Preventing radiocontrast-induced nephropathy in chronic kidney disease patients undergoing coronary angiography

Radiocontrast-induced nephropathy(RCIN) is an acute and severe complication after coronary angiography,particularly for patients with pre-existing chronic kidney disease(CKD).It has been associated with both short-and long-term adverse outcomes,including the need for renal replacement therapy,increased length of hospital stay,major cardiac adverse events,and mortality.RCIN is generally defined as an increase in serum creatinine concentration of 0.5 mg/dL or 25%above baseline within 48 h after contrast administration.There is no effective therapy once injury has occurred,therefore,prevention is the cornerstone for all patients at risk for acute kidney injury(AKI).There is a small but growing body of evidence that prevention of AKI is associated with a reduction in later adverse outcomes.The optimal strategy for preventing RCIN has not yet been established.This review discusses the principal risk factors for RCIN,evaluates and summarizes the evidence for RCIN prophylaxis,and proposes recommendations for preventing RCIN in CKD patients undergoing coronary angiography.

The gene expression of adenosine receptors in the processes of contrast induced nephropathy in mouse kidney

Objective: Contrast induced nephropathy (CIN) is the third leading cause of hospital acquired renal failure. The mechanism of CIN is not fully understood. The objectives of this study were to investigate the expression changes of the four subtypes of adenosine receptors (A1AR, A2AAR, A2BAR, and A3AR) following administration of contrast media in mice. Methods: C57BL/6J mice were randomized into treatment and control groups. Iodixanol (IDX) was administered to two treatment groups through retroorbital injection at two different dosages, 0.75 gI/kg and 2.75 gI/kg. Phosphate buffered saline (PBS) was given to the control group. Mice kidneys were harvested at day 3 and day 7 after Iodixanol administration. Kidney injuries and function were evaluated according to Hematoxylin and eosin stain, Ki67 protein expression, and TUNEL assay of paraffin embedded kidney sections, and plasma creatinine assay. RNA and protein were extracted from the kidney specimens. A1AR, A2AAR, A2BAR, and A3AR RNA and protein level of the samples were assessed using qRT-PCR and Western blotting, with GAPDH as an endogenous control. Results: H&E staining showed no significant histopathology injuries after Iodixanol administration. No evidence of kidney injury and functional impairment was found. However, there was an increased number of A1AR, A2AAR, A2BAR, and A3AR RNA transcripts detected in the kidney 3 days after Iodixanol injection. The RNA levels in all the four subtypes of adenosine receptors were increased 2-3 fold in the day 3 specimens and back to normal at day 7. Western blot demonstrated that A1AR, A2AAR, and A3AR expression increased 1.5 to 2 fold at day 3 and day 7 following Iodixanol injection. A2BAR baseline expression was low in normal physiological conditions and no significant change was detected by Western blot. Conclusions: Iodixanol significantly increases adenosine receptors gene expression in mice. This suggests that adenosine receptors may play a role in the development of CIN.

Contrast Induced Nephropathy after Radial or Femoral Access for Invasive Management of Acute Coronary Syndrome

Background: Percutaneous coronary intervention is now the best way of management of acute coronary syndrome (ACS). Contrast induced nephropathy is a serious complication and greatly dependent on several factors. It is still unclear whether the vascular access migrates CIN risk. Objective: To study the impact of Radial Access (RA) compared with Femoral Access (FA) on developing contrast-induced nephropathy (CIN) in patients undergoing invasive management of acute coronary syndrome (ACS). Methods: Sixty patients eligible for invasive management of ACS at cardiology department (Menoufia University hospital and National Heart Institute) were randomized into two groups. Group I: included 30 patients with femoral approach and Group II: included 30 patients with radial approach. The occurrence of CIN estimated by KDIGO definition (absolute increase in serum creatinine (SCr) by ≥0.5 mg/dl within 48 hours;or increase in SCr to ≥25% of baseline) was estimated in both groups. Results: Only 9 patients (15%) developed CIN, 5 patients (55.6%) of them underwent PCI through FA without statistically significant difference between the two approaches.Conclusion: CIN is considered a potential complication of percutaneous coronary intervention (PCI). Our study did not show the preference of using an approach over the other.

Contrast induced nephropathy after percutaneous coronary intervention： risk factors and preventive strategy

Objective To analyze the risk factors and clinical outcome of contrast induced nephropathy （CIN） in patients with coronary artery disease （CAD） after percutaneous coronary intervention （PCI） and discuss its prevention. Methods Fifty-four patients with C1N among 729 patients who received PCI were retrospectively studied and the related risk factors, cardiovascular events and preventive strategy were analyzed. Results C1N was strongly associated with pre-procedure chronic renal failure, diabetes mellitus and large-dose contrast. The incidence of cardiac mortality and major adverse cardiac events 1 year after PCI in CIN group was higher than that in group without CIN. Conclusion Chronic renal failure, diabetes mellitus and dosage of contrast agent were three independent risk factors of CIN. CIN could affect the patients＇ prognosis. A well overall perioperative management of CAD patients following PCI, especially hydration therapy, is the most important strategy for prevention of CIN.

Contrast Agents and Contrast-Induced Nephropathy

Recent advances in medical sciences, especially in imaging, have dramatically increased the use of contrast agents. The constantly changing nature of medicine and the availability of new information, such as new pharmaceutical formulations, have necessitated periodic revisions and drafting of new guidelines for the safe use of intravenous contrast agents in radiology. This study examined the majority of guidelines, articles, and authoritative references available on the use of intravenous contrast agents in adults to reduce the risk of contrast-induced nephropathy. The search engines of PubMed, Web of Science, Scopus, and Google Scholar were used, and relevant English articles cited at least twice between 1979 and 2014 were studied. Review of the collected papers showed no consensus among them for guidelines on the incidence of contrast-induced nephropathy in patients at risk. Different formulas were used to calculate estimated glomerular filtration rate, which could be problematic in some cases. Further studies are needed for unification of existing guidelines.

Contrast-Induced Nephropathy in Patients with Hepatocellular Carcinoma Undergoing Transcatheter Arterial Chemoembolization

Purpose: The purpose of this retrospective study was to assess the incidence and the risk factors of contrast-induced nephropathy (CIN) following transcatheter arterial chemoembolization (TACE) in patients with hepatocellular carcinoma (HCC). Materials and Methods: We performed a retrospective review of 186 sessions of TACE in 122 patients with HCC. We examined the incidence and factors associated with risk of CIN, defined as an increase of at least 0.5 mg/dl (44.2 μmol/l) or 25% of the baseline serum creatinine level between 48 and 72 hours after TACE. Results: CIN developed in 14 (7.5%) of the 186 sessions after TACE. A univariate analysis showed that the Child-Pugh class B or C [10/14 (71%) vs. 70/172 (41%), P = 0.046], a low albumin level (3.0 ± 0.5 vs. 3.4 ± 0.6, P = 0.018), and a low hemoglobin level (10.6 ± 2.0 vs. 11.8 ± 2.0, P = 0.035) were significantly associated with the development of CIN. Multivariate analysis revealed that the hemoglobin value was associated with CIN [odds ratio (OR) 1.6;P = 0.038]. Conclusions: CIN after TACE is closely associated with the severity of liver cirrhosis, and with low levels of albumin and hemoglobin. Effective preventive methods remain to be considered in patients with HCC and advanced LC who are undergoing TACE.

Contrast-Induced Nephropathy in Patients Undergoing Elective Coronary Angiography： Incidence and Risk Factors

Contrast-Induced Nephropathy （CIN） is a considerable complication in cardiac procedures. Several conditions for CIN have been identified after Coronary Angiography （CA）. The purpose of this study was to assess the incidence and clinical predictors of CIN 24 h after Coronary Angiography. A total of 1,137 consecutive patients with coronary artery syndrome undergoing CA were prospectively enrolled the study. Serum creatinine （Cr） at baseline and 24 h after CA, as well as demographic and clinical characteristics of patients were measured. Contrast-induced nephropathy was defined as a rise in Cr _0.3 mg/dL after CA. Univariable and multivariable logistic regression analysis were performed to identify independent predictors of CIN. The overall incidence rate was 56 （4.9%） in total study population. In multivariate analysis, baseline Cr 〉 1.5 （odds ratio [OR] 4.8, 95% confidence interval [CI] 1.04 to 8.3; P〈 0.001）, Contrast volume 〉 100 mmL （OR 3.4, 95% CI 0.7 to 8.1; P〈 0.002）, Baseline GFR 〈 30 （OR 14.2, 95% CI 8 to 2; P 〈 0.000）; Baseline GFR 30-60 （OR 8.7, 95% CI 2.3 to 13.8; P 〈 0.000） were predictors for CIN. CIN was more frequent in older patients, with higher serum creatinine level and Grater usage of contrast media, and diuretic. N-acetylcysteine （NAC） and hydration cannot prevent the occurrence of CIN.

Contrast-induced acute kidney injury:A review of practical points

Contrast-induced acute kidney injury(CI-AKI) is oneof the most common causes of AKI in clinical practice.CI-AKI has been found to be strongly associated with morbidity and mortality of the patients.Furthermore,CI-AKI may not be always reversible and it may be associated with the development of chronic kidney disease.Pathophysiology of CI-AKI is not exactly understood and there is no consensus on the preventive strategies.CI-AKI is an active research area thus clinicians should be updated periodically about this topic.In this review,we aimed to discuss the indications of contrastenhanced imaging,types of contrast media and their impact on nephrotoxicity,major pathophysiological mechanisms,risk factors and preventive strategies of CI-AKI and alternative non-contrast-enhanced imaging methods.

Contrast-induced acute kidney injury in kidney transplant recipients: A systematic review and meta-analysis

AIM To evaluate the incidence of contrast-induced acute kidney injury(CIAKI) in kidney transplant recipients. METHODS A literature search was performed using MEDLINE, EMBASE, and the Cochrane Database of Systematic Reviews from the inception of the databases through July 2016. Studies assessing the incidence of CIAKI in kidney transplant recipients were included. We applied a randomeffects model to estimate the incidence of CIAKI.RESULTS Six studies of 431 kidney transplant recipients were included in the analyses to assess the incidence of CIAKI in kidney transplant recipients. The estimated incidence of CIAKI and CIAKI-requiring dialysis were 9.6%(95%CI: 4.5%-16.3%) and 0.4%(95%CI: 0.0%-1.2%), respectively. A sensitivity analysis limited only to the studies that used low-osmolar or iso-osmolar contrast showed the estimated incidence of CIAKI was 8.0%(95%CI: 3.5%-14.2%). The estimated incidences of CIAKI in recipients who received contrast media with cardiac catheterization, other types of angiogram, and CT scan were 16.1%(95%CI: 6.6%-28.4%), 10.1%(95%CI: 4.2%-18.0%), and 6.1%(95%CI: 1.8%-12.4%), respectively. No graft losses were reported within 30 d post-contrast media administration. However, data on the effects of CIAKI on long-term graft function were limited.CONCLUSION The estimated incidence of CIAKI in kidney transplant recipients is 9.6%. The risk stratification should be considered based on allograft function, indication, and type of procedure.

Quantitative Assessment of Protective Effects of Antioxidant Agents against Drug-Induced Nephrotoxicity Using Dynamic Contrast-Enhanced Computed Tomography

Purpose: The purpose of this study was to develop a method for quantifying the extent of renal dysfunction due to drug-induced nephrotoxicity using dynamic contrast-enhanced computed tomography (DCE-CT) and to investigate the protective effects of various antioxidant agents against cis-dichlorodiammineplatinum (cisplatin)-induced nephrotoxicity in rats using this method. Materials and Methods: The DCE-CT studies were performed in 8-week-old male Sprague-Dawley rats. The CT scanning started 4 s before a bolus intravenous injection of iodinated contrast agent (CA) (150 mgI/kg) from the tail vein using an automatic injector and lasted 90 s at 1-s intervals. The contrast clearance per unit renal volume (K1) was estimated from the DCE-CT data using the Patlak model. The renal volume (V) was calculated by manually delineating the kidney on the CT image. The contrast clearance of the entire kid-ney (K) was obtained by . First, to investigate the effect of CA itself, the DCE-CT studies were performed without injecting cisplatin 2, 4, and 7 days after the first DCE-CT study on day 0. Second, to investigate the effect of injected dose of cisplatin, the DCE-CT study was performed after the intraperitoneal (i.p.) injection of cisplatin (1.8 mg/kg) and was repeated every other day for one week. Finally, to investigate the protective effects of antioxidant agents [L-arginine (300 mg/kg), N-acetylcysteine (500 or 1000 mg/kg), methimazole (40 mg/kg), captopril (60 mg/kg), and taurine (750 mg/kg)], the DCE-CT studies were performed on days 0, 2, 4, and 7 after the i.p. injection of cisplatin (3.6 mg/kg). For comparison, the DCE-CT data were also acquired without injecting the antioxidant agents (CDDP group). Results: When cisplatin was not injected, there were no significant changes in the K value as compared to that on day 0 within the studied period. The K valuesignificantly (p < 0.05) decreased with increasing dose of cisplatin. Although some differences were observed in the extent of change in the K value normalized by that on day 0, depending on the antioxidant agents and their injected dose and schedule, the normalized K values on day 7 in the groups injected with the antioxidant agents were significantly higher than those in the CDDP group, suggesting that the antioxidant agents studied here had protective effects against cisplatin-induced nephrotoxicity in varying degrees. Conclusion: Our method appears useful for quantitatively evaluating the protective effects of antioxidant agents against cisplatin-induced nephrotoxicity and for investigating the optimal injected dose and schedule of the agents, because it allows repeated measurements of split renal function in a single animal.

The Study on the Relationship between Serum Vascular Endothelial Growth Factor and Proteinuria in Adriamycin induced Nephrotic Rats

To study the relationship between serum vascular endothelial growth factor (VEGF) and proteinuria in adriamycin induced nephrotic rats, a rat model of adriamycin induced nephrotitis was developed by injection of adriamycin into a tail vein in a rat. At different time points, 24 h urinary protein excretion was measured by using Coomassie brilliant blue method and the serum VEGF levels detected by using ELISA assay. The interventional effect of VEGF on this model was observed. The results showed that: (1) The adriamycin induced nephrotic syndrome rat model was developed successfully; (2) Serum VEGF levels and proteinuria were significantly increased at 7th day after intravenous injection of adriamycin. There was a positive correlation between serum VEGF levels and 24 h urinary protein excretion ( r=0.67, P <0.05). (3) The 24 h urinary protein excretion was significantly increased in the rats receiving administration of VEGF ( P <0.05). It was concluded that VEGF might play an important role in the pathogenesis of proteinuria in adriamycin induced nephrotic rats.

Hydrogen effect on the mechanical behaviour and microstructural features of a Fe-Mn-C twinning induced plasticity steel

The influences of hydrogen on the mechanical properties and the fracture behaviour of Fe-22Mn-0.6C twinning induced plasticity steel have been investigated by slow strain rate tests and fractographic analysis.The steel showed high susceptibility to hydrogen embrittlement,which led to 62.9%and 74.2%reduction in engineering strain with 3.1 and 14.4 ppm diffusive hydrogen,respectively.The fracture surfaces revealed a transition from ductile to brittle dominated fracture modes with the rising hydrogen contents.The underlying deformation and fracture mechanisms were further exploited by examining the hydrogen effects on the dislocation substructure,stacking fault probability,and twinning behaviour in pre-strained slow strain rate test specimens and notched tensile specimens using coupled electron channelling contrast imaging and electron backscatter diffraction techniques.The results reveal that the addition of hydrogen promotes planar dislocation structures,earlier nucleation of stacking faults,and deformation twinning within those grains which have tensile axis orientations close to<111>//rolling direction and<112>//rolling direction.The developed twin lamellae result in strain localization and micro-voids at grain boundaries and eventually lead to grain boundary decohesion.

“Contrast nephropathy” in renal transplantation:Is it real?

The risk of contrast-induced nephropathy(CIN) in renal transplant recipients is increased in diabetics, patients with impaired basal kidney function, patients in shock, patients presenting with acute emergency and in old age recipients. Approximately one-third of all hospitalized patients with acute kidney injury is attributed to CIN. In the United States, it is the third leading cause of hospital-acquired renal failure. Therefore, efforts should be directed to minimize CIN-related morbidity and mortality as well as to shorten hospital stay. While the role of peri-procedural prophylactic hydration with saline is unequivocal; the use of acetyl cysteine is not based on robust evidence. The utility of theophylline, aminophylline, calcium channel blockers, natriuretic peptide, and diuretics does not have proven role in attenuating CIN incidence. We aim to analyze the evidence for using various protocols in published literature to limit CIN-associated morbidity and mortality, particularly during surveillance of the renal allograft survival.

Laser-induced Interstitial Thermotherapy via a Single-needle Delivery System: Optimal Conditions of Ablation, Pathological and Ultrasonic Changes

Summary： This study aimed to examine the optimal conditions of laser-induced interstitial ther- motherapy （LITT） via a single-needle delivery system, and the ablation-related pathological and ultra- sonic changes. Ultrasound （US）-guided LITT （EchoLaser system） was performed at the output power of 2--4 Wattage （W） for 1-10 min in ex vivo bovine liver. Based on the results of the ex vivo study, the output power of 3 and 4 W with different durations was applied to in vivo rabbit livers （n=24）, and VX2 tumors implanted in the hind limbs of rabbits （n=24）. The ablation area was histologically determined by hematoxylin-eosin （HE） staining. Traditional US and contrast enhanced ultrasound （CEUS） were used to evaluate the treatment outcomes. The results showed： （1） In the bovine liver, ablation disruption was grossly seen, including a strip-like ablation crater, a carbonization zone anteriorly along the fiber tip, and a surrounding gray-white coagulation zone. The coagulation area, 1.2 cm in length and 1.0 cm in width, was formed in the bovine liver subjected to the ablation at 3 W for 5 min and 4 W for 4 rain, and it extended slightly with the ablation time. （2） In the rabbit liver, after LITT at 3 W for 3 min and more, the coagulation area with length greater than or equal to 1.2 cm, and width greater than or equal to 1.0 cm, was found. Similar coagulation area was seen in the implanted VX2 carcinoma at 3 W for 5 min. （3） Gross examination of the liver and carcinoma showed three distinct regions： ablation cra- ter/carbonization, coagulation and congestion distributed from the center outwards. （4） Microscopy re- vealed four zones after LITT, including ablation crater/carbonization, coagulation, edema and conges- tion from the center outwards. A large area with coagulative necrosis was observed around a vessel in the peripheral area with edema and hyperemia. （5） The size of coagulation was consistent well to the CEUS findings. It was concluded that EchoLaser system at low power can produce a coagulation area larger than 1.0 cm×1.0 cm during a short time period. The real-time US imaging can be used to effec- tively guide and assess the treatment.

High Glucose Promotes the CTGF Expression in Human Mesangial Cells via Serum and Glucocorticoid-induced Kinase 1 Pathway

The role of serum and glucocorticoid-induced kinase 1 （SGK1） pathway in the connective tissue growth factor （CTGF） expression was investigated in cultured human mesangial cells （HMCs） under high glucose. By using RT-PCR and Western blot, the effect of SGK1 on the CTGF expression in HMCs under high glucose was examined. Overexpression of active SGK1 in HMCs transfected with PIRES2-EGFP- S422D hSGK1 （SD） could increase the expression of phosphorylated SGK1 and CTGF as compared with HMCs groups transfected with PIRES2-EGFP （FP） under high glucose or normal glucose. Overexpression of inactive SGK1 in HMCs transfected with PIRES2-EGFP- K127N hSGK1 （KN） could decrease phosphorylated SGK1 and CTGF expression as compared with HMCs groups transfected with FP under high glucose. In conclusion, these results suggest that high glucose-induced CTGF expression is mediated through the active SGK1 in HMCs.

Significance and Expression of Serum and Glucocorticoid-inducible Kinase in Kidney of Mice with Diabetic Nephropathy

Summary: To investigate the expression and the role of three isoforms of Serum and Glucocorticoid-inducible Kinase (SGK) in experimental diabetic nephropathy (DN), 12 male C57BL/6 mice of 8-weeks-old were divided into two groups. Streptozotocin (STZ)-induced diabetic nephropathy and normal controls were analyzed at the end of the 4th week after the induction of diabetes. Renal hemodynamics and histological studies were performed. The expression of SGK1 mRNA, SGK2 mRNA and SGK3 mRNA of kidney cortex were measured by RT-PCR, and the cortical SGK1 protein was detected with Western blotting. Our results showed that the blood glucose, blood HbA1c, 24-h urinary protein, creatinine clearance and the renal index were all increased in DN group. More extracellular matrix (ECM) accumulation was observed. The level of cortical SGK1 mRNA and protein were up-regulated in DN group in comparison with control group. SGK2 and SGK3 mRNA were elevated in DN mice. In DN, mRNA level of three SGK isoforms and SGK1 protein were increased significantly. It is concluded that SGKs may contribute to the early renal injury of DN.

Prevention of iodinated contrast-induced nephropathy

Objective To lessen the occurrence of contrast-induced nephropathy （CIN）, the preventive measures of CIN were reviewed. Data sources The data used in this review were from PubMed with relevant English articles and from Chinese Knowledge Information （CNKI） published from 1989 to 2009. The search terms were ＂contrast medium＂, ＂contrast-induced nephropathy＂ and ＂prevention＂. Articles involved in prevention of CIN were selected. Study selection CIN is the third most common cause of acute kidney injury and is associated with an unfavorable prognosis. The best treatment is prophylaxis because CIN can not be reversed or ameliorated. Results Thirty articles were included. Among various preventive measures, pericatheterization hydration is almost universally accepted as an appropriate and safe measure to prevent CIN, although there is no agreement as to composition, amount, and timing of hydration. Based on the use of concomitant nephrotoxic agents or high doses of contrast medium （CM） is one of risk factors for CIN, discontinuation of potentially nephrotoxic drugs 2-3 days before and after the procedure until renal function recover, and using the lowest possible dose of CM can decrease the risk of CIN. It is promising that removing the majority of CM from the coronary sinus, before it enters the systemic circulation, during coronary angiography can reduce the risk for CIN in animal studies and in limited clinical trials. Inconsistent data exist with respect to application of some vasodilators （endothelin antagonists and adenosine antagonists） and antioxidants （N-acetylcysteine and statins） in preventing CIN in high-risk patients, and new vasodilators and antioxidants continue to be tested. Conclusions Pericatheterization hydration, discontinuation of nephrotoxic drugs, and using the lowest possible dose of CM are effective measures to lessen the risk for CIN. Other prophylactic strategies and some drugs are promising, but further confirmation is required.

Prediction of contrast-induced nephropathy in diabetics undergoing elective percutaneous coronary intervention： role of the ratio of contrast medium volume to estimated glomerular filtration rate

Background Diabetic patients undergoing percutaneous coronary intervention （PCI） have a higher incidence of contrast-induced nephropathy （CIN） than nondiabetic patients, and no pharmacological approach has been demonstrated to offer consistent protection. Therefore, identifying individuals who are at increased risk becomes essential. This study was designed to assess the predictive role of the ratio of contrast medium volume to estimated glomerular filtration rate （CMV/eGFR） in diabetic patients undergoing elective PCI who developed ClN.Methods We retrospectively investigated clinical factors associated with the development of CIN in 114 diabetic patients who had undergone elective PCI. The risk factors for CIN included age, gender, body mass index （BMI）, left ventricular ejection fraction （LVEF）, hemoglobin （Hb）, fasting plasma glucose （FPG）, hemoglobin A1c （HbA1c）, volume of contrast medium, basic levels of serum creatinine （Scr）, the number of treated vessels and the number of stents used.We conducted a stepwise regression analysis to evaluate the predictive role of these risk factors in the incidence of CIN.Results The incidence of CIN was 18.4% （21/114）. There were no significant differences in age, gender, BMI, LVEF, Hb,FPG, HbA1c, and incidence of hypertension and number of acute myocardial infarction （AMI） in patients between the CIN （n=21） and the non-CIN （n=93） groups. However, the eGFR was significantly lower （（72.0±12.5） ml·min-1·1.73 m-2 vs.（82.0±16.5）ml·min-1·1.7m-2, P=0.010）, and the basic serum creatinine level （（1.07±0.12） mg/dl vs.（0.97±0.19） mg/dlP=0.014） was significantly higher in the CIN group. In addition, the volume of contrast medium was significantly larger （（253±75）ml vs. （211±71）ml, P=0.017） and the CMV/eGFR ratio was significantly greater （3.64±1.26 vs.2.70±1.11, P=0.001） in the CIN group. Stepwise regression analysis showed that the CMV/eGFR ratio was a significant independent predictor for the development of CIN （P=0.001）. At a cut-off point of 〉3.1, the CMV/eGFR ratio exhibited 71% sensitivity and 70% specificity for detecting CIN.Conclusion The CMV/eGFR ratio could be a valuable predictor of CIN for diabetic patients after elective PCI. At a cut-off point of〉3.1, the CMV/eGFR ratio was an optimal predictor for the incidence of CIN.

Safety and efficacy of anisodamine on prevention of contrast induced nephropathy in patients with acute coronary syndrome

Background Previous studies have proved the renal protective effects of anisodamine in patients with septic shock. The aim of this study was to investigate anisodamine for the prevention of contrast induced nephropathy （CIN） in patients with acute coronary syndrome （ACS）. Methods Consecutive ACS patients undergoing elective percutaneous coronary intervention （PCI） were randomly assigned to one of two groups： patients in the anisodamine group （ANI group） were assigned to receive intravenous infusions of anisodamine by an adjusted-dose （0.1-0.2 μg·kg^-1·min^-1） from the PCI procedure to 24 hours after PCI, and the control group （CON group） received 0.9% isotonic saline of the same volume. All patients were hydrated for 6 to 12 hours before and 12 hours after PCI. Blood samples were taken on the day of PCI and at 24, 48 and 72 hours after PCI to measure the serum creatinine （SCr）. Results A total of 177 patients were involved in the study, 88 in the ANI group and 89 in the CON group. In both groups, the SCr concentrations significantly increased after PCI, with the peak value occurring at 48 hours. At 72 hours, the SCr concentration in the ANI group retuned to the baseline level （P 〉0.05）, but the SCr concentration in CON group was still higher than baseline level （P 〈0.01）. The SCr concentrations at 48 and 72 hours after PCI were much lower in the ANI group than those in the CON group （both P 〈0.01）. The estimated glomerular filtration rate （eGFR） significantly decreased after PCI, the lowest value occurred at 48 hours. In the ANI group, the eGFR at 72 hours was similar to the baseline level. In the CON group, the eGFR failed to return to baseline at 72 hours （P〈0.01）. The eGFR at 24, 48 and 72 hours after PCI were higher in the ANI group （all P 〈0.05）. The incidence of CIN in the ANI group was lower than that in the CON group within 72 hours after PCI （P〈0.05）. The results of multiple Logistic regression proved that both diabetes and left ventricular ejection fraction （LVEF） were independent predictors of CIN, and treatment with anisodamine was an independent preventive factor of CIN （OR 0.369 and 95% Cl 0.171 to 0.794, P=0.011）. No serious side effects were found in the ANI group. Conclusion Intravenous infusion of anisodamine during and after elective PCI may safely prevent the occurrence of CIN in ACS patients.

Preventive effects of anisodamine against contrast-induced nephropathy in type 2 diabetics with renal insufficiency undergoing coronary angiography or angioplasty

Background Anisodamine is widely used in therapy for treating acute glomerulonephritis and diabetic nephropathy because it can improve renal microcirculation. We performed a study to evaluate the preventive effects of anisodamine against contrast-induced nephropathy （CIN） in type 2 diabetics with renal insufficiency undergoing coronary angiography or angioplasty. Methods A total of 260 patients with type 2 diabetes and an estimated glomerular filtration rate （eGFR） of 60 ml^-1 - min^-1·1.73 m^-2 or less, who were undergoing coronary angiography or angioplasty, were randomly assigned to receive an infusion of either sodium chloride （control group, n=128） or anisodamine （treatment group, n=132）. Patients in the treatment group received an infusion of anisodamine at a rate of 0.2 μg · kg^-1 · min^-1 from 12 hours before to 12 hours after coronary angiography or angioplasty, while patients in the control group received an infusion of sodium chloride with the same volume as the treatment group. All patients received intravenous sodium chloride hydration. CIN was defined as a 25% increase in serum creatinine from baseline or an absolute increase of 〉0.5 mg/dl within three days after contrast exposure. The primary end point was the incidence of CIN. The secondary end point was a 25% or greater reduction in eGFR. Results There were no significant differences between the two groups with regard to age, gender, risk factors, laboratory results, medications and interventions. The incidence of CIN was 9.8% （13/132） in the treatment group and 20.3% （26/128） in the control group （P 〈0.05）. The secondary end point was 6.0% （8/132） in the treatment group and 16.4% （21/128） in the control group （P〈0.05）. Conclusion These results indicate the preventive effects of anisodamine against CIN in type 2 diabetics with renal insufficiency who are undergoing coronary angiography or angioplasty.