References:
- Tepel M, van Der GM, Schwarzfeld C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 2000; 343(3):180-184.
- Mueller C, Buerkle G, Buettner HJ, Petersen J, Perruchoud AP, Eriksson U, Marsch S, Roskamm H. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med 2002; 162(3):329-336.
- Mehran R, Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at risk. Kidney Int Suppl 2006;(100):S11-S15.
- Rihal CS, Textor SC, Grill DE, Berger PB, Ting HH, Best PJ, Singh M, Bell MR, Barsness GW, Mathew V, Garratt KN, Holmes DR, Jr. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002; 105(19):2259-2264.
- Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, Mintz GS, Lansky AJ, Moses JW, Stone GW, Leon MB, Dangas G. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004; 44(7):1393-1399.
- Tepel M, Aspelin P, Lameire N. Contrast-induced nephropathy: a clinical and evidence-based approach. Circulation 2006; 113(14):1799-1806.
- Barrett BJ, Parfrey PS. Clinical practice. Preventing nephropathy induced by contrast medium. N Engl J Med 2006; 354(4):379-386.
- Solomon R, Deray G. How to prevent contrast-induced nephropathy and manage risk patients: practical recommendations. Kidney Int Suppl 2006;(100):S51-S53.
- Mueller C. Prevention of contrast-induced nephropathy with volume supplementation. Kidney Int Suppl 2006;(100):S16-S19.
- Marenzi G, Assanelli E, Marana I, Lauri G, Campodonico J, Grazi M, De Metrio M, Galli S, Fabbiocchi F, Montorsi P, Veglia F, Bartorelli AL. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med 2006; 354(26):2773-2782.
- Merten GJ, Burgess WP, Gray LV, Holleman JH, Roush TS, Kowalchuk GJ, Bersin RM, Van Moore A, Simonton CA, III, Rittase RA, Norton HJ, Kennedy TP. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA 2004; 291(19):2328-2334.
- Briguori C, Airoldi F, D'Andrea D, Bonizzoni E, Morici N, Focaccio A, Michev I, Montorfano M, Carlino M, Cosgrave J, Ricciardelli B, Colombo A. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL). A Randomized Comparison of 3 Preventive Strategies. Circulation 2007.
- Aspelin P, Aubry P, Fransson SG, Strasser R, Willenbrock R, Berg KJ. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003; 348(6):491-499.
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Question 3) - What other factors have been previously described as possible contributors to the risk of CIN?
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a) Dehydration |
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b) Therapy with ACE-inhibitors |
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c) Diabetes mellitus |
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d) Therapy with NSAIDS |
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e) Therapy with diuretics |
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f) Female gender |
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g) Preexisting kidney disease |
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h) Volume of contrast media |
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i) Hypotension, shock |
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j) Need for vasopressor support |
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k) Older age |
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l) Intra-aortic balloon counterpulsation (IABP) |
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m) Proteinuria |
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n) Congestive heart failure |
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o) Nephrotoxic medications |
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p) Liver cirrhosis |
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q) Anemia |
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r) None of the above |
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s) All of the above |
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The correct answer is "s", ALL of the above-mentioned conditions may contribute to the development of CIN.
Comment to Question 3:
Previous trials concerning CIN have revealed numerous risk factors for CIN (3,6,7). A possible classification is:
A) Preexisting factors negatively influencing renal perfusion / oxygen supply (e.g. low volume status, shock, hypotension, consecutive vasopressor use, sepsis, IABP, NSAIDS, ACE-I, congestive heart failure, anemia, liver cirrhosis ?)
B) Preexisting renal damage (chronic kidney disease, proteinuria, arterial hypertension, older age, multiple myeloma ?)
C) Additional nephrotoxin application (e.g. NSAIDS, antibiotics, diuretics ?)
D) Unknown or genetic factors (female gender?)
Obviously, this classification system does not allow a sharp differentiation and several of the above-mentioned factors may well be placed into another or several groups at the same time.
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After stratifying the present patient as a patient at risk for developing a CIN, the crucial question is the best way of management.
The patient from the vignette should receive i.v. fluid before and after contrast application. We used to give normal saline by 80 to 100 ml/h i.v. 12 hrs before and 12 hrs after PCI.
In case of an outpatient setting, an alternative to a 24hrs i.v. fluid regimen can be to advice the patient to drink 1 liter within the last ten hrs prior to contrast application and then to start high volume i.v. hydration (e.g. 300ml/h for 6 to 8 hrs) ?on call? for the intervention (9). The advise should be given to use a low-osmolality contrast agent and the lowest possible volume by omitting a left ventricular angiogram. We apply N-acetylcysteine 600 mg bid orally for 2 days (before and after) (1). Although N-acetylcysteine is not without controversy we in accordance to many others use N-acetylcysteine since the cost and risks of side-effects are low. In case of emergency angiography, the scheme of Marenzi et al (10) with a single shot NAC i.v. prior to angiography might be preventive. However, in this study high volumes of contrast media (approximately a mean of 260 ml) were used, so general recommendations cannot be made for high dose N-acetylcysteine (10).
In case of treatment with loop diuretics, if clinically possible, we stop these drugs at least for the day of the examination. We would not stop the ACE-inhibitor in the case of the vignette.
Concerning CIN, the last years have generated several publications with possibly new insights into prophylaxis and treatment.
Question 5) - Which of the following statements concerning CIN trial and interpretation are true?
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a) Giving normal saline (0.9% NaCl) intravenously 80ml/h for 12 hrs before and 12 hrs after PCI is an efficient mode for prophylaxis. |
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b) It has clearly been shown that isoosmolar contrast agents are superior to low-osmolality contrast agents in terms of risk reduction. |
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c) Bicarbonate infusion may be superior to normal saline infusions in terms of risk reduction. |
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d) Serum creatinine measurements may be insufficient to assess all patients at risk. |
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e) The occurrence of CIN does not influence hard end-points such as in-hospital death or long-term mortality. |
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f) Answers #1, #3 and #4 are true. |
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Comment to Question 5:
Answer #1 describes an appropriate approach to optimize the volume status of the patient. However, two recent studies have challenged the role of normal saline as the optimal fluid substitution (11) (12). Bicarbonate infusion has been postulated to be superior to normal saline first by Merten et al. (11). They administered a 154 mEq/L sodium bicarbonate solution: 3ml/kg for one hour prior and 1 ml/kg for 6 hours after contrast application. However, these authors used a rather short and presumably insufficient hydration regimen in the normal saline control group (720 ml of normal saline in an 80 kg patient) and they did not administer N-acetylcysteine. In contrast Briguori et al in a very recent publication (12) stratified their patients to receive either the Merten bicarbonate scheme plus N-acetylcysteine or a higher amount of normal saline (1562±585ml) plus N-acetylcysteine. All patients received NAC orally at a dose of 1200 mg twice daily on the day before and the day of administration of the contrast agent (total of 2 days).
They included patients undergoing coronary angiography or peripheral procedures with relatively severely impaired renal function (mean baseline GFR was approximately 34 ml/min). The contrast agent was iodixanol (an iso-osmolar, nonionic contrast agent = Visipaque®, approximately 175±95 ml). The incidence of CIN was defined as a serum creatinine increase of 25% in 48 hrs. There was a significantly lower risk for CIN in the bicarbonate group compared to the normal saline group: 2% versus 10%. Therefore, the Merten bicarbonate scheme appears to be a superior alternative especially for the outpatient setting but also proved to be superior to a scheduled 24 hrs normal saline i.v. scheme. No serious side effects were recorded: Urine pH increased from 5.4±0.6 to 6.6±0.9; serum potassium decreased from 4.8±0.6 to 4.4±0.6 mmol/L (the latter change being similar in the normal saline group).
Aspelin et al have investigated the difference between the iso-osmolar contrast iodixanol and the low-osmolality contrast iohexol (13). They found in a study with 129 patients a superior outcome for the iso-osmolar contrast agent concerning the risk for CIN. However, these results need to be confirmed before a general recommendation can be made: The group of patients with the low-osmolality iohexol contrast had more PCI (possible blood pressure drop?) and a longer history of diabetes (18 versus 12 years).
It needs to be pointed out that serum creatinine may be insufficient in identifying all patients at risks. The (calculated) creatinine clearance can help to identify patients with severely reduced renal function despite serum creatinine still being within the normal range. Calculating the GFR with e.g. MDRD formula is also possible in the patient from the vignette only a couple of hours ahead from the PCI (just with "spot" blood drawing).
Although definite, prospective data are still missing, it is clear that CIN is more than just a temporary change of a biomarker. CIN is associated with increased morbidity and mortality (6). However, it still needs to be elucidated, whether CIN is just a reflection for the presence of severe circulatory disturbances or whether CIN exerts an independent effect upon morbidity and mortality (CIN being a marker of versus being a mediator for reduced patient outcome).
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