***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: Contrast-induced nephropathy ( CIN ) is an important cause of mortality and morbidity in patients undergoing angiography . This study investigated whether statins decrease incidence of CIN in the setting of  percutaneous coronary intervention ( PCI )  and evaluated the influence of such potential benefit on long-term outcome . Four-hundred thirty-four patients undergoing PCI were prospect ively enrolled and followed up to 4 years . Patients were stratified according to preprocedural statin therapy ( 260 statin treated , 174 statin naive ) . CIN was defined as a postprocedural increase in serum creatinine of > or=0.5 mg/dl or>25 % from baseline . Follow-up assessment included 4-year occurrence of major adverse cardiac events .  Statin-treated patients had a significantly lower incidence of CIN ( 3 % vs 27 % , p<0.0001 ; 90 % risk decrease ) and had better postprocedural creatinine clearance ( 80+/-20 vs 65+/-16 ml/min , p<0.0001 ) . Benefit of statin before treatment was observed in all subgroups , except in patients with a pre-existing creatinine clearance<40 ml/min . During follow-up , CIN was a predictor of poorer outcome ; 4-year survival free of major adverse cardiac events was highest in statin-treated patients without CIN ( 95 % , p < or=0.015 ) and lowest in statin-naive patients with CIN ( 53 % , p < or=0.018 ) . In conclusion , patients receiving statins before PCI have a significant decrease of CIN ; this early protective effect translates into better long-term event-free survival . These results may lend further support to utilization of statins as adjuvant pharmacologic therapy before PCI Contrast-induced nephropathy limits the outcomes of percutaneous coronary intervention ( PCI ) . The present study compared the protective effects of different statin doses on renal function . A total of 228 patients with acute coronary syndrome undergoing selective PCI were r and omly divided into simvastatin 20-mg group ( S20 , n = 115 ) and simvastatin 80-mg group ( S80 , n = 113 ) . Serum creatinine was measured at admission , the day of PCI , and 24 and 48 hours after PCI . The creatinine clearance was calculated using the Cochcroft-Gault formula . High-sensitive C-reactive protein , P-selectin , and intercellular adhesion molecule-1 were also measured before and after the procedure . Contrast-induced nephropathy was defined as a postprocedure increase in serum creatinine of > or = 0.5 mg/dl or > 25 % from baseline . The serum creatinine significantly increased after PCI , with the peak value occurring at 24 hours , and then began to decrease . At 48 hours , the serum creatinine had decreased to the baseline level in the S80 group , but it had failed to do so in the S20 group . At 24 and 48 hours after PCI , the serum creatinine was lower in the S80 group than in the S20 group ( p < 0.05 and p < 0.001 , respectively ) . The creatinine clearance significantly decreased after PCI , with the lowest value occurring at 24 hours , and then it began to increase . In the S80 group , the creatinine clearance recovered to baseline level at 48 hours , but it failed to do so in the S20 group . The creatinine clearance was greater at 24 and 48 hours in the S80 group than that in the S20 group . Although the procedure caused a significant increase in high-sensitive C-reactive protein , P-selectin , and intercellular adhesion molecule-1 levels , the value was lower in the S80 group than in the S20 group ( p < 0.001 ) . In conclusion , pretreatment with simvastatin 80 mg before PCI could further decrease the occurrence of contrast-induced nephropathy compared with simvastatin 20 mg . This benefit was associated with the lowering of high-sensitive C-reactive protein , P-selectin , and intercellular adhesion molecule-1 levels We investigated the efficacy of short-term high-dose atorvastatin in decreasing the risk of contrast-induced nephropathy ( CIN ) in patients with chronic kidney disease ( CKD ) subjected to coronary angiography and /or angioplasty . CIN occurs in up to 15 % of patients with pre-existing CKD and affects clinical outcome . The protective effect of statin therapy against CIN is still controversial . A prospect i ve , single-center study of 304 patients with baseline estimated creatinine clearance < 60 ml/min were r and omized to receive atorvastatin 80 mg/day or placebo for 48 hours before and 48 hours after contrast medium administration . All patients received intravenous saline hydration and oral N-acetylcysteine 1,200 mg 2 times/day . Iso-osmolar contrast medium was used . CIN was defined as an absolute increase of serum creatinine > or = 0.5 mg/dl within 5 days after the procedure . CIN occurred in 31 patients ( 10 % ) , 16 ( 11 % ) in the placebo group and 15 ( 10 % ) in the atorvastatin group ( p = 0.86 ) . Mean increase in creatinine was not significantly different in the 2 groups ( 0.59 + or - 0.17 in placebo group vs 0.72 + or - 0.26 mg/dl in atorvastatin group , p = 0.31 ) . Persistent kidney injury , defined as 1-month increase from baseline creatinine value > or = 25 % , was observed in 30 % in the placebo group and in 31 % in the atorvastatin group ( p = 0.58 ) . In conclusion , a short-term administration of high doses of atorvastatin before and after contrast exposure , in addition to st and ard intravenous hydration and oral N-acetylcysteine , does not decrease CIN occurrence in patients with pre-existing CKD Objectives : To investigate whether preprocedural high-dose atorvastatin decreases the incidence of contrast-induced nephropathy ( CIN ) and protects the renal function after emergency percutaneous coronary intervention ( PCI ) . Methods : Statin-naive patients with acute ST-segment elevation myocardial infa rct ion ( STEMI ) undergoing emergency PCI ( n = 161 ) r and omly received atorvastatin ( 80 mg , n = 78 , ATOR group ) or placebo [ n = 83 , control ( CON ) group ] followed by long-term atorvastatin ( 40 mg/day ) . The primary end point was incidence of CIN . Results : In the ATOR group , 2.6 % of the patients developed CIN versus 15.7 % in the CON group ( p = 0.01 ) . In the ATOR group , postprocedural serum creatinine was significantly lower ( 93.4 ± 17.1 vs. 112.6 ± 23.3 µmol/l at 48 h and 84.2 ± 14.2 vs. 95.3 ± 17.7 µmol/l at 72 h , both p < 0.0001 ) and in the CON group , peak serum cystatin C was lower ( 0.51 ± 0.14 vs. 0.61 ± 0.13 mg/l , p < 0.0001 ) . Atorvastatin pretreatment was independently associated with a decreased risk of CIN ( OR 0.084 , 95 % CI 0.015–0.462 , p = 0.004 ) . The proportion of alanine aminotransferase > 3 × upper limit of the normal value within 1 month was 3.85 versus 1.20 % ( ATOR vs. CON group , p = 0.57 ) . Conclusion : Preprocedural high-dose atorvastatin prevents CIN and protects the renal function in patients with acute STEMI undergoing emergency PCI Background and aims . Gentamicin ( GM ) is still considered to be an important antibiotic against life-threatening , gram-negative bacterial infections despite its known nephrotoxic effects . We aim ed to evaluate the potential protective effect of atorvastatin ( ATO ) against GM-induced nephrotoxicity in rats . Material s and methods . The rats were r and omly divided into five groups of six animals each : control , GM ( 100 mg/kg/day ) , ATO ( 10 mg/kg/day ) , GM + ATO , and GM + Vehicle .  Kidney function tests , tissue oxidative stress parameters , and histopathological and immunohistochemical studies clarified GM nephrotoxicity . Results . GM caused a marked reduction in renal functions and increased oxidative stress parameters . Histopathological examination revealed tubular necrosis especially in the renal cortex in GM rats . On immunohistochemical evaluation , GM rat showed more intense expressions of mitogen-activated protein kinase ( MAPK ) , nuclear factor kappa B ( NF‐kB ) , and inducible nitric oxide synthase ( iNOS ) compared with control . Kidney function tests and tissue oxidative stress parameters were normalized in the GM + ATO group . Histopathological and immunohistochemical pictures were also greatly ameliorated . Conclusions . ATO acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GM via the inhibition of MAPK and NF-kB signaling pathways and iNOS expression A decline in kidney function after contrast exposure is associated with a high risk of morbidity and mortality during hospitalization and over long-term periods . Several retrospective and recent prospect i ve clinical trials have shown that statin therapy might prevent contrast-induced nephropathy in patients undergoing percutaneous coronary intervention . In this study , we aim ed to assess the effects of statin therapies on renal function parameters in patients undergoing elective coronary angiography . One hundred and sixty patients undergoing elective coronary angiography were r and omized equally into two groups : atorvastatin 40 mg/day group ( statin started 3 days before coronary angiography ) and an untreated control group . An additional 80 patients were included as a chronic statin therapy group . Serum creatinine , serum cystatin C , and glomerular filtration rate ( GFR ) were measured before and 48 h after coronary angiography . Cockcroft – Gault and Modification of Diet in Renal Disease ( MDRD ) equations were used to determine GFR . After coronary angiography , serum creatinine and GFR determined by MDRD were significantly better in patients using atorvastatin than those in controls ( P = 0.002 and P = 0.004 , respectively ) . Postprocedure serum creatinine , cystatin C , and GFR determined by MDRD were also significantly better in chronic statin therapy group than those in controls ( P = 0.006 , P = 0.003 , and P = 0.004 , respectively ) . There were no differences in renal function parameters between the short-term atorvastatin group and the chronic statin therapy group . Our data demonstrate that the use of short-term atorvastatin and chronic statin therapy may have a role in protecting renal function after elective coronary angiography Contrast-induced nephropathy ( CIN ) impairs clinical outcome in patients undergoing angiographic procedures . The aim of this study was to investigate whether short-term high-dose atorvastatin load decreases the incidence of CIN after percutaneous coronary intervention ( PCI ) .  Statin-naive patients with acute coronary syndrome undergoing PCI ( n = 241 ) r and omly received atorvastatin ( 80 mg 12 hours before intervention with another 40-mg preprocedure dose , n = 120 ) or placebo ( n = 121 ) . All patients had long-term atorvastatin treatment thereafter ( 40 mg/day ) . Primary end point was incidence of CIN defined as postintervention increase in serum creatinine ≥0.5 mg/dl or > 25 % from baseline . Five percent of patients in the atorvastatin arm developed CIN versus 13.2 % of those in the placebo arm ( p = 0.046 ) . In the atorvastatin group , postprocedure serum creatinine was significantly lower ( 1.06 ± 0.35 vs 1.12 ± 0.27 mg/dl in placebo , p = 0.01 ) , creatinine clearance was decreased ( 80.1 ± 32.2 vs 72.0 ± 26.6 ml/min , p = 0.034 ) , and C-reactive protein peak levels after intervention were decreased ( 8.4 ± 10.5 vs 13.1 ± 20.8 mg/l , p = 0.01 ) . Multivariable analysis showed that atorvastatin pretreatment was independently associated with a decreased risk of CIN ( odds ratios 0.34 , 95 % confidence interval 0.12 to 0.97 , p = 0.0 
    Output:
    
This review concluded that  chronic statin user may be less prone to contrast-induced nephropathy ( CIN ) compared with statin  non-users .
Short-term high dose statin administration may also reduce the incidence of CIN in  statin  naïve patients .
This renoprotective effect of statins against CIN is seen in low risk patients with normal kidney function or mild kidney dysfunction , but probably not in patients with moderate to severe renal dysfunction .