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| REVIEW ARTICLE |
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| Year : 2013 | Volume
: 14
| Issue : 3 | Page : 106-116 |
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Contrast-induced nephropathy
Nazar M. A. Mohammed1, Ahmed Mahfouz2, Katafan Achkar3, Ihsan M Rafie1, Rachel Hajar1
1 Department of Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
2 Department of Pharmacy, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
3 Department of Nephrology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
| Date of Web Publication | 28-Jan-2014 |
Correspondence Address:
Nazar M. A. Mohammed
Department of Cardiology, Heart hospital, Hamad Medical Corporation, Doha, PO BOX 3050
Qatar
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1995-705X.125926
 Abstract | | |
Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures resulting from the administration of contrast media (CM). It is the third most common cause of hospital acquired acute renal injury and represents about 12% of the cases. CIN is defined as an elevation of serum creatinine (Scr) of more than 25% or ≥0.5 mg/dl (44 μmol/l) from baseline within 48 h. More sensitive markers of renal injury are desired, therefore, several biomarkers of tubular injury are under evaluation. Multiple risk factors may contribute to the development of CIN; these factors are divided into patient- and procedure-related factors. Treatment of CIN is mainly supportive, consisting mainly of careful fluid and electrolyte management, although dialysis may be required in some cases. The available treatment option makes prevention the corner stone of management. This article will review the recent evidence concerning CIN incidence, diagnosis, and prevention strategies as well as its treatment and prognostic implications. Keywords: Contrast-induced nephropathy, definition, management of contrast-induced nephropathy, risk scoring and stratifications
How to cite this article:
Mohammed NM, Mahfouz A, Achkar K, Rafie IM, Hajar R. Contrast-induced nephropathy. Heart Views 2013;14:106-16 |
| Introduction | |  |
Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures and results from administration of iodinated contrast media (CM). [1],[2],[3]
CIN is the third most common cause of hospital acquired acute renal injury representing about 12% of the cases. The incidence of CIN varies between 0 and 24% depending on patient's risk factors. [4] It is generally a transient and reversible form of acute renal failure. [5] However, the development of CIN is associated with a longer hospital stay, an increased morbidity and mortality, in addition to a higher financial cost.
Treatment of CIN is mainly supportive, consisting of careful fluid and electrolyte management, although dialysis may be required in some cases. [6] The limitation in the available treatment options makes prevention the cornerstone of management.
This article will review the recent evidence concerning CIN incidence, diagnosis, and prevention strategies as well as its treatment and prognostic implications.
Definition
CIN is defined as an elevation of serum creatinine (Scr) of more than 25% or ≥0.5 mg/dl (44 μmol/l) from baseline within 48 h after excluding other factors that may cause nephropathy, such as nephrotoxins, hypotension, urinary obstruction, or atheromatous emboli. It is self-limited in most instances, with Scr levels peaking in 3-5 days and gradually returning to baseline levels within 7-10 days. [7],[8],[9]
Prevalence
CIN is one of the major causes of hospital-acquired acute kidney injury (AKI) [10] and represents about 12% of the cases. [11] It is the third most common cause after renal hypoperfusion (42%) and postoperative renal injury (18%).
The reported incidence of CIN after percutaneous coronary intervention (PCI) varies between 0 and 24%, depending on the prevalence of associated risk factors, with the higher incidence being reported after emergency PCI. [12],[13],[14],[15]
A meta-analysis that included 40 studies, found a 6% incidence of CIN after contrast enhanced computed tomography (CT), [16] 9% after peripheral angiography, [17] and 4% after intravenous pyelography. [18]
The incidence of CIN is low in patients with normal renal function (0-5%). [19] However, several prospective controlled trials reported an incidence of 12-27% in patients with preexisting renal impairment. [7],[19],[20] Furthermore, in one study, an incidence as high as 50% was reported in patients with diabetic nephropathy undergoing coronary angiography in spite of the use of low-osmolar CM (LOCM) and adequate hydration. Notably, up to 15% of them required dialysis. [21] Development of CIN is associated with a longer hospital stay, an increased morbidity and mortality, in addition to a higher cost. [1],[2],[3]
Elevation of post-PCI Scr may have prognostic significance regardless of initial kidney function. In fact, even a slight elevation in Scr (25-35 μmol/l) is associated with an increase in 30-day mortality. [22] Furthermore, post-PCI Scr elevation has been reported to be associated with a higher 1-year mortality than periprocedural myonecrosis. [23]
| The Pathophysiology | | |
Although the definite mechanism of CIN is not well-understood, several mechanisms have been proposed
- Renal medullary hypoxia due to either a decrease in vasodilators (nitric oxide or prostaglandins), or an increase in vasoconstrictors (adenosine and endothelin).
- Direct toxicity of CM which could be related to harmful effects of free radicals and oxidative stress. It is thought that activation of cytokine-induced inflammatory mediators by reactive free radicals is the responsible mechanism. Conversely, the inhibition or reduction of free radicals formation might reduce CIN by alkalinizing tubular cells. [24],[25],[26],[27],[28],[29]
- In addition, apoptosis may also play a role in the development of CIN. [24],[30]
Risk factors
Multiple risk factors may contribute to the development of CIN; these factors are divided into two groups; patient- and procedure-related.
Preexisting renal insufficiency (estimated glomerular filtration rate (eGFR) <60 ml/min) and diabetes mellitus are the most important patient-related risk factors. Others, include age >75 years, uncontrolled hypertension, hypotension requiring inotropes, congestive heart failure (CHF), use of intra-aortic balloon pump (IABP), anemia, hypoalbuminemia, and liver cirrhosis.
Procedure-related factors include high contrast volume, osmolality or viscosity, and repeated exposures to CM within 72 h. Other factors that may increase the risk of CIN include the concomitant use of diuretics or nephrotoxic drugs (nonsteroidal anti-inflammatory drugs (NSAIDs) and aminoglycosides). [11],[27],[28],[31],[32],[33]
| Risk Scoring and Stratifications | | |
Several risk stratification scoring systems have been developed to assess the risk of developing CIN. [33],[34],[35],[36] One of the main goals of these scoring systems is to help clinicians and patients weigh the risk of the exposure versus its benefit.
Bartholomew and his colleagues used a database of 20,479 patients to develop a risk scoring system of eight variables (creatinine clearance <60 ml/min, use of IABP, urgent coronary procedure, diabetes, CHF, hypertension, peripheral vascular disease, and contrast volume). In this scoring system, the population with the highest risk score had a 28% incidence of CIN and a 17% risk of death. [35]
Mehran et al., used a database of 8,357 interventional cardiology patients (mean age 63.6 years, 28.8% females) to develop a CIN risk scoring system. This system is based on eight variables: i) hypotension for more than 1 h requiring inotropes, ii) use of IABP within 24 h of the procedure, iii) CHF New York Heart Association (NYHA) class III or IV, iv) age >75 years, v) anemia with hematocrit value <39% for men and <36% for women, vi) diabetes mellitus, vii) contrast volume (1 point for each 100 ml), and viii) baseline Scr >1.5 mg/dl (132 μmol/l). The incidence of CIN and dialysis increased with higher risk score (CIN incidence; 7.5, 14, 26.1, and 57.3%) if total risk score ≤5 (low), 6-10 (moderate), 11-16 (high), and ≥16 (very high), respectively. [33] Of note, no prospective validation of published risk scores has been done.
Diagnosis
Elevation of Scr of more than 25% above baseline and within 48 h post CM administration is the key diagnostic criteria after excluding other causes. Additional laboratory findings such as acidosis and/or hyperkalemia may be present. In regards to urine output; patient may be oliguric, anuric, or have normal urine output. Findings on urine examination are usually nonspecific. [36]
There is usually a 24-48 h delay between contrast exposure and the change in Scr. This delay makes creatinine a late indicator of renal function changes, [37] therefore more sensitive markers of renal injury are desirable. In fact, several biomarkers of tubular injury have been under evaluation
- Plasma neutrophil gelatinase-associated lipocalin (NGAL), also known as human neutrophil lipocalin, is an early predictive biomarker of AKI. It is a small protein of the lipocalin superfamily that was first isolated in 1993 from the supernatant of activated human neutrophils. Subsequent studies have identified tubularly secreted NGAL as a novel and specific biomarker for the early detection of AKI after contrast agent administration and in critically ill patients. NGAL as a marker of AKI is increasingly studied since its serum and urinary levels increase well before the increase of Scr and have a better sensitivity than Scr alone for AKI detection. A significant increase occurs in patients with CIN after 2 h. [38],[39],[40],[41]
- Plasma cystatine-C (CysC) is a low molecular weight protein produced at a constant rate by all nucleated cells, is freely filtered across the glomerular membrane and is neither secreted nor reabsorbed along the nephron. Because it is almost completely catabolized in the proximal tubule, its renal clearance cannot be measured, but its concentration in serum or plasma reflects the GFR. It is significantly increase in patients with CIN after 8 h. Nevertheless, the increment has also been noted in other conditions including corticosteroids administration, thyroid dysfunction, systemic inflammation, neoplasia, age, and an increase in the muscular mass. [42]
- Urinary NGAL (uNGAL or lipocalin-2 (LCN2)), is an iron-transporting protein rapidly accumulating in the kidney tubules and urine after nephrotoxic and ischemic insults, it has been put forward as an early, sensitive, noninvasive biomarker for AKI. A study was done by Zappitelli et al., in 150 patients with AKI concluded that uNGAL serves well in predicting AKI before a rise in SCr becomes apparent and patients who will have persistent AKI. In spite of a significant increase of these urinary biomarkers in patients with CIN as early as 2 h, its use is still experimental. [43]
- Urinary interleukin-18 (IL-18, interferon gamma inducing factor) is a specific biomarker of proximal acute tubular necrosis. The value of more than 60 pg/ml after 24 h exposure to CM is regarded as significant. [44]
- Urinary liver-type fatty acid-binding protein (L-FABP) is expressed in renal proximal tubule cells and secreted into urine in response to hypoxia caused by decreased peritubular capillary blood flow. FABPs are known as intracellular lipid chaperones that transport lipids to a specific component in the cell. Even though it is significantly elevated in patients with CIN after 24 h, it might have a low specificity due to interferences from different systemic processes regularly found in critically-ill patients. [45]
- Urinary kidney injury molecule-1 (KIM-1) is a transmembrane protein that is not detectable in normal kidney tissue but is expressed at very high levels in the differentiated proximal tubule epithelial cells in human and rodent kidneys after ischemic or toxic injury. [46],[47]
Treatment
There is no definitive treatment available for established CIN; therefore, the benefit for CM-based diagnostic studies or interventional procedures should always be weighed against the risk of CIN. In addition, repeated exposure to CM within a short period of time should be avoided whenever possible.
Prevention strategies
Several pharmacological and nonpharmacological approaches have been evaluated for the prevention of CIN. The prevention strategies are most important in patients at high risk for CIN, such as those with AKI or preexisting chronic kidney disease (CKD). It is well established that minimizing the volume of CM, preventing volume depletion and avoiding activation of renal vasoconstriction are the most effective measures to prevent CIN. In addition, the concomitant use of diuretics or nephrotoxins (e.g. nonsteroidal anti-inflammatory drugs (NSAIDs), cytotoxic drugs, and aminoglycosides) should be avoided. [4]
| Nonpharmacological Approach | | |
Contrast medium related factors
CM is a diagnostic iodinated material used to enhance the visibility of blood vessels. It is mainly excreted through the kidneys with less than 1% eliminated via extrarenal routes in patients with normal kidney function. [48] The half-life of CM is about 2 h with 75% excreted within 4 h and 98% within 24 h. [49],[50]
In the renal tubules, the excreted CM generates osmotic force causing marked increase in sodium and water excretion. This diuresis will increase intratubular pressure, which will reduce the GFR, contributing to the pathogenesis of acute renal failure. [51] The effect of CM on the kidney depends on its volume, osmolality, and viscosity.
CM volume is a risk factor for CIN, correlation between the CM volume and risk of CIN was investigated in patients at high-risk for CIN.
Brown and his group attempted to identify the relationship between CM volumes, body weight, and baseline renal function in patients who received CM, with a goal to identify a maximum acceptable contrast dose (MACD). MACD was determined by the following formula: (Contrast ml = 5 × body weight (kg))/(88.4 × SCr (μmol/l)). They concluded that patients who received CM volumes more than the calculated MACD had a higher incidence of CIN and dialysis requirement than those who did not exceed the calculated MACD. [52] Nyman, et al., studied the relation between CM dose (Gram's iodine; GI), estimated GFR (eGFR; ml/min), and the incidence of CIN in patients who underwent primary PCI following ST-segment elevation acute myocardial infarction. The study showed that CIN incidence increased with high CM dose/eGFR ratio. [53] McCullough et al., found that the risk of CIN is low in patients with normal kidney function receiving less than 100 ml of CM. [1] However, the risk remains high in patients with CKD receiving less than 100 ml of CM with possible need for dialysis or progression to end-stage renal disease. [21],[54]
LOCM is more expensive than high-osmolar one and it has been shown to lower the incidence of CIN. Nevertheless, there has been no significant difference between high-osmolar and low-osmolar iodinated CM in patients with normal kidney function. The nephrotoxic effect of high osmolar CM is higher in patients with preexisting CKD or in the presence of significant risk factors for CIN. [20],[55],[56]
The benefit of iso-osmolar CM (IOCM) over LOCM in patients with preexisting CKD or those at high risk for CIN is debatable. Some clinical trials found no benefit of nonionic IOCM (i.e. iodixanol) compared to nonionic LOCM (i.e. iopamidol, iopromide, ioversal, iomeprol, iobitridol, and iopentol), [21],[57],[58],[59],[60],[61],[62],[63] while other trials found reduction in the incidence of CIN with IOCM (i.e. iodixanol) compared to nonionic LOCM (i.e. iohexol, iopromide, and ioxaglate). [64],[65],[66] It appears that iohexol, iopromide, and ioxaglate have a higher incidence of CIN than other LOCM, while no similar data are available for the nonionic LOCM.
It has been initially thought gadolinium-based CM would be safer than iodinated CM in patients with preexisting CKD or those at high risk for CIN. [67] Nevertheless, case reports and small studies reported evidence of nephrotoxicity using gadolinium-based CM, especially when used in high doses in patients with preexisting CKD or those at high risk for CIN. A long half-life of gadolinium-based CM and its lower clearance due to a small volume of distribution (V d ), and its excretion through glomerular filtration may contribute to the nephrotoxic effect. [68],[69],[70],[71],[72] More importantly, gadolinium-based CM have been associated with the development of nephrogenic systemic fibrosis in patients with significant decrease in GFR. Therefore, its use is contraindicated in patients with GFR less than 30 ml/min/1.73 m 2 and it should be used with caution in patients with GFR between 30 and 60 ml/min/1.73 m 2.[73] Gadolinium-based CM might be a reasonable option in patients with severe allergy to iodine or iodine CM. [74]
| Hemodialysis and Hemofiltration | | |
Intermittent hemodialysis or peritoneal dialysis has been shown to efficiently remove CM from the circulation; several studies have been carried out to evaluate the effectiveness of prophylaxis dialysis strategy. [75],[76] A study by Lee et al., showed a protective effect, [77] all other clinical trials did not find any benefit of immediate hemodialysis after exposure to CM in patients with preexisting CKD undergoing angiography. [78],[79],[80]
Hemofiltration is another preventive strategy that have been studied for CIN prevention in patients at high risk. [81],[82],[83] Marenzi et al., found that periprocedural hemofiltration for 24 h after CM exposure was an effective strategy for the prevention of CIN in patients with preexisting CKD leading to a decrease in the in-hospital mortality and a better long-term outcomes. [84] However, these modalities are not yet supported with sufficient evidence. Additionally, these modalities require intensive care unit (ICU) admission and may not be practical in most settings.
| Pharmacological Approach | | |
Volume expansion
Volume expansion is the most effective strategy in prevention of CIN. The exact mechanism by which volume expansion reduces the risk of CIN is not well-known. One possible mechanism is the dilution of CM by more fluid reduces the concentration of CM and subsequently it may minimize the risk of CM exposure and reduce the nephrotxic effect. Another possible mechanism is that volume expansion reduces the intrarenal hemodynamic alterations by inhibition of renin-angiotensin-aldosterone system (RAAS) minimizing the renal vasoconstriction. [85],[86]
Multiple randomized controlled trials were performed in the past 20 years and confirmed the beneficial role of intravenous fluid administration in the prevention of CIN. [87],[88],[89],[90] In several recent trials, the common approach for adequate intravenous volume expansion was isotonic saline (0.9% NaCl) or hypotonic saline (0.45% NaCl) at a rate of (1.0-1.5 ml/kg/h) for 3-12 h prior the procedure and continued for 6-24 h after the procedure aiming to maintain the urine flow rate more than 150 ml/h. [91],[92] One study compared isotonic saline (0.9% NaCl) with half saline in dextrose 5% water (D5W 0.45% NaCl) in patients undergoing elective or emergency coronary angioplasty. In this study, the incidence of CIN was significantly less with isotonic saline than hypotonic saline. [89]
The renoprotective effects of oral and intravenous administration of fluids were compared in patients at high risk for CIN. One randomized trial showed no difference in the incidence of CIN between the two routes. [93] However, another trial ( n = 53) found a lower incidence of CIN in patients receiving intravenous saline than those received fluids orally. [94] In a recent observational study, the effects of oral fluid intake in patients undergoing CT angiography that had normal kidney function was closely correlated with the percentage changes in SCr and the absolute changes in eGFR. [95]
Patients with CKD and left ventricular dysfunction (left ventricular (LV) ejection fraction <40%), are at increased risk for volume overload. Therefore, volume expansion should be done after a careful assessment of clinical and volume status.
Sodium bicarbonate
Sodium bicarbonate may reduce the risk of CIN by decreasing free radicals formation through an alkaline pH that reduces the production and increases the neutralization of oxygen. [96],[97],[98]
Nevertheless, conflicting results were derived from the clinical trials on the efficacy of sodium bicarbonate. In several clinical trials and meta-analyses; intravenous sodium bicarbonate showed a significant risk reduction of CIN compared to intravenous isotonic saline with or without N-acetylcysteine (NAC), even though there was no difference in the need for dialysis, in-hospital mortality, or heart failure. [87],[90],[99],[100],[101],[102],[103],[104]
Meanwhile, other studies, published and unpublished [105],[106] did not show any beneficial effect. This included a prospective randomized trial comparing sodium bicarbonate to isotonic saline with NAC in patients undergoing coronary angiography with creatinine clearance (CrCl) <60 ml/min. [107] Furthermore, one retrospective cohort study conducted at Mayo clinic found that the incidence of CIN increased with intravenous sodium bicarbonate. [108]
In conclusion, the role of sodium bicarbonate in prevention of CIN is yet to be determined, and the decision to use sodium bicarbonate in the prevention of CIN should be made on an individual basis. A large prospective randomized multicenter trial is needed to clarify this question.
Antioxidants (NAC and ascorbic acid)
N-Acetylcysteine
NAC has an antioxidant effect; scavenging oxygen-derived free radicals, which may lead to improved endothelium-dependent vasodilatation. [109],[110]
Intravenous and oral NAC have been studied in the prevention of CIN in patients with or without renal impairment. While NAC is indicated for the treatment of acetaminophen intoxication, it is not approved by the Food and Drug Administration (FDA) for the prevention of CIN. High intravenous doses of NAC (used in treatment of acetaminophen intoxication) may have detrimental effects on myocardium and the coagulation system. [111],[112] In addition, high incidence of anaphylactoid reactions (up to 48%) and one death in an asthmatic patient have been reported. [113],[114] However, when intravenous NAC is used for CIN prophylaxis, a much lower dose of 1,200 mg twice/day is the usual dose. [115]
The protective effect of NAC has been demonstrated in several clinical studies even though there were significant limitations in these trials, such as a relatively small sample size, heterogeneity, and publication bias. [116],[117],[118],[119]
However, the enthusiasm for using NAC has faded away after a large randomized controlled trial and meta-analyses failed to show any added renoprotective benefit or efficacy of NAC in patients with CKD versus placebo. [12],[120],[121]
This large randomized trial, Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT), enrolled 2,308 patients undergoing coronary or peripheral vascular angiography with at least one risk factor (>70-year-old, diabetes mellitus, renal failure, heart failure, or hypotension). These patients were randomized to receive NAC (two doses of 1,200 mg before and two doses of 1,200 mg after angiographic procedure) versus placebo.
The incidence of CIN (primary endpoint) was 12.7% in the NAC group and 12.7% in the control group (relative risk (RR), 1.00; 95% CI, 0.81-1.25; P = 0.97). The same results were observed in all subgroups analyzed, including those with renal impairment. [12]
Ascorbic acid
Ascorbic acid is an antioxidant which has been studied in the prevention of CIN. One randomized controlled trial ( n = 231) found that ascorbic acid reduced the incidence of CIN in patients undergoing coronary angiography in comparison with placebo. [122] However, another randomized double-blind trial ( n = 143) failed to show benefit of ascorbic acid in the prevention of CIN in patients with renal dysfunction. [123] A recently published randomized controlled trial ( n = 212) compared a high dose of NAC to a high dose of ascorbic acid in patients with renal dysfunction (CrCl < 60 ml/min) undergoing coronary angiography. The study found that the incidence of CIN was higher in patients receiving ascorbic acid than those who received NAC; however, the difference was not statistically significant. [124] Therefore, the use of ascorbic acid is not recommended in the prevention of CIN.
Theophylline
Theophylline is a xanthine derivative and a nonselective adenosine receptor antagonist (A1 and A2). Oxygen consumption or decreased intracellular adenosine triphosphate (ATP) will lead to increase level of adenosine that will contribute to afferent arteriolar vasoconstriction after CM exposure. Katholi et al.,[125] have shown that theophylline prevented the decrease in GFR after CM exposure. These findings were supported by other trials. [126],[127] Additionally, a recent study showed theophylline plus bicarbonate prophylaxis significantly reduced the incidence of CI-AKI compared to bicarbonate alone. [128] However, many recent clinical trials, meta-analyses, and systemic review did not support the beneficial effect of theophylline in prevention of CIN. [129],[130],[131],[132],[133]
Since the results of studies using theophylline were inconsistent and the relevant clinical benefit is doubtful, current recommendation does not support its use in the prevention of CIN. In addition, there is the possibility of gastrointestinal, neurological and cardiovascular side effects with theophylline.
HMG CO A reductase inhibitors
The HMG-CoA reductase inhibitors (statins) are mainly used as cholesterol-lowering agents, but they are also known to have antioxidative and anti-inflammatory properties so they may reduce the risk of CIN. [134],[135]
Some studies suggested that the chronic use of statin has a protective effect against CIN, with a reduction in the incidence of dialysis and long-term mortality. [136],[137]
In a recent systematic review and meta-analysis; chronic statin treatment (≥7 days) reduced the risk of CIN ( P < 0.05), whereas a short-term high-dose therapy did not. [138]
Nevertheless, other studies have reported a null effect for statin use and an even higher incidence of CIN in the statin group. [139],[140]
The role of statin use in preventing CIN is inconclusive, and this could be attributed in part to the variability of statin dosing and length of use. [141],[142] A large controlled randomized trial is needed to assure the beneficial effect of statins in preventing CIN.
Calcium channel blockers
The data available for the use of CCBs is limited. CCBs are known to have an attenuating affect both the magnitude and duration of renal vasoconstriction after CM exposure, suggesting its potential benefit in reducing CIN. [143] In fact one trial showed a beneficial effect of starting CCBs shortly prior to PCI in reducing CIN. [144] However, this benefit was not observed in other trials. [145],[146]
Allopurinol
Allopurinol is a xanthine oxidase inhibitor which may limit the fall in the GFR after CM exposure by limiting oxygen-free radical formation, inhibiting adenine nucleotide degradation and by decreasing the vasodilatation response to intrarenal adenosine in the renal vasculature. In one study, allopurinol (4 mg/kg) was given orally starting 24 h before CM exposure and showed a protective effect against CIN. [27]
A recent trial ( n = 159) randomized patients undergoing coronary procedures (Scr > 1.1 mg/dl) to allopurinol (300 mg orally) with hydration or hydration alone. This trial found allopurinol may protect against CIN in high-risk patients receiving CM. [147]
The beneficial effect of allopurinol in the prevention of CIN needs further studies.
Fenoldopam
Fenoldopam mesylate is a selective dopamine-1 receptor agonist known to produce both systemic and renal arteriolar vasodilatation. It has been shown to reduce the incidence of CIN in high risk patients undergoing PCI in one study; [148] however, a large randomized controlled trial ( n = 52,315) failed to show any protective effect against CIN. [149]
Dopamine
Dopamine (in a renal dose 0.5-2.5 μg/kg/min) has a dilatory effect on the renal vasculature and has an ability to increase renal blood flow and GFR with a potential benefit in the prevention of CIN. Positive trials were small, non-randomized, inadequately powered, and with questionable end-points of clinical significance. [150]
On the other hand, negative trial, were large, randomized, controlled, and with adequate statistical power; [151],[152] therefore, the use of dopamine in prevention of CIN is no longer recommended.
Prostaglandin E1 (alprostadil)
Prostaglandin E1 is a well-known vasodilator that improves renal blood flow. It has shown some benefit in small clinical studies. [153],[154] Nevertheless, the risk of CIN increased with higher infusion rate, likely due to prostaglandin (PG)-induced hypotension. Further large trials are required to prove the protective effect and address the safety concerns.
Avoidance of nephrotoxic drugs
The common potential nephrotoxic drugs include angiotensin converting enzymes inhibitors (ACEIs), angiotensin receptor antagonists, aminoglycosides, amphotericin B, diuretics, NSAIDs/cyclooxygenase (COX)-2 inhibitors, and antiviral drugs like acyclovir and foscarnet. The concomitant use of these drugs with CM administration should be avoided when possible in order to reduce the risk of CIN. [155]
Metformin is mainly eliminated via the kidneys (90%). As a result, metformin will accumulate in the event of AKI. [156],[157] It is recommended that metformin should be held 24-48 h before CM exposure to avoid the risk of lactic acidosis and restarted when clinically appropriate (e.g. no development of CIN or when renal function returns to baseline).
| Conclusion and Recommendations | | |
Iodinated CM remains the sole agent for diagnostic and interventional vascular procedures. Since there is no effective therapy available to treat established CIN, it is imperative to maintain adequate volume expansion in the periprocedure period, minimize the volume of CM used, and avoid the use of nephrotoxic medications whenever possible.
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