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Year : 2005  |  Volume : 15  |  Issue : 3  |  Page : 307-308
Contrast induced nephropathy (CIN): Can we minimize its effects?


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How to cite this article:
Kohli A. Contrast induced nephropathy (CIN): Can we minimize its effects?. Indian J Radiol Imaging 2005;15:307-8

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Kohli A. Contrast induced nephropathy (CIN): Can we minimize its effects?. Indian J Radiol Imaging [serial online] 2005 [cited 2020 Dec 3];15:307-8. Available from:
Contrast induced nephropathy is an impairment exacerbaration of previously demonstrated impairment in renal function occurring within 3 days following intravascular administration of contrast medium. This is in the absence of an alternative aetiology for the detiorating renal function. An increase in serum Creatinine of more than 0.5 mg/dl or 25% above the baseline serum Creatinine is considered the criteria to determine contrast induced nephropathy. The ideal method is actually to determine serial creatinine clearance. This is extremely sensitive and detects subtle changes in renal function, however this test is not practical as well as not cost effective, therefore serum creatinine measurements are used as the marker for contrast induced nephropathy. CIN is by no means uncommon. It is the third most common cause of acute renal failure in patients admitted to hospital. [1] The incidence is estimated to be 1% with intravenous contrast medium, 2-7% with intra-arterial contrast medium. [2] In diabetics with normal renal function it rises to 16%. [2] Patients with a preexisting renal insufficiency prior to receiving contrast media have 33% incidence of developing CIN. [3] Diabetics with associated renal insufficiency are at the greatest risk for developing CIN. Other risk factors for developing CIN are dehydration, hypotension, nephrotic syndrome, multiple myeloma, higher dose of contrast media, and repeated doses of contrast media within 48hrs, higher osmolar contrast media and concurrent use of nephrotoxic drugs.

The mechanism by which contrast induces nephropathy is complex and not very clear. It is considered to be a combination of renal ischemia and direct tubular epithelial cell toxicity. The renal ischemia occurs due to alterations in nitric oxide metabolism leading to renal vasoconstriction and a consequent drop in renal perfusion and acute renal failure. Contrast media is also considered to be directly toxic to the renal tubules most likely due to the formation of free radicals in the acidic tubular environment.

CIN most commonly clinically manifests either as a nonoliguric or an oliguric nephropathy. In the nonoliguric variety there is a transient decline in renal function. Serum Creatinine levels begin to rise within 24 hours of contrast administration, peaking at 3-5 days and then returning to baseline in 10-15 days. In the oliguric variety, which is the more, sever form; there is a drop in urine output to less than 400 ml in 24 hours. Serum Creatinine levels peak in 5-10 days, returning to normal in 14-21 days. In a small percentage the serum creatinine continues to rise, urine output drops; these indivuals need then to be put on dialysis. Mortality from contrast induced nephropathy is also well documented. [4]

Can we reduce contrast induced nephropathy with some preventive or prophylactic measures How do we do it, it is easy to say do not use contrast. This is a radical statement as the incidence is CIN is low and if we take adequate care we can minimize it considerably. So how do we minimize it?

Universal usage of low osmolar contrast media. High osmolar contrast media - ionic contrast media have a higher incidence of CIN as compared to low osmolar contrast media. The price difference between these two are now approximately 20-30% as compared to 400-500% a decade ago. Isoosmolar contrast media were introduced a few years back with a landmark publication that they further reduced the incidence of CIN to very low levels. (5) Unfortunately that publication has been followed up by numerous studies that have not substantiated this fact, in fact in some studies the reverse has been found to be true. [6]

Volume Expansion: The most important risk factor for CIN after preexisting renal insufficiency and diabetes is dehydration. Hydration is the most effective means available to decrease the incidence and severity of contrast induced nephropathy. Conventionally patients are asked to remain nil by mouth 3-4 hrs prior to a contrast study for CT Scan. This induces dehydration. The main rational for asking patients to remain nil by mouth was due to the fact that they may vomit after intravascular administration of contrast media and the consequent danger of aspiration. This was particularly with ionic contrast media. Today with practically a universal usage of nonionic contrast media the incidence of vomiting has considerably reduced. Infact this is paradoxical as patients for abdominal CT receive a liter of oral contrast medium including a table dose, of a few 100 ml just seconds before the onset of the CT study. It is therefore prudent to ask patients to remain of solids for 3-4 hrs prior to administration of contrast but not liquids. In fact patients should be encouraged to hydrate themselves well prior to administration of contrast as well as after the study.

Instructions to patients should actually simulate the instructions for sonography, no solids but plenty of liquids prior to the exam. Hydration can also be achieved by using the intravenous route. Initial studies recommended use of IV normal saline for 12 hours prior and 12 hours after contrast administration to reduce contrast induced nephropathy. Recent publications have recommended the use of sodium bicarbonate rather than sodium chloride as in addition to volume expansion the sodium bicarbonate neutralises the acidic medium in the tubules leading to a reduced release of free radicles and thus lowering of contrast induced nephropathy. 3ml/kg/per hour of sodium bicarbonate is administered for 1 hour prior to the study. After the study 1ml/kg per hour is administered for 6 hours. Multiple myeloma is a risk factor for CIN. High amounts of protein and contrast get deposited in the tubules causing as obstructive nephropathy. Adequate hydration avoids contrast induced nephropathy in multiple myeloma as it does not permit the development of an obstructive uropathy.

N acetyl Cystine is a free radical scavenger, thereby has been assumed to reduce the incidence of contrast induced nephropathy. It is administered in doses of 1200 mg in two divided doses a day prior to the administration of contrast or 150 mg/kg intravenously half an hour prior to contrast administration. There is a great amount of confusion regarding the utility of N acetyl cystine, there are numerous reports which reveal there is a reduction in the incidence of CIN and numerous which reveal no benefit. The metaanalysis have also not provided a clear idea of the merits demerits of N acetyl Cystine. This an extremely cheap drug. The general consensus is since it is cheap and easy to administer this drug it should be used as a prophylactic in high risk indivuals till larger studies prove whether it is efficacious or not.

To minimize the effects of CIN it is important to have a specific protocol in place. It is ideal to obtain serum Creatinine levels in all indivuals receiving contrast media. This may not be feasible in all centers, then in all indivuals at a high risk to develop CIN serum Creatinine levels obtained. If the levels are high above 1.6 it should be first evaluated whether another imaging modality may be used, if not, the risks versus benefit for administration of IV contrast should be considered. If IV contrast is necessary then adequate measures to minimize nephropathy should be undertaken. All indivuals receiving IV contrast must be adequately hydrated using an oral or IV route. N acetyl cystine at present is cheap and harmless. Nephrotoxic drugs should be avoided 48 hours before and after adminstration of contrast material.

Contrast induced nephropathy is a serious adverse event following administration of contrast medium. It is incumbent on every radiologist to avoid or minimize the risk of contrast induced nephropathy.

   References Top

1.Mccullough P. Sandberg K. Epidemiology of contrast induced nephropathy. Rev Cardiovasc Med 2003:4(suppl 5): S3-S9  Back to cited text no. 1    
2.Narang R, Sakhare M, Bahl VK: Contrast Induced Nephropathy : Indian Heart journal Jan-Feb 2004 Vol 56, No 1, 13-20  Back to cited text no. 2    
3.Barrett BJ, Parfrey PS, Vavasour HM, McDonald J, Kent G, Hefferton D, et al. Contrast nephropathy in patients with impaired renal function; high versus low osmolar media. Kidney Int 1992; 41: 1274-127933  Back to cited text no. 3  [PUBMED]  
4.Mccullogh PA, Wolyn R, Racher LL, Levin RN, O'Neil WW. Acute Renal Failure after coronary intervention: incidence, risk factors and relationship to mortality. Am J Med 1997:103:368-375  Back to cited text no. 4    
5.Aspelin P, Aubry P, Fransson S-G, Strasser R, Willenbrock R,Berg KJ for the NEPHRIC study investigators. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003;348:491-9.  Back to cited text no. 5    
6.Sharma Samin K, Kini Annapoorna : Effect of Nonionic radiocontrast agents on the occurance of contrast induced nephropathy in patients with mild - moderate chronic renal insufficiency : Catheterisation and Cardiovascular interventions 65:386-393 (2005)  Back to cited text no. 6    

Correspondence Address:
Anirudh Kohli

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-3026.29141

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