Prevention of contrast induced nephropathy: recommendations for the high risk patient undergoing cardiovascular procedures

Catheterization and Cardiovascular Interventions 69:135–140 (2007) Prevention of Contrast Induced Nephropathy: Recommendations for the High Risk Patient Marc J. Schweiger,1,2* MD, Charles E. Chambers,3 MD, Charles J. Davidson,4 MD, Shaoheng Zhang,5 James Blankenship,6 MD, Narinder P. Bhalla,7 MD, Peter C. Block,8 MD, John P. Dervan,9 MD, Christine Gasperetti,10 MD, Lowell Gerber,11 MD, Neal S. Kleiman,12 MD, Ronald J. Krone,13 MD, William J. Phillips,14 MD, Robert M. Siegel,15 MD, Barry F. Uretsky,16 MD, and Warren K. Laskey,17 MD Contrast induced nephropathy (CIN) is the third leading cause of hospital aquired renalfailure and is associated with significant morbidity and mortality. Chronic kidney dis-ease is the primary predisposing factor for CIN. As estimated glomerular filtration rate<60 ml/1.73 m2 represents significant renal dysfunction and defines patients at highrisk. Modifiable risk factors for CIN include hydration status, the type and amount ofcontrast, use of concomitant nephrotoxic agents and recent contrast administration.
The cornerstone of CIN prevention, in both the high and low risk patients, is adequateparenteral volume repletion. In the patient at increased risk for CIN it is often appropri-ate to withhold potentially nephrotoxic medications, and consider the use of n-acetyl-cysteine. In patients at increased risk for CIN the use of low or iso-osomolar contrastagents should be utilized and strategies employed to minimize contrast volume. Inthese patients serum creatinine should be obtained forty-eight hours post procedureand it is often appropriate to continue withholding medications such as metformin ornon steroidal anti-inflammatories until renal function returns to normal.
Key words: hydration; contrast induced nephropathy; radiographic contrast media;renal failure 1Division of Cardiology, Baystate Medical Center, Springfield, MA 12Division of Cardiology, Baylor College of Medicine, Houston, 2Department of Medicine, Tufts University School of Medicine, 13Division of Medicine, Washington University, St. Louis, Missouri 3Division of Medicine & Radiology, Penn State University Col- 14Division of Cardiology, Central Maine Heart and Vascular 4Division of Medicine, Northwestern University Medical School, 15Division of Medicine, Mesa General Hospital, Mesa, Arizona 16Division of Cardiology, University of Texas, Galveston, Texas 5Shanghai Institute of Cardiovascular Disease, Fudan Univer- 17Division of Medicine, University of New Mexico, Albequer- sity, Zhongshan University, Shanghai, China 6Division of Medicine, Geisenger Clinic, Danville, Pennsylvania7Division of Medicine, Carillon Roanoke Memorial Hospital, *Correspondence to: Marc J. Schweiger, Division of Cardiology, Bay- state Medical Center, 759 Chestnut St, Springfield, MA 01199, USA.
8Division of Medicine, Emory University, Atlanta, Georgia 9Division of Medicine, Stony Brook University Medical Center,Stony Brook, New York Received 6 September 2006; Revision accepted 6 September 2006 10Division of Cardiology, Deborah Heart & Lung Institute,Brown Mills, New Jersey 11Division of Medicine, Northeast Regional Medical Center, Published online 30 November 2006 in Wiley InterScience (www.
Adapted from Kozak M, Robertson BJ, Chambers, CE. Cardiac catheterization laboratory: Diagnosticand therapeutic procedures in the adult patient. In: Kaplan, JA, editor. Kaplan’s Cardiac Anesthesia,5th ed. p. 307. Copyright ' 2006, with permission from Elsevier.
Ultravist is a registered trademark of Berlex Laboratories. Isovue is a registered trademark of BraccoDiagnostics. Omnipaque and Visipaque are registered trademarks of GE Medical, Inc. Optiray is aregistered trademark of Mallinckrodt Medical, Inc. Oxilan and Hexabrix are registered trademarks ofGuerbet, S.A. LOCM, low-osmolality contrast media; IOCM, iso-osmolar contrast media.
TABLE II. Equations to Estimate CrCl and GFR I. Cockcroft–Gault (C&G) estimates CrCl (ml/min) ð140 ageÞÂweight ðkgÞÂ0:85 ðif femaleÞ Adverse reactions have been the major disadvantage of RCM since their introduction for urinary tract visual- II. Modification of diet in renal disease (MDRD) estimates GFR ization in 1923. High-osmolar (>1,600 mOsm/l) ionic RCM (HOCM) were the first agents developed and areproduced using the meglumine and sodium salts of diatri- 170ÂðSCrÂ0:011ÞÀ0:999ÂðageÞÀ0:176ÂðSUrÂ2:801ÞÀ0:170 ðSA1bÂ0:1Þ0:318Â1:180 ðif blackÞÂ0:762 ðif femaleÞ zoic acid. Low-osmolar (<850 mOsm/l) RCM (LOCM),both ionic and nonionic, have increasingly supplanted SCr, serum creatinine; SUr, serum urea; SAlb, serum albumin. The cal-culator for MDRD is located on the internet at: http://www.kidney.org/ HOCM in clinical practice as they have less systemic professionals/kdoqi/gfr_calculator.cfm OR http://www.nkdep.nih.gov/pro- adverse effects. These agents (Table I) are predominantly monomeric, non-ionic agents with the exception of the aThis does not require patient weight.
two dimers: ioxaglate (ionic) and iodixanol (non-ionic).
Chronic kidney disease (CKD) is the primary predis- posing factor for CIN [5]. Definitions of CKD in the medical literature have varied and have relied on the The invasive/interventional cardiologist uses radio- SCr rather than creatinine clearance (CrCl) or glomeru- graphic contrast media (RCM) on a daily basis and lar filtration rate (GFR). Equations for estimating CrCL must strive to minimize the risks associated with these and GFR (Table II) are based upon age, body weight, agents. One such risk, contrast induced nephropathy and sex, and with Modification of Diet in Renal Dis- (CIN), is defined as a worsening of renal function after ease (MDRD), race, and serum albumin. MDRD is RCM administration. The medical literature varies in preferred in the obese or elderly patient [6,7]. Both the definition of CIN, typically using a change in se- formulae are more accurate measures of intrinsic renal rum creatinine (SCr) over baseline by 48 hr, such as !25% above baseline or an absolute increase of >0.25 Though limitations exist with each method/formulae or 0.5 mg/dl [1–3]. Albeit an infrequent event in un- [8], the MDRD is recommended to estimate GFR in the selected population-based studies, CIN is the third adult patient with cardiovascular disease [9]. It should leading cause of all cases of hospital-acquired renal be noted that there are two versions of the MDRD equa- tion; the abbreviated version requires fewer measured In recognition of the need for a document on the parameters while providing essentially the same results.
prevention of CIN, the Society for Cardiovascular These are available online: http://www.kidney.orgprofes- Angiography and Interventions (SCAI) proposes the sionals/kdoqi/gfr_calculator.cfm or http://www.nkdep.nih.
following recommendations based on the available evi- gov/professionals/gfr_clculators/mdrd_con.htm.
dence in the literature, and where inconclusive, supple- In addition to CKD, there are patient-related risk factors for CIN [10–13]. Table III summarizes the Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.
Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Prevention of Contrast Induced Nephropathy TABLE III. Pre-procedural Clinical Risk Factors for CIN half normal saline with the incidence of CIN significantly decreased in the isotonic saline group compared withhalf-normal saline (0.7% vs. 2.0%) [21]. Importantly, all studies agree parenteral volume repletion is the corner- The critical aspect is to ensure optimal volume repletion prior to the procedure. With many protocols published but no one specific regimen identified, it isstrongly recommended to parenterally administer a most commonly encountered modifiable and non-modi- total of at least 1 L of isotonic saline beginning at fiable pre-procedural clinical features associated with least 3 hrs before and continuing at least 6–8 hrs after the procedure. Initial infusion rates of 100–150 ml/hr The risk of CIN is inversely related to the calculated are recommended with adjustment post procedure as estimated GFR (eGFR) [13]. An eGFR of <60 ml/ clinically indicated. Appropriate caution should be min/1.73 m2 represents significant renal dysfunction applied in the patient with known reduced left ventric- [14] and is used to define the patient at high risk for ular function or congestive heart failure. To accom- plish this regimen, outpatients should be scheduled for Several predictive algorithms have been proposed to early arrival or later procedure times; prior-day admis- estimate the risk for CIN. These algorithms generally sion may be required in selected patients.
include intraprocedural factors limiting their use prior Sodium Bicarbonate. The use of isotonic sodium to the procedure with none prospectively validated.
bicarbonate has been demonstrated in one study to be Mehran developed a risk score for predicting CIN [10] marginally superior to isotonic sodium chloride (saline) that includes congestive heart failure, hypotension, age in preventing CIN in the high risk patient [23]. This >75 years, anemia, diabetes, RCM volume, and CKD protocol used an infusion of 3 ml/kg/hr for 1 hr beforedefined as a SCr >1.5 mg/dl or an eGFR of <60/ml/ and 1 ml/kg/hr for 6 hrs after the procedure. Although min/1.7 m2. Of note, the risk of CIN increases in a additional studies are needed, these data suggest that a graded fashion as the eGFR decreases from <60/ml/ modified regimen with sodium bicarbonate may be The development of CIN is strongly associated with significant morbidity and mortality. Among hospital survivors who undergo percutaneous coronary interven- Pre-procedural management of patients at risk for tion (PCI), patients who develop CIN are at an CIN requires a review of the patient’s medications and increased risk of death or myocardial infarction (MI) withholding, as clinically appropriate, potentially ne- at 6 months, 1 year, and 5 years [15,16]. Rihal reported phrotoxic drugs, including aminoglycoside antibiotics, an in-hospital mortality of 22% in the 254 patients who anti-rejection medications, and nonsteroidal anti-inflam- developed CIN following PCI, from a patient population matory drugs (NSAID). Although optimizing volume of 7,586 [13]. Acute hemodialysis was uncommon status is essential, the decision to interrupt diuretic ther- except in patients with severe CKD, especially when di- apy must be individualized [13,17,21]. Angiotensin con- abetes was present. McCullough studied 1,826 patients verting enzyme inhibitor therapy may be continued but undergoing PCI with an in-hospital mortality of 1.1% in neither initiating nor changing dose should be consid- patients without CIN, 7.1% in patients with CIN with- ered until the patient is safely past the risk period for out dialysis, and 35.7% in dialyzed patients with CIN CIN following RCM. Although not a risk factor for developing CIN, metformin should be withheld after theprocedure until it is clear that renal function has notsignificantly deteriorated [24].
PRE-PROCEDURAL MANAGEMENT FOR THEHIGH RISK PATIENT Table IV summarizes the multiple pharmacologic Multiple trials have addressed type, amount, duration, approaches to mitigate the risk for CIN [25]. Many and route of volume repletion to prevent CIN [17–20].
agents studied have not shown a consistent benefit in Small numbers, different patient populations and end- reducing the incidence of CIN when compared to vol- points, and various repletion regimens have hindered ume repletion alone. These include mannitol [17], comparison of these studies. Mueller randomized 1,620 post-procedural diuretics [17], dopamine [26], fenoldo- patients undergoing PCI to isotonic (normal) saline or pam [27], atrial natriuretic peptide [28], non-selective Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.
Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
TABLE IV. Approach to Prevention of CIN Based on Possible TABLE V. Summary of Randomized Clinical Trials Concerning Type of RCM and Relative Risk of CIN in High Risk PatientsUndergoing Angiographic Procedures Possibly beneficialAminophylline/theophylline RCM, radiographic contrast media; RR, relative risk; CIN, contrast-induced nephropathy; CI, confidence interval; IOCM, iso osmolar con- endothelin receptor antagonists [29], and calcium chan- trast media; LOCM, low osmolar contrast media; HOCM, high osmolar nel blockers [30]. Potential benefits may occur with prostaglandin E1 [31], aminophylline or theophylline[32], statins [33], and ascorbic acid [34] but more data priate if the clinical situation permits. However, there are needed before any of these agents can be system- are limited data regarding the timing for a repeat pro- cedure with RCM. With creatinine elevation post RCM Despite multiple single studies, as well as several occurring by 48–72 hrs, it is recommended to consider meta-analyses, the true benefit of N-acetylcysteine avoiding subsequent RCM during this period.
(NAC) is still unclear [35–37]. However, NAC remainsthe most frequently prescribed medication in this set- ting, as a likely consequence of its low cost and lack Table V summarizes the randomized clinical trials of serous side effects. If chosen, 600 mg of NAC (RCTs) regarding the type of RCM and the incidence should be administered orally q 12 hrs  4 doses by mixing it with soda or orange juice and begun prior to Overall, there is evidence that LOCM lessens the risk for CIN in the high risk patient compared withHOCM [44]. It is unclear whether significant differen-ces in nephrotoxicity exist among individual LOCM [46]. One RCT has demonstrated a lessened risk for development of CIN in the high risk patient with iso- osmolar contrast media compared to a single LOCM Total case RCM volume is a risk factor for CIN [10,13]. Intuitively, the less RCM administered, the Gadolinium chelates are used extensively in mag- lower the risk for CIN. However, there are no studies netic resonance imaging, and reports of CIN are rare.
that prospectively evaluate this hypothesis. Retrospective These agents have been proposed as an alternative to analyses have suggested that a total dose of <30 ml for iodinated agents in the high risk patient for CIN, but diagnostic studies and <100 ml for interventional proce- no benefit has been reported to date [47].
dures lessen the risk for CIN [10]. In a study by Free-man, RCM doses above 5 cc  body weight (kg)/SCr were associated with a need for dialysis while unad- justed RCM dose was not a univariate predictor of con-trast induced dialysis [38].
The complexity and unpredictability of PCI pre- Continuation of pre-procedure parenteral volume cludes a strict recommendation of the RCM dose for a repletion is the mainstay of post-procedural manage- ment in the high risk patient for CIN. To ensure decrease RCM volume in the high risk patient include adequate hydration, urine output should be monitored.
small catheter size, biplane or rotational coronary angi- Though a urine output of 150 ml/hr is preferred [20], ography, and avoidance of left ventriculography. Per- individual assessment is required. The risk/benefit ratio forming diagnostic and interventional procedures at for bladder catheterization to monitor urine output separate sessions, often referred to as staging, is appro- Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.
Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Prevention of Contrast Induced Nephropathy TABLE VI. Recommendations for Prevention of CIN should be considered, e.g. cholesterol embolization, which is commonly associated with skin lesions [51].
i. Schedule outpatient for early arrival or delay procedure time to allow time to accomplish the hydration.
ii. Consider the following recommendations (No. 2–No. 5).
The risk of CIN varies from 2–30% in unselected a. Withhold, if clinically appropriate, potentially nephrotoxic drugs patients undergoing cardiovascular angiographic proce- including aminoglycoside antibiotics, anti-rejection medications and dures. It is associated with a significant increase in nonsteroidal anti-inflammatory drugs (NSAID).
patient morbidity and mortality. Recognition of the b. Administer N-acetylcysteine (equivocal data, see text) i. 600 mg administered orally q 12 hrs  4 doses beginning high risk patient coupled with appropriate peri-proce- dural management can reduce the incidence of CIN.
3. Manage Intravascular Volume (Avoid Dehydration) The routine use of eGFR is strongly recommended as a. Administer a total of at least 1 L of isotonic (normal) saline a method to identify the patient at risk for CIN. The beginning at least 3 hrs before and continuing at least 6–8 hrs after available evidence to date supports vigorous parenteral the procedure.
i. Initial infusion rate 100–150 ml/hr adjusted post procedure as volume repletion, limiting contrast volume, and the use of low- or iso-osmolar contrast media to decrease the b. Sodium bicarbonatea (limited data, see text) incidence of CIN in the high risk patient.
i. 154 mEq/l @3 ml/kg/hr starting 1 hr before contrast.
ii. 154 mEq/L @ 1 ml/kg/hr for 6 hrs following contrast.
b. Low- or iso-osmolar contrast agents (on going data, see text).
1. King B, Segal G, Berg G, et al. for the Committee on Drugs and Contrast Media of the American College of Radiology.
a. Obtain follow-up SCr 48 hrs post procedure.
Manual on Contrast Media. Version 5.0. Reston, VA: American b. Consider holding appropriate medications until renal function returns to normal, i.e. metformin, NSAID.
2. Thomsen HS, Morcos SK. Contrast media and the kidney: Euro- CIN, contrast-induced nephropathy; eGFR, estimated glomerular filtration pean Society of Urogenital Radiololgy (ESUR) guidelines. Br J rate; NSAID, nonsteroidal anti-inflammatory drug; SCr, serum creatinine.
a154 mEq/L is 3 A NaNaHCO3 in 1 L of either D5W or sterile water.
3. Morcos SK, Thomsen HS, Webb JAW, et al. Contrast media- induced nephrotoxicity: A consensus report. Eur J Radiol1999;9:1602–1613.
4. Gupta R, Birnbaum Y, Uretsky BF. The renal patient with coro- nary artery disease. Current concepts and dilemmas. J Am CollCardiol 2004;44:1343–1353.
Hemodialysis has been shown to remove RCM but 5. Sadeghi HM, Stone GW, Grines CL et al. Impact of renal insuf- not to prevent CIN [48]. Hemofiltration allows increased ficiency in patients undergoing primary angioplasty for acute hemodynamic stability compared with hemodialysis myocardial infarction. Circulation 2003;108:2769–2775.
6. Cockcroft DW, Gault MH. Prediction of creatinine clearance while permitting 10–15 times the usual hydration with- from serum creatinine. Nephron 1976;16:31–41.
out adding intravascular volume. Though promising in 7. Levey AS, Bosch JP, Lewis JB, et al. A more accurate method small studies, hemofiltration is invasive and logistically to estimate glomerular filtration rate from serum creatinine: A complex [49,50]. It will need to be established in larger new prediction equation. Ann Intern Med 1999;130:461–470.
trials before it can be widely recommended.
8. Stevens LA, Coresh J, Greene T, Levey A. Assessing kidney function—Measured and estimated glomerular filtration rate. NEngl J Med 2006; 54:2473–2483.
9. Brosius FC, Hostetter TH, Kelepouris A, et al. AHA science ad- visory. Detection of chronic kidney disease in patients with or at Management following RCM administration depends increased risk of cardiovascular disease. Circulation 2006; on the risk for CIN, with little follow-up required for 10. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score the low risk patient. In the high risk patient, SCr for prediction of contrast-induced nephropathy after percutane- should be obtained at 48–72 hrs following RCM as 24 ous coronary intervention: Development and initial validation.
hr values will miss a significant minority of these J Am Coll Cardiol 2004;44:1393–1399.
events. It should also be noted that the peak decrement 11. Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of in renal function may not appear until 1 week. Restart- ionic and nonionic contrast media 1196 patients: A randomizedtrial. Kidney Int 1995;47:254–261.
ing medications such as NSAID’s and metformin is de- 12. Cochran ST, Wong WS, Roe DJ. Predicting angiography- pendent upon the return to baseline renal function induced acute renal function impairment: Clinical risk model.
[25]. Should renal dysfunction occur, other causes Am J Roentgenol 1983;141:1027–1033.
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.
Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
13. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic A randomized, double-blind, placebo controlled study. Am J importance of acute renal failure after PCI. Circulation 2002; 32. Bagshaw SM, Ghali WA. Theophylline for prevention of con- 14. National Kidney Foundation. K/DOQI clinical practice guide- trast-induced nephropathy: A systemic review and meta-analysis.
lines for chronic kidney disease: Evaluation, classification and Arch Intern Med 2005;165:1087–1093.
stratification. Am J Kidney Dis 2002;39 (Suppl. 1):S1–S266.
33. Khanal S, Attallah N, Smith DE, et al. Statin therapy reduces 15. McCullough PA, Wolyn R, Rocher LL, et al. Acute renal failure contrast induced nephropathy: An analysis of contemporary PCI.
after PCI: Incidence, risk factors, and relationship to mortality.
34. Spargias K, Alexopoulos E, Kyrzopoulos S, et al. Ascorbic acid 16. Gruberg L, Mintz GS, Mehran R, et al. The prognostic implica- prevents contrast-mediated nephropathy in patients with renal tions of further renal function deterioration within 48 hrs of dysfunction undergoing coronary angiography or intervention.
interventional coronary procedures in prospective trial. Ann In- 35. Nallamothu BK, Shojania KG, Saint S, et al. Is acetylcysteine 17. Solomon R, Werner C, Mann D, D’Elia J, Silva P. Effects of effective in preventing contrast-related nephropathy? A meta- saline, mannitol, and furosemide to prevent acute decreases in analysis. Am J Med 2004;117:938–947.
renal function induced by radiocontrast agents. N Engl J Med 36. Hoffman U, Fischreder M, Kruger B, et al. The value of N-ace- tylcysteine in the prevention of radiocontrast agent-induced ne- 18. Taylor AJ, Hotchkis D, Morse RW, McCabe J. PREPARED: phropathy seems questionable. J Am Soc Nephrol 2004;15:407– Preparation for angiography in renal dysfunction. A randomized trial of inpatient vs outpatient hydration protocols for cardiac 37. Marenzi G, Assanelli E, Marana I, et al. N-Acetylcysteine and catheterization in mild to moderate renal dysfunction. Chest contrast induced nephropathy in primary angioplasty. N Engl J 19. Trivedi HS, Moore H, Nasr S, et al. A randomized prospective 38. Freeman RV, O’Donnell M, Share D, et al. Nephropathy requir- trial to assess the role of saline hydration on the development ing dialysis after percutaneous coronary intervention and the of contrast nephropathy. Nephron Clin Pract 2003;93:C29– critical role of an adjusted contrast dose. Am J Cardiol 20. Stevens MA, McCullough PA, Tobin KJ, et al. A prospective 39. Taliercio CP, Vlietstra RE, Ilstrup DM, et al. A randomized randomized trial of prevention measures in patients at high risk comparison of the nephrotoxicity of iopamidol and diatrizoate in for contrast nephropathy: Results of the P.R.I.N.C.E. Study. Pre- high risk patients undergoing cardiac angiography. J Am Coll vention of radiocontrast induced nephopathy clinical evaluation.
J Am Coll Cardiol 1999;33:403–411.
40. Schwab SJ, Hlatky MA, Pieper KS, et al. Contrast nephrotox- 21. Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast icity: A randomized controlled trial of a nonionic and an media-associated nephropathy. Arch Intern Med 2002;162:329– ionic radiographic contrast agent. N Engl J Med 1989;320: 22. Bader BD, Berger ED, Heede MB, et al. What is the best hydra- 41. Barrett BJ, Parfrey PS, Vavasour HM, et al. Contrast nephropa- tion regimen to prevent contrast media-induced nephrotoxicity? thy in patients with renal dysfunction: High versus low osmolar media. Kidney Int 1992;41:1274–1279.
23. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast- 42. Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in induced nephropathy with sodium bicarbonate—A randomized high-risk patients undergoing angiography. N Engl J Med controlled trial. JAMA 2004;291:2328–2334.
24. Heupler FA Jr. Guidelines for performing angiography in 43. Chalmers N, Jackson RW. Comparison of iodixanol and iohexol patients taking metformin. Members of the Laboratory Perform- in renal impairment. Br J Radiol 1999;72:701–703.
ance Standards Committee of the Society for Cardiac Angiog- 44. Barret BJ, Carlisle EJ. Meta-analysis on the relative nephrotox- raphy and Interventions. Cathet Cardiovasc Diagn 1998;43: icity of high- and low-osmolality iodinated contrast media. Radi- 25. Tepel M, Aspelin P, Lameire N. Contrast induced nephropathy: 45. McCullough PA, Bertrand ME, Brinker JA, et al. A meta-analysis A clinical and evidenced-based approach. Circulation 2006;113: of the renal safety of isosmolar iodixanol compared with low- osmolar contrast media. J Am Coll Cardiol 2006;48:692–699.
26. Gare M, Haviv YS, Ben-Yehuda A, et al. The renal effect of 46. Solomon R. The role of osmolality in the incidence of contrast- low-dose dopamine in high-risk patients undergoing coronary induced nephropathy: A systematic review of angiographic con- angiography. J Am Coll Cardiol 1999;34:1682–1688.
trast media in high risk patients. Kidney Int 2005;68:2256–2263.
27. Stone GW, McCullough PA, Tumlin JA, et al. Fenoldopam 47. Briguori C, Colombo A, Airoldi F, et al. Gadolinium-based con- mesylate for the prevention of contrast-induced nephropathy: A trast agents and nephrotoxicity in patients undergoing coronary ar- randomized controlled trial. JAMA 2003;290:2284–2291.
tery procedures. Catheter Cardiovasc Interv 2006;67:175–180.
28. Kurnik BR, Allgren RL, Genter FC, et al. Prospective study of 48. Sterner G, Frennby B, Kurkus K, Nyman U. Does post-angio- atrial natriuretic peptide for the prevention of radiocontrast- graphic hemodialysis reduce the risk of contrast medium ne- induced nephropathy. Am J Kidney Dis 1998;31:674–680.
phropathy? Scand J Urol Nephrol 2000;34:323–326.
29. Wang A, Holcslaw T, Bashore RM, et al. Exacerbation of radio- 49. Marenzi G, Marana I, Lauri G, et al. The prevention of radio- contrast nephrotoxicity by endothelin receptor antagonism. Kid- contrast-agent-induced nephropathy by hemofiltration. N Engl J 30. Khoury Z, Schlicht JR, Como J, et al. The effect of prophylactic 50. Marenzi G, Lauri G, Campodonico J, et al. Comparison of two nifedipine on renal function in patients administered contrast hemofiltration protocols for prevention of contrast-induced ne- media. Pharacotherapy 1995;15:59–65.
phropathy in high risk patients. Am J Med 2006;119:155–162.
31. Sketch MH Jr, Whelton A, Schollmayer E, et al. Prevention of 51. Cuddy E, Robertson S, Cross S, Isles C. Risks of coronary angi- contrast media induced renal dysfunction with prostaglandin E1: Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.
Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

Source: http://www.uphs.upenn.edu/renal/renal%20curr%20pdfs/core%20curr.pdf

spirig-healthcare.ch2

Patienteninformation des Arzneimittel-Kompendium der Schweiz® AMZVWas ist Montelukast Spirig HC und wann wird es angewendet?Montelukast Spirig HC enthält einen Wirkstoff, welcher die Wirkung von körpereigenen Substanzen, den sog. Leukotrienen, hemmt. Leukotriene verursachen die Verengung und Schwellung der Atemwege in Ihren Lungen. Die Blockierung der Leukotriene führtzur Besserung der Ast

Australian shareholders agreements - iba guide - jan 2013

AUSTRALIAN SHAREHOLDERS’ AGREEMENTS - AN INTERNATIONAL GUIDE Liability limited by a scheme approved under the Professional Standards Legislation This paper provides guidance on Australian shareholder agreements in a format adopted by the International Bar Association. Guides on shareholders’ agreements for other jurisdictions http://www.ibanet.org/LPD/Corporate_Law_Section/Clsly

Copyright © 2010-2014 Medical Pdf Finder