future studies are required to assess the reliability of serum creatinine-based estimates of GFR to assess change in renal function , particularly among individuals with normal serum creatinine levels Objective . Autosomal dominant polycystic kidney disease ( ADPKD ) is progressive , result ing in end-stage kidney failure in most patients . Experimental and clinical studies have suggested that statins may slow the progression of chronic kidney disease in general and ADPKD specifically . Material and methods . This r and omized open-label clinical trial was conducted to assess the effect of pravastatin 20 mg on kidney function and urinary protein excretion in patients with ADPKD . Sixty patients were initially recruited but 49 of these received either pravastatin 20 mg or no treatment for 2 years . Trial visits were conducted every 3 months , assessing kidney function by estimated glomerular filtration rate and 24 h urine creatinine clearance and urinary protein excretion . Results . There were no significant ( p > 0.05 ) changes in markers of kidney function or urinary protein excretion between groups over the 2 years despite a significant fall in total serum cholesterol in pravastatin-treated patients ( p = 0.029 ) . Conclusion . This trial found that taking 20 mg pravastatin for 2 years had no significant effect on kidney function or urinary protein excretion in patients with ADPKD . The lack of statistical power limits the external validity of these findings . A larger , longer duration study using a higher dose of a more potent statin is required BACKGROUND Chronic kidney disease ( CKD ) is associated with an increased risk of incident cardiovascular disease ( CVD ) ; however , the role of statins for the primary prevention of acute cardiovascular events in patients with CKD and the effect of statins on kidney function loss in persons without prevalent CVD have not been studied . STUDY DESIGN Post hoc analysis of the Air Force/Texas Coronary Atherosclerosis Prevention Study . SETTING & PARTICIPANTS Multicenter , r and omized , double-blind , placebo-controlled trial of 5,608 men and 997 women without CVD r and omly assigned to treatment with lovastatin or placebo .  INTERVENTION Placebo or lovastatin , 20 mg/d . OUTCOMES & MEASUREMENTS First major acute cardiovascular event in participants with mild CKD and kidney function loss in persons with or without CKD .  Estimated glomerular filtration rate was calculated using the 4-variable Modification of Diet in Renal Disease Study equation . RESULTS At baseline ,  mean estimated glomerular filtration rate in participants with CKD ( n = 304 ) was 53.0 + /- 6.0 mL/min/1.73 m(2 ) . After an average follow-up of 5.3 + /- 0.8 years , the incidence of a fatal and nonfatal CVD event was lower in participants with CKD receiving lovastatin than in those receiving placebo ( adjusted relative risk [ RR ] , 0.31 ; 95 % CI , 0.13 - 0.72 ; P = 0.01 ) . Tests for interaction suggested that the benefit of lovastatin was independent of the presence of CKD . Lovastatin did not reduce the annualized mean decrease in estimated glomerular filtration rate ( -1.3 + /- 0.07 vs -1.4 + /- 0.07 mL/min/1.73 m(2)/y , respectively ; P = 0.1 ) or the frequency of a > or = 25 % decrease in kidney function ( adjusted RR , 1.10 ; 95 % CI , 0.96 - 1.28 ; P = 0.2 ) or incident CKD ( adjusted RR , 1.04 ; 95 % CI , 0.86 - 1.27 ; P = 0.6 ) . LIMITATIONS Unable to determine the cause and duration of kidney disease , and information regarding proteinuria was not available . CONCLUSIONS Lovastatin is effective for the primary prevention of CVD in patients with CKD , but is not effective in decreasing kidney function loss in persons with no CVD In this study 43 patients with idiopathic nephrotic syndrome were r and omly distributed into 2 age- and sex-matched groups . The first group was given fluvastatin while the second was used as control . The cases in the 2 groups were evaluated clinical ly , biochemically ( creatinine clearance , albumin , 24-hour proteinuria , and lipogram ) , neurologically , and histopathologically ( examination of renal biopsies obtained basally and after 1 year of treatment with fluvastatin ) . In the fluvastatin-treated group but not in the control group , we observed a significant reduction in cholesterol , low-density lipoprotein , and triglyceride . Clinical and laboratory assessment showed satisfactory tolerance of the drug by the patients . Proteinuria , serum albumin and creatinine clearance values were significantly better in the statin-treated patients . There was no difference in glomerular sclerosis between the 2 groups while interstitial fibrosis and renal fat deposits were less in the statin-treated group . The reduction in renal fat deposits in the statin-treated group was highly significant , while that of interstitial fibrosis was not . We conclude that : ( 1 ) statin can be safely and effectively used in the treatment of dyslipidemia in patients with persistent idiopathic nephrotic syndrome ; ( 2 ) control of dyslipidemia in nephrotic patients is associated with better control of proteinuria and creatinine clearance ; ( 3 ) statin treatment may cause regression of renal fat deposits in patients with nephrotic syndrome , and ( 4 ) longer term studies are still required to study further possible beneficial effects on renal histology and disease progression BACKGROUND The effect of atorvastatin on kidney function was assessed in patients with stages 2 - 4 chronic kidney disease . METHODS We conducted a r and omised , double-blind , placebo-controlled trial in chronic kidney disease clinics in Northern Tasmania and enrolled 132 patients with serum creatinine levels > 120 μmol/l , not taking lipid-lowering therapy and at all levels of proteinuria and serum cholesterol . Patients were r and omly assigned to receive either 10 mg of atorvastatin/day ( 64 ) or placebo ( 68 ) and were followed with trial visits 3-monthly for a mean of 2.5 yrs . The primary outcome was the rate of both MDRD eGFR and Cockcroft-Gault creatinine clearance ( C-G CrCl ) decline . Analysis was based on intention to treat and included all patients that had at least one follow-up visit . RESULTS The rate of MDRD eGFR decline was 29 % lower ; 1.04 ± 3.84 vs. 1.47 ± 3.74 ml/min/1.73 m(2)/yr ( P=0.53 ) , and the C-G CrCl was 20 % lower ; 1.88 ± 5.07 vs. 2.36 ± 4.61 ml/min/1.73 m(2)/yr ( P=0.58 ) in atorvastatin-treated , compared with placebo-treated patients . Although blood pressure decreased in both atorvastatin and placebo-treated groups there were no differences between groups . In addition , there was no difference in concomitant medication intake including angiotensin converting enzyme inhibitors and angiotensin receptor blockers between groups . CONCLUSIONS There was a trend toward a slower eGFR decline in the atorv 
    Output:
    
CONCLUSIONS Statin therapy does not reduce the risk for kidney failure events in adults not receiving dialysis for whom kidney disease outcomes were reported , but may modestly reduce proteinuria and rate of eGFR decline