| Objective: Contrast induced nephropathy(CIN) means acute renal damage happened after using contrast agent 24-28 hours. Contrast induced acute acute renal damage has been ranked third position in the hospital, due to the wide application of contrast agent in modern imaging and interventional PCI. And there is a significant increase in CIN incidence with increased interventional therapy of cardiovascular disease. Hydration therapy is now widely used to prevent CIN and has been recognized as the most effective means. Some study showed using atorvastatin before the interventional therapy may reduce the occurence of CIN. In this study, we explored by using preoperative strenthening atorvastatin and adequate hydration treatment on pateints underwent coronary angiography, to show its effect on CIN and liver transaminase.Method: Selected 80 patients underwent elective coronary intervention treatment in Department of Cardiology, Baoding Second City Center Hospital, during period of 2014 January to July. Include 51 male and 29 female; average age 57.8±9.1. All patients voluntarily joined this study with informed consents. Criteria for inclusion: patients with contrast examination and treatment for coronary indications, and preoperative serum creatinine(Scr) < 105μmol/L. Criteria for exclusion:(1) Radiography agent allergy;(2) infectious diseases;(3) autoimmune disorder;(4) cancer;(5) has used contrast agent within 1 week;(6) has received lipid-lowering therapy in 2 weeks;(7) severe heart failure patients, with left ventricular ejection fraction <40%. The 80 patients were randomly divided into conventional therapy group and intensive treatment group, 40 patients each group. Patients from two groups have no significant difference in age, sex, BMI, blood pressure, diabetes, smoke, amount of contrast agent, number of vascular lesions. Conventional therapy group: give atorvastatin 20 mg 24 hours before operative, then 20 mg atorvastatin, once per night. Apply 0.9% Na Cl injection as 1ml.kg/h intravenous drip 4 hours before operative and 6 hours after operative. Intensive treatment group: give atorvastatin 60 mg 24 hours before operative, then 40 mg atorvastatin, once per night. Apply 0.9% Na Cl injection as 1ml.kg/h intravenous drip 4 hours before operative and 6 hours after operative. Fasting blood samples were taken to test urea nitroge(BUN), creatinine(Scr), blood β2 microglobulin, high sensitivity C- reactive protein(Hs CRP) before operative and the 1st, 3rd, 7th day after operative. Urina sanguinis were also taken to test urinary N-acetyl beta-D- amino dextran enzym(NAG), urinary β2 microglobuli(β2-MG). The alanine aminotransferase(ALT) and aspertate aminotransferase(AST) were also tested at the 7th day blood test. The criteria for CIN was set as blood CREA level increased 44 μmol/L or increased 25% by the basic value after radiography 24-28 hours. We analysised the change of BUN, Scr, blood β2-MG, Hs CRP, urinary NAG, urinary β2-MG at different time point and the effect of high dose stating on liver aminotransferase.Results:1 The change of renal function index before and after treatment of two groups. Before PCI, conventional therapy group: BUN(5.46±0.23) mmol/L, Scr(74.43±10.26) umol/L, blood β2-MG(2.10±0.24) mg/L, urinary β2-MG(174.78±11.88) ug/L, urinary NAG(23.63±3.11) U/L; intensive treatment group: BUN(5.55±0.53) mmol/L, Scr(73.45±7.33) umol/L, blood β2-MG(2.13±0.33) mg/L, urinary β2-MG(173.58±17.81) ug/L, urinary NAG(23.89±2.56) U/L. There is no significant different between two groups(P>0.05). The first day after PCI, conventional therapy group: BUN(5.70±0.21) mmol/L, Scr(89.71±8.60) umol/L, blood β2-MG(3.05±0.20) mg/L, urinary β2-MG(297.69±17.11) ug/L, urinary NAG(42.38±3.17) U/L, there is a significant increased compared to the level before PCI(P<0.05). Intensive treatment group: BUN(5.75±0.30)mmol/L,Scr(85.51±8.85)umol/L,blood β2-MG(2.82±0.24)mg/L,urinary β2-MG(267.44±16.99)ug/L,urinary NAG(26.22±3.28)U/L,the results showed significant increased compared to the figure before PCI(P<0.05). There is a strong increasing of Scr, blood β2-MG, urinary β2-MG and urinary NAG in conventional therapy group(P<0.05), and there is no significant difference in change of BUN(P>0.05). The third day after PCI, conventional therapy group: BUN(5.85±0.71) mmol/L, Scr(113.98±12.65) umol/L, blood β2-MG(2.80±0.22) mg/L, urinary β2-MG(286.15±21.13) ug/L, urinary NAG(39.61±4.75) U/L. The results significantly higher than the levels before PCI(P<0.05). Intensive treatment group: Scr(93.02±8.81) umol/L, blood β2-MG(2.48±0.23) mg/L, urinary β2-MG(234.31±19.04) ug/L, urinary NAG(27.62±4.46) U/L, all showed a significant increase compared to before PCI(P<0.05). The level of BUN(5.85±0.71) mmol/L showed no significant different(P<0.05). The results of Scr, blood β2-MG, urinary β2-MG showed more significant increase between two groups(P<0.05), no significant difference in BUN level(P<0.05). The 7th day after PCI, conventional therapy group: BUN(5.62±0.34) mmol/L, Scr(84.08±10.46) umol/L, blood β2-MG(2.41±0.28) mg/L, urinary β2-MG(226.77±19.12) ug/L, urinary NAG(30.92±4.49) U/L, all showed a significant increase compared to before PCI(P<0.05). Intensive treatment group: Scr(80.13±8.82) umol/L, urinary β2-MG(198.33±21.78) ug/L, urinary NAG(25.15±3.81) U/L, all showed a significant increase compared to before PCI(P<0.05). The level of BUN(80.13±8.82) mmol/L, and blood β2-MG(2.12±0.24) mg/L, showed no significant difference(P>0.05). The level of BUN, Scr, blood β2-MG, urinary β2-MG and urinary NAG all showed significant decrease compared to the first day after PCI(P<0.05). The level of blood β2-MG and urinary β2-MG in conventional therapy group was significantly higher than the intensive treatment group(P<0.05). The level of BUN, Scr and urinary NAG showed no significant difference between two groups(P>0.05). There was no CIN happened in two groups.2 The change of hs CRP before and after PCI in two groups. Conventional therapy group: hs CRP before PCI(2.68±0.32)mg/L, 1st day after PCI(3.16±0.33)mg /L, 3rd day after srugery(4.05±0.23)mg /L, 7th day after srugery(3.00±0.25)mg /L, the level after PCI showed significant increase compared to the level before PCI(P<0.05). Intensive treatment group: hs CRP before PCI(2.49±0.30)mg /L, first day after PCI(2.83±0.28)mg /L, showed no significant difference(P>0.05); third day after PCI(3.12±0.20)mg /L, showed significantly higher than the level before PCI(P<0.05), the 7th day after PCI(2.30±0.25)mg/L, showed significantly lower then the level before PCI(P<0.05).3 The change of aminotransferase before and after PCI in two groups. Conventional therapy group: before PCI AST(28.47±8.76)U/L,ALT(26.55±10.86)U/L; 7st day after PCI AST( 28.91±8.84) U/L, ALT( 25.59±10.93) U/L. Intensive treatment group: before PCI AST(27.72±7.69)U/L, ALT(26.83±9.30)U/L; 7th day after PCI AST(21.62±8.82)U/L,ALT(22.93±8.95)U/L. There is no significant differene compared between groups or in groups(P>0.05).Conclusion:1 The results showed increased of BUN, Scr, blood β2-MG and urinary β2-MG after PCI in both groups. However, there was an improvement in renal function index in intensive treatment group, this may indicate the protective effect of atorvastatin on the renal function was dosage dependent.2 The level of hs CRP on the 1st day and 3rd day after PCI showed significant increase compared to the level before PCI in both groups, the level of conventional therapy group increased higher than the intensive treatment group. Then the level of hs CRP decreased significantly after PCI 7 days, may indicat the protective renal function by reduce inflammation of atorvastatin, and the high dose use showed more strong effect.3 There was no significant increase of liver aminotransferase in intensive treatment group. |
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