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Saudi Journal of Kidney Diseases and Transplantation
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REVIEW ARTICLE Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 5  |  Page : 753-765
Prevention of iodinated contrast induced acute kidney injury (ICI­-AKI) - what have we learnt so far?

Department of Medicine, Nephrology Section, Hamad General Hospital, Doha, Qatar

Click here for correspondence address and email

Date of Web Publication2-Sep-2009


The use of imaging modalities and endovascular procedures has escalated phenol­menally in the last two decades. In view of increasing number of elderly patients, rising incidence of chronic kidney disease and diabetes along with the complication of nephrogenic systemic fibrosis with gadolinium, a large patient population will be at risk of developing iodinated contrast induced acute kidney injury (ICI-AKI) which is associated with significant morbidity and mortality and increased health care costs. Hence a search for more effective ways to prevent ICI­AKI continues to be a focus within the medical community.

How to cite this article:
Asim M. Prevention of iodinated contrast induced acute kidney injury (ICI­-AKI) - what have we learnt so far?. Saudi J Kidney Dis Transpl 2009;20:753-65

How to cite this URL:
Asim M. Prevention of iodinated contrast induced acute kidney injury (ICI­-AKI) - what have we learnt so far?. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2022 Sep 29];20:753-65. Available from: https://www.sjkdt.org/text.asp?2009/20/5/753/55357

   Introduction Top

Iodinated contrast media (ICM), by virtue of their ability to enhance the visibility of vascular structures and organs during radiographic pro­cedures, have greatly facilitated the diagnosis and treatment of many diseases. Conversely, their use has been associated with serious com­plications like acute kidney injury (AKI). This resulted in a trend towards the use of gado­linium-based contrast media in patients with pre-existing renal impairment. However, over the past few years, gadolinium-based contrast media is linked with the development of a severe, life-threa­tening condition, i.e. nephrogenic systemic fib­rosis, especially in patients with advanced kidney disease. Thus far, over 400 patients with nephrogenic systemic fibrosis have been re­ported. [1],[2] More than 95% of the evaluated pa­tients had been exposed to gadolinium within three months prior to the onset of disease. Consequently, ICM continue to be utilized as the main radiocontrast agents for imaging pro­cedures in patients with renal impairment. The purpose of this article is to provide an up to date of strategies for preventing AKI secon­dary to the use of ICM. This will help in translating the available evidence into daily clinical practice.

   Nomenclature Top

"What's in a name? That which we call a rose, by any other name would smell as sweet" (William Shakespeare)

Uniformity of medical terminology and the abbreviations is important to clarify and en­hance international medical scientific commu­nication and to avoid misunderstanding. Kee­ping in line with this concept, the terminology in the field of Nephrology has evolved with time and new terms have been coined e.g. "Acute Kidney Injury" and "Chronic Kidney Disease".
"Contrast induced Nephropathy" has been the most frequently used term to describe kidney injury seen after exposure to ICM. The word "nephropathy" has recently been replaced by "Acute kidney injury" (emphasizing that it is an acute renal insult resulting in abrupt change in serum creatinine/urine output), leading to the new term "Contrast induced Acute Kidney Injury" (CI-AKI). Various materials are used as contrast agents for radiological imaging e.g. Barium Sulphate, Iodine based contrast media, Gadolinium and Carbon dioxide. Though there are reports of AKI induced by Gadolinium­based CM, [3],[4] for all practical purposes, when­ever we talk of "CI-AKI", we refer to AKI induced by iodinated contrast media. Similarly, the pathogenesis, risk factors and preventive strategies that have been studied and recom­mended in literature apply only to ICM. Hence, to avoid confusion, "Iodinated Contrast Induced Acute Kidney Injury" (ICI-AKI) is preferable to describe this clinical entity.

"The beginning of wisdom is to call things by their right names." (Chinese proverb)

   How Do ICM Damage the Kidneys? Top

"You can discover what your enemy fears most by observing the means he uses to frighten you"

(Eric Hoffer)

Various pathophysiologic mechanisms form the basis of rationale for using various strate­gies to reduce the risk of ICI-AKI [5],[6] [Figure 1].

The predominant mechanism appears to be ischemia in outer medulla which is supplied by vasa recta- small diameter blood vessels with high vascular resistance. Because of the coun­ter current mechanism, metabolic activity and therefore oxygen consumption is very high in this area. This might result in a thin balance of supply and demand of oxygen and possibility of hypoxia with any metabolic stress. ICM ad­ministration potentiates hypoxia by increasing the demand and reducing the supply of oxygen to this area. ICM activate adenosine, renin­angiotensin system and endothelin on one hand; and inhibit nitric oxide and vasodilatory pros­taglandins on the other, resulting in vasocons­triction of vasa recta. They also increase the osmolality/viscosity of blood making the blood flow sluggish and increasing tubular activity to excrete the administered osmotic load. Osmotic natriuresis and diuresis activates tubuloglome­rular feedback mechanism leading to vaso­constriction of glomerular afferent arterioles thus decreasing glomerular filtration rate (GFR).

Another proposed mechanism is direct tubular cytotoxicity as evidenced by intense vacu­lization of the proximal tubular cells, loss of brush border and sometimes frank tubular necrosis after the injection of ICM. [7] However, these findings may represent ICM exposure rather than a true nephrotoxicity, since kidney ische-mia molecule (KIM-1), an indicator of tubular necrosis has not been detected in urine in clinical ICI-AKI. [8]

Hypo perfusion of tissues and direct tubulo­toxicity can lead to production of reactive oxy­gen species, oxidative stress and inflammation that contributes to additional injury causing death of tubular cells.

Finally, tubular plugging can take place se­condary to cast formation from aggregation of Tamm-horsfall proteins, increased tubular fluid viscosity and increased urate excretion with tubular precipitation.

   Reducing the Risk of ICI-AKI Top

"Intellectuals solve problems; geniuses prevent them." (Einstein)

Since ICI-AKI is an iatrogenic complication with predictable timing, it is amenable to pre­ventative strategies. These can be broadly divi­ded into five categories:

  1. Peri-procedural intravascular volume ex­pansion
  2. Withdrawal of potentially nephrotoxic me­dication
  3. Adjunctive pharmacotherapy
  4. Selection of type and dose of ICM and
  5. Prophylactic extra-corporeal therapy

   Peri-Procedural Intravascular Volume Expansion Top

"We never know the worth of water 'til the well is dry" (English Proverb)

Volume supplementation increases renal blood flow by expanding plasma volume, down-re­gulating the renin-angiotensin-alsodterone axis and reducing the levels of vasoconstrictive hormones. Increased urinary flow by fluid ad­ministration shortens the intratubular transit time of ICM reducing the duration of nephron exposure to the ICM. It also helps dilute the ICM and prevent tubular obstruction. [9]

There have been no randomized controlled trials (RCTs) directly comparing intravascular volume expansion with no volume expansion but most patients with ICI-AKI reported in the early literature were volume depleted; many of them intentionally to increase the concentra­tion of ICM in the urinary tract for best visua­lization. [10],[11] Effectiveness of hydration therapy was recognized in 1980s. [12],[13]

Search for the best type of intravenous (IV) fluid has been ongoing for the last two de­cades. Recommendations for the use of half normal saline [14] changed in favor of normal saline after randomized data in patients under­going coronary angioplasty demonstrated added advantage by isotonic hydration. [15] Later, Merten et al in a RCT showed that sodium bicarbonate was more effective than normal saline in re­ducing ICI-AKI. [16] Both types of fluids were infused at a rate of 3 mL/kg per hour for 1 hour immediately before ICM injection followed by 1 mL/kg per hour during the contrast exposure and for 6 hours after the procedure. Following this a number of randomized, prospective trials in patients undergoing coronary angiography/ percutaneous coronary intervention (PCI) using intra-arterial ICM found that bicarbonate had a protective effect that was equal to or greater than that of normal saline. [17],[18],[19],[20],[21] However, in a retrospective cohort study of about 8000 pa­tients at Mayo clinic comparing the effect of sodium bicarbonate and N-acetylcysteine used together and alone, From et al demonstrated that bicarbonate was associated with an in­creased incidence of ICI-AKI despite the favo­rable baseline risk profile in the bicarbonate group. [22] The authors speculated that contrary to the earlier belief, bicarbonate may actually possess pro -oxidant properties. The most recent and largest prospective RCT showed no advantage of bicarbonate over normal saline in patients with chronic kidney disease (GFR < 60 mL/min/1.73m 2 ) and additional risk markers for ICI-AKI who were undergoing coronary angiography. [23] Procedure duration, contrast volume and hydration protocol was similar in both groups (3 mL/kg for 1 hr pre and 1.5 mL/ kg/hr during and up to 4 hrs post-procedure) though the sodium content and osmolality of the two intravenous fluids differed. The results of these studies have blunted the enthusiasm about the use of sodium bicarbonate. Another disadvantage of sodium bicarbonate solution is that it is not readily available in hospitals and has to be prepared.

In conclusion, isotonic hydration remains the gold standard prophylactic hydration therapy. Rate and duration of IV fluid administration must be tailored to the patient's cardiac status. Forced diuresis is however not recommended [24],[25] as both mannitol and frusemide have been shown to increase the risk of ICI-AKI. [14],[26]

   Withdrawing Potentially Nephrotoxic Medication Top

In patients with GFR < 60mL/ min/1.73m 2 , every effort should be made to withhold drugs that have nephrotoxic potential at least 24 hours prior to a planned ICM study. These recom­mendations are mostly "opinion-based" since there are no RCTs addressing this issue.

Nonsteroidal anti-inflammatory drugs and cy­clo-oxygenase-2 inhibitors should be withdrawn as they adversely affect renal hemodynamics by inhibiting the vasodilatory prostaglandins. Dipyridamol should also be avoided as it en­hances the effect of ICM by increasing renal adenosine. [27] Diuretics, unless required for pul­monary odema, should be discontinued as they aggravate ICM tubulo-toxicity. [14],[24],][25],[26] Concomi­tant use of Aminoglycosides, Vancomycin and Amphotericin is best avoided but if not po­ssible, then drug levels should be monitored closely.

It is controversial if angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) should be withheld or not. Some reports have shown decreased [28],[29] and others increased [30],[31] risk of ICI-AKI with ACEIs. A recent prospective RCT of 220 pa­tients by Rosenstock et al showed that with­holding ACEIs and ARBs 24 hours before coronary angiography did not influence the incidence of ICI-AKI in stable patients with chronic kidney disease (CKD) stages 3-4. [32] Based on this study and considering their be­neficial effects, these agents can be continued as long as hypotension is avoided.

Metformin should also be discontinued on the day of procedure and resumed after 2-3 days if no increase in creatinine is seen since toxicity can be enhanced if ICI-AKI sets in.

   Adjunctive Pharmacotherapy Top

Many pharmacological agents have been evaluated for reduction in the risk of ICI-AKI, but none has shown a consistent trial evidence to receive approval from regulatory authorities for clinical use.

Pharmacological manipulation aiming at pre­venting ICM induced vasoconstriction failed to yield beneficial effects in RCTs using do­pamine, [33] atrial natriuretic peptide, [34] calcium channel blockers, [35] non-selective endothelin receptor antagonists [36] and Fenoldopam. [37] Inte­restingly, use of vasodilators such as dopamine and atrial natriuretic peptide may actually exa­cerbate medullary ischemia by causing redis­tribution of blood flow from the medulla to the cortex.

N-Acetyl Cysteine (NAC), by virtue of its anti­oxidant and vasodilator properties was widely accepted as a prophylactic measure after the first prospective placebo controlled study sho­wed benefit in patients with renal insufficiency undergoing computed tomography with a non­ionic, low-osmolality contrast agent. [38] Nume­rous studies have been published since then in support and against the efficacy of NAC. [39] The divergent results were partly due to significant heterogeneity among studies reflecting diffe­rence in patient population, definition of ICI­AKI, route of administration, types and volumes of ICM, types of imaging procedures and dosing regimens of NAC. Even a series of meta-analysis failed to clarify the efficacy of NAC. [40],[41],[42],[43],[44],[45],[46],[47],[48],[49] A most comprehensive meta-analysis of 41 RCTs by Kelly et al involving 6379 pa­tients showed more effective reduction in ICI­AKI risk by periprocedural NAC than by any other pharmacological agent. [50] Results of all these meta-analyses must be interpreted with caution since it is difficult to derive a summary effect given the heterogeneous results of indi­vidual trials. Furthermore, recent demonstra­tion by Hoffmann et al of lowered serum crea­tinine without change in serum cystatin C levels following the use of NAC suggested possible changes in muscle metabolism or re­nal tubular secretion rather than a true change in GFR. [51] IV and combined IV and oral routes have been utilized for patients undergoing emergency coronary interventions but once again showing mixed results. [52],[53],[54],[55] Safety remains an additional concern with IV use of NAC. There is also evidence that higher dose of NAC (1200 mg orally twice daily) might be more effective than the standard dose [56],[57] but this still needs to be explored further. In summary, consensus on the benefit of NAC has not been reached, however, since it is safe, economical and readily available, it has found a place in the preventive strategies adopted by several societies including the American College of Radiology [58] and the Canadian Association of Radiologists. [59]

Theophylline and aminophylline cause intra­renal vasodilatation by non-selective adenosine antagonism but their use has been limited be­cause of the narrow therapeutic index with potential adverse effects and inconsistent re­sults across studies. Pooled results of 7 trials by Ix et al revealed renoprotective effect [60] but a meta-analysis by Bagshaw et al including 9 RCTs [61] and a recent meta-analysis by Kelly et al did not find a statistically significant bene­ficial effect. [50]

Recognizing the antioxidant potential of As­corbic acid, Spargias et al conducted a rando­mized, double-blind, placebo-controlled trial of 231 patients with a serum creatinine concen­tration > 1.2 mg/dL who underwent coronary angiography and/ or intervention. [62] 3 g of As­corbic acid, at least 2 hours before the pro­cedure and 2 g in the night and the morning after the procedure, or placebo was adminis­tered orally. ICI-AKI occurred in 9% of pa­tients in the ascorbic acid group and in 20% patients in the placebo group. Additive pro­tective effect was however not seen when Ascorbic acid was used in combination with NAC in the REMEDIAL trial. [63] Boscheri et al evaluated the efficacy of ascorbic acid as an adjunct to hydration in a randomized, double­blind, prospective, single center-study. [64] 143 consecutive patients with CKD who were undergoing coronary angiography/intervention were randomly assigned to receive 1 g ascorbic acid or placebo as adjunct to saline hydration prior to and after angiography. No significant difference was detected in the incidence of ICI-AKI in the two groups (Vitamin C 6.8% patients; placebo 4.3% patients).

Statins increase nitric oxide production, re­duce oxidative stress and have anti-inflamma­tory properties. Attallah et al in a retrospective study of 1002 patients with CKD undergoing cardiac catheterization showed that prophylac­tic administration of statins along with hydra­tion was associated with less (17% VS 22%) ICI-AKI (defined as 50% increase in crea­tinine). [65] This beneficial effect was confirmed in retrospective and prospective studies in patients undergoing PCI. [66],[67] More recently, Bouzas-Mosquera et al did not observe a pro­tective effect of statins in 589 consecutive patients with acute myocardial infarction who underwent primary angioplasty. [68] Hence there is not enough evidence to support routine ini­tiation of statin therapy in patients at risk of ICI-AKI, in whom these agents are not other­wise indicated.

In summary, conflicting results, rather than convincing conclusions have been observed in the studies of pharmacological agents and additional large prospective RCTs are needed before any of these agents become the standard of care for ICI-AKI prevention. These trials should use clinically relevant outcomes like doubling of serum ceatinine/ requirement for dialysis and all cause mortality rather than using surrogate end-points. Head to head stu­dies of different agents will identify the most effective prophylactic pharmacologic preventive regimen.

"He who would search for pearls, must dive deep below" (John Dryden)

   Selection of Type of ICM Top

"Know your enemy. The supreme art of war is to subdue the enemy without fighting." (Sun Tzu)

Strategies to attenuate toxicity of ICM have focused on reducing protein binding (to mini­mize anaphylactoid reactions), manipulating hydroxyl groups and adding calcium ions (to improve neural and cardiac tolerance) as well as on reducing the osmolality and ionicity (for reno-protection).

The chemical structure of ICM consists of benzoic acid molecule where each benzene ring has 3 Iodine atoms. From the radiological point of view, the higher the number of Iodine atoms in a contrast molecule, the better the opacifica­tion with fewer number of contrast molecules and therefore lesser osmotic load. If there is only one benzene ring in each molecule, we call it a monomer; and dimmer if there are 2 ben­zene rings (joined by a side chain) in each mo­lecule. In addition, ICM can be ionic if there is a carboxyl group coupled with a cation (usually Na or meglumine) - or non-ionic if there is no carboxyl group attached [Figure 2].

Based on osmolality, ICM are classified as hyper-osmolar (HO-ICM) with osmolality of up to 2000 mOsm/L, low-osmolar (LO-ICM) with osmolality of 600-900 mOsm/L or iso­osmolar (IO-ICM) with osmolality approaching that of blood. It should be noted that though LO-ICM are "low-osmolar" compared to the first generation HO-ICM, their osmolality is still 2-3 times higher than that of blood.

There is evidence that nephrotoxic potential of ICM is related to their osmolality.

Large trial by Rudnick et al (comparing Iohexol, a LO-ICM with Diatrizoate, a HO­ICM) and a meta-analysis of comparative randomized trials by Barrett et al convincingly showed that in patients with CKD, incidence of ICI-AKI was much less with the use of LO­ ICM as compared to HO-ICM. [69],[70] But whether IO-ICM are safer than LO-ICM with regards to their nephrotoxicity is debatable as a clear benefit has not been shown in many studies. The reason might be that despite having the same osmolality as that of blood, IO-ICM have higher viscosity compared to LO-ICM which leads to increased resistance to flow in micro vessels.

When administered intravenously, no advan­tage of IO-ICM over LO-ICM was seen in ACTIVE, [71] (comparing Iodixanol and Iomeprol), IMPACT [70] and PREDICT [72] studies (comparing Iodixanol and Iopamidol). This reduced the inte­rest in the use of the Iodixanol which in NEPHRIC [73] study was shown to be less neph­rotoxic than Iohexol in high risk patients ha­ving angiographic studies. On the other hand, after intra-arterial administration, the LO-ICM Iohexol was documented to be of greater toxic potential than IO-ICM Iodixanol in diabetic patients with CKD. [74] Similarly, Ioxaglate, an ionic dimeric LO-ICM was found to be more nephrotoxic than its competitor Iodixanol in RECOVER study [75] that recruited patients with creatinine clearance < 60 mL/min undergoing coronary angiography with or without percu­taneous coronary intervention. However there is a wide range of LO-ICM in the non-ionic monomers group that is approved for intra­vascular use. Out of these, Iopamidol was de­monstrated to have lower incidence of ICI­ AKI than Iohexol. [76],[77],][78]

The American College of Cardiology/American Heart Association guidelines [79] recommend the use of IO-ICM in CKD patients undergoing angiography, whereas the American College of Radiology, [58] Canadian Association of Radio­logists [57] and European Society of Urogenital Radiology guidelines [80] recommend the use of either LO-ICM or IO-ICM in patients at in­creased risk of ICI-AKI. NKF KDOQI guide­lines recommend use of IO-ICM in dialysis patients with residual renal function. [81]

   Minimizing the Dose of ICM Top

Both retrospective and prospective studies have shown that the risk of ICI-AKI directly correlates with the dose of ICM administered, which is an independent predictor of ICI­-AKI. [82],[83],[84] There are no cut-off doses below which ICM are absolutely safe; the toxic "volume-threshold" of ICM decreases as the CKD progresses, since the filtered load of the ICM per surviving nephron is increased. In other words, it's the dose of ICM relative to the level of renal function that best reflects ICI-AKI risk and it is the load of ICM per functioning nephron that is the best measure of contrast dosage (approximated by mg of Iodine/ eGFR ratio). [85] Laskey et al showed that the volume of ICM to the creatinine clearance (V/Creatinine clearance) ratio > 3.7 was a sig­nificant and independent predictor of ICI-AKI after PCI. [86] Earlier, in a study of 115 patients with CKD who underwent cardiac catheteriza­tion and angiography, Sigarroa et al suggested that safe limit could be calculated by the for­mula: 5 mL of ICM per kg body weight (max 300 mL) divided by creatinine in mg/dL. [87] Using Renografin, a HO-ICM, they found out that ICI-AKI (defined as an increase in serum creatinine greater than or equal to 1.0 mg/dL) occurred in 21% patients if this limit was ex­ceeded and in 2% if the limit was not ex­ceeded. A correction multiplying factor of 1.5 was later established for low osmolar mono­meric ICM. [88]

   Avoiding Repeated, Closely Spaced Exposures to ICM Top

Repeated ICM studies in a short period of time increase the cumulative dose of ICM administered and at the same time expose the functional nephrons that might be recovering from the previous insult. Ranucci et al showed that cardiac surgery performed on the day of cardiac catheterization was independently asso­ciated with increased risk of postoperative AKI and suggested that delaying cardiac sur­gery after exposure to ICM can potentially decrease the incidence of ICI-AKI in patients undergoing elective cardiac surgery. [89\ In the absence of randomized controlled trial data, it is reasonable to allow a renal "recess" of atleast three days between ICM studies. [90],[91] If serum creatinine rises during this time, the next study should be delayed until creatinine dec­reases and stabilizes or ideally, decreases to pre-study level.

   Prophylactic Extracorporeal Therapy Top

Since most cases of ICI-AKI have been re­ported in patients having coronary angiograms and interventions, a novel strategy would be to remove the blood rich in ICM from the coro­nary sinus, into which major cardiac veins drain, thus preventing/ reducing renal exposure to these agents. [92],[93] While this has not become possible in humans, attempts have been made to remove ICM soon after the systemic expo­sure using extracorporeal therapy.

Except for a very small, uncontrolled study [94] all studies have shown that prophylactic hemo­dialysis (HD) is either ineffective in reducing the risk or even harmful though it eliminates the administered ICM effectively from the intravascular and interstitial compartments. [95],[96],[97],[98],[99] This raises the possibility that by the time HD is initiated, renal damage has already in­curred. One interesting development with re­gards to renoprotection by prophylactic HD is a recent RCT by Lee et al of 82 patients with advanced CKD (creatinine > 3.5 mg/dL and Cr Cl < 25 mL/min) undergoing coronary angio­grams using low volumes (100 mL) of LO­ICM, Iohexol. [100] Patients were assigned ran­domly to receive either normal saline and high flux HD or fluids only. Prophylactic dialysis group in this study maintained creatinine clea­rance and had reduced risk for renal injury requiring temporary or permanent dialysis. Lar­ger multicenter studies are warranted before routine prophylactic HD therapy can be reco­mmended in this subgroup of patients.

Effect of continuous veno-venous hemofiltra­tion (CVVH) as a prophylactic procedure in high risk patients undergoing PCI was studied twice by Marenzi et al. In the first study, CVVH was initiated before exposure to ICM and continued for 18-24 hrs after. [101] Authors' conclusion was that CVVH treatment preven­ted ICI-AKI. The second study compared the effect of pre-and-post to only-post-ICM expo­sure-CVVH to find that pre-ICM exposure CVVH was essential component for obtaining maximum clinical benefit. [102] Both the studies have been heavily criticized since the apparent beneficial effect seen from CVVH could have been due to confounding factors such as hy­dration, alkalinizing effect of bicarbonate based replacement fluid and heparin therapy during CVVH. A more recent but small study of multimorbid CKD patients (eGFR < 40 mL/min) undergoing interventional radiolo­gical cardiovascular procedures involving an IO-ICM (Visipaque) has suggested effectiveness of post ICM exposure CVVH. [103] Nevertheless, before such an expensive and invasive prophy­laxis is recommended, it is important that fur­ther studies are done to establish its efficacy, and to define the subgroup of CKD population that would benefit most from such treatment.

   Conclusion Top

ICM are used for majority of intravascular contrast enhanced imaging procedures. Although a causal relationship has not been established, observational studies have shown that short­term and long-term mortality is increased in patients who develop ICI-AKI [104] . Hence these agents should be utilized in a way that opti­mizes the imaging study but at the same time minimizes risk to the patient. Expert consensus has been reached on the benefit of isotonic hydration, discontinuation of nephrotoxic me­dication and administration of the smallest dose of ICM consistent with a diagnostic re­sult. Use of IO-ICM and adjunct pharmaco­therapy is recommended/ practiced by some but not all due to inconsistent trial evidence.

"In necessary things, unity; in doubtful things, liberty" (Ann Baxter)

   Caution Top

CKD is recognized as an independent risk factor for the development of coronary artery disease. It adversely affects the prognosis from cardiovascular disease including increased mor­tality after an acute coronary syndrome and after PCI. [105],[106] The risk of death due to cardio­vascular disease in patients with CKD is in fact much higher than the risk of eventually requiring renal replacement therapy. [107],[108] Con­sidering this, patients with CKD should not be denied the benefits of diagnostic/ therapeutic coronary interventions just because of the con­cern of possible ICI-AKI, when cardiac be­nefits clearly outweigh the potential risks.

"And the day came when the risk to remain tight in a bud was more painful than the risk it took to bloom"(Anais Nin)

   Acknowledgement Top

I thank Hania Asim for her assistance with graphics.

   References Top

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Correspondence Address:
Muhammad Asim
Department of Medicine, Nephrology Section, Hamad General Hospital P.O. Box 3050, Doha
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