***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: INTRODUCTION Diabetic Nephropathy ( DN ) is one of the main complications of diabetes mellitus , mostly ending to end-stage renal disease . Leptin and C-reactive protein ( CRP ) , as inflammatory markers implicated in the progression of DN , increase in diabetes mellitus , while transferrin and albumin , as members of anti-oxidant defense mechanism , are found to decline . MATERIAL S AND METHODS In a controlled clinical trial , 65 patients with type 2 DN were assigned to receive lovastatin or placebo , for 3 months , to assess statins ' impact on serum levels of leptin , CRP , transferrin , albumin , and lipid profile . RESULTS Serum levels of CRP ( 3.52 + /- 4.16 mg/dL to 2.84 + /- 3.06 mg/dL , P = .02 ) , leptin ( 10.78 + /- 8.30 mg/dL to 7.80 + /- 5.41 mg/dL , P = .006 ) , low-density lipoprotein cholesterol ( 116.16 + /- 46.54 mg/dL to 85.46 + /- 29.22 mg/dL , P = .001 ) , and total cholesterol ( 199.00 + /- 43.33 mg/dL to 164.67 + /- 35.19 mg/dL , P = .001 ) were lowered after lovastatin therapy . Mean serum level of high-density lipoprotein cholesterol increased ( 40.00 mg/dL to 42.80 mg/dL , P = .005 ) after the treatment . Lovastatin had no significant effect on albumin and transferrin . Placebo did not change any of the parameters after 3 months . CONCLUSIONS The effect of statins on the inflammatory markers involved in the development of DN is a new approach to evidence supporting the pleiotropic effect of this drug group 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 AIM We aim ed to assess the effects of rosuvastatin treatment on lipid levels , a biomarker of oxidative stress , albuminuria , and kidney function in patients with diabetic nephropathy . METHODS We conducted a prospect i ve , open-label , parallel group , controlled study of 104 patients with diabetic nephropathy , low-density lipoprotein cholesterol ( LDL-C ) levels of > 120 mg/dL , and well-controlled blood pressure who were undergoing treatment with renin angiotensin system inhibitors .  Patients were r and omly assigned to two groups : the rosuvastatin group ( n = 52 ; 2.5 mg/day rosuvastatin , increased to 10 mg/day ) and the control group ( n = 52 ; no rosuvastatin administered ) . We determined the efficacy of rosuvastatin by monitoring serum lipid profiles , high sensitivity C-reactive protein ( hs-CRP ) , malondialdehyde-modified LDL ( MDA-LDL ) , and cystatin C levels . In addition , urinary albumin , 8-hydroxydeoxyguanosine ( 8-OHdG ) and liver-type fatty acid-binding protein ( L-FABP ) levels were measured before and 6 months after rosuvastatin was added to the treatment . RESULTS Rosuvastatin effectively reduced total cholesterol , LDL-C , triglycerides , non-high-density lipoprotein cholesterol ( non-HDL-C ) levels , and the LDL-C/ HDL-C ratio in the rosuvastatin group . These parameters remained unchanged in patients who were not treated with rosuvastatin . Although there was no significant change in the estimated glomerular filtration rate level , serum cystatin C levels and urinary albumin excretion rates were significantly decreased in the rosuvastatin group . In addition , rosuvastatin significantly reduced hs-CRP and MDA-LDL levels . Moreover , urinary 8-OHdG and L-FABP levels at baseline ( 13.5±5.1 and 41.7±26.1 ng/mgCr , respectively ) decreased significantly at 6 months ( 11.5±4.0 and 26.9±13.4 ng/mgCr , respectively ) , and there was a significant correlation ( r = 0.48 , p < 0.01 ) . Multivariate analysis revealed that albuminuria was significantly correlated with only rosuvastatin use ( p = 0.0006 , R(2)= 0.53 ) . CONCLUSION Rosuvastatin administration reduced albuminuria , oxidative stress , and serum cystatin C levels , independent of blood pressure and lipid levels OBJECTIVE Liver-type fatty acid-binding protein ( l-FABP ) is expressed in renal proximal tubules and is reported to be a useful marker for progression of chronic glomerulonephritis . The aim of this study was to determine whether urinary l-FABP levels are altered at various stages of diabetic nephropathy and whether pitavastatin affects urinary l-FABP levels in early diabetic nephropathy . RESEARCH DESIGN AND METHODS Fifty-eight patients with type 2 diabetes ( 34 men and 24 women , median age 52 years ) and 20 healthy , age-matched subjects ( group E ) were recruited for the study . The diabetic patients included 12 patients without nephropathy ( group A ) , 20 patients with microalbuminuria ( group B ) , 14 patients with macroalbuminuria and normal renal function ( group C ) , and 12 patients with chronic renal failure but not undergoing hemodialysis ( blood creatinine > 1.2 mg/dl ; mean 2.5 mg/dl , group D ) . Twenty group B patients were r and omly assigned to receive 1 mg/day pitavastatin ( 10 patients , group B1 ) or placebo ( 10 patients , group B2 ) . Treatment was continued for 12 months . Urinary l-FABP levels were measured by enzyme-linked immunosorbent assay . Urinary 8-hydroxydeoxyguanosine and serum free fatty acids ( FFAs ) were also measured in group B. RESULTS Urinary l-FABP levels in groups A-D were 6.2 + /- 4.6 microg/g creatinine , 19.6 + /- 13.5 microg/g creatinine , 26.8 + /- 20.4 microg/g creatinine , and 52.4 + /- 46.8 microg/g creatinine , respectively . Urinary l-FABP levels in groups B-D were significantly higher than those in healthy subjects ( group E , 5.8 + /- 4.0 microg/g creatinine ) ( group B , P < 0.05 ; group C , P < 0.01 ; group D , P < 0.01 ) . In group B1 , urinary albumin excretion ( UAE ) and urinary l-FABP levels were decreased after pitavastatin treatment ( UAE before , 110 + /- 74 microg/min ; 6 months , 88 + /- 60 microg/min , P < 0.05 ; 12 months , 58 + /- 32 microg/min , P < 0.01 ; l-FABP before , 18.6 + /- 12.5 microg/g creatinine ; 6 months , 12.2 + /- 8.8 microg/g creatinine , P < 0.05 ; 12 months , 8.8 + /- 6.4 microg/g creatinine , P < 0.01 ) . In group B2 , UAE and l-FABP levels showed little change during the experimental period . In group B1 , urinary 8-hydroxydeoxyguanosine was decreased 12 months after pitavastatin treatment ( before 32.5 + /- 19.5 ng/mg creatinine , after 18.8 + /- 14.5 ng/mg creatinine , P < 0.01 ) , but in group B2 , these showed little difference during the experimental period . In both groups B1 and B2 , serum FFAs showed little difference during the experimental period . CONCLUSIONS Urinary l-FABP levels appear to be associated with the progression of diabetic nephropathy , and pitavastatin may be effective in ameliorating tubulointerstitial damage in early diabetic nephropathy Background / Aims : To determine whether cerivastatin , a newly developed novel synthetic potent statin , exerts a renoprotective effect , we assessed urinary albumin excretion ( UAE ) and plasma and urinary endothelin (ET)-1 concentrations in normotensive microalbuminuric type 2 diabetes patients with dyslipidemia . Methods : Sixty normotensive type 2 diabetic patients ( 38 men and 22 women ; mean age 56.5 years ) with microalbuminuria ( 20–200 µg/min ) and dyslipidemia ( total cholesterol > 200 mg/dl , LDL cholesterol > 160 mg/dl , HDL cholesterol < 35 mg/dl , and triglyceride > 150 mg/dl ) were enrolled in a double-blind study for 6 months , receiving either cerivastatin ( 0.15 mg/day ) or placebo . Plasma and urinary ET-1 concentrations were measured by radioimmunoassay . Results : Cerivastatin did not affect serum creatinine and HbA1c levels , and reduced systolic blood pressure slightly , but not significantly . Plasma levels of total cholesterol and LDL cholesterol were significantly reduced ( p < 0.01 ) , and plasma triglyceride levels were also reduced significantly ( p < 0.05 ) after 6 months of cerivastatin treatment . A concomitant significant decrease in UAE ( p < 0.01 ) , and urinary and plasma ET-1 concentrations ( p < 0.01 ) were found during this period . Conclusion : The use of cerivastatin is associated with decreased microalbuminuria and plasma and urinary ET-1 levels in microalbuminuric patients with type 2 diabetic mellitus and speculate that this may represent an amelioration of renal injury The effects of pravastatin on plasma lipid levels , in vitro 
    Output:
    
In general , our study demonstrated that statins might have beneficial effects on reducing albuminuria in diabetic kidney disease patients .
However , there was no strong evidence that the same intervention had an effect on overt proteinuria or eGFR outcomes in these patients