Contrast nephropathy

Refers to acute renal impairment after the intravascular administration of radiocontrast in the absence of another identifiable cause of renal failure.

Contrast-associated acute kidney injury is characterized by a decrease in kidney function that occurs within days after the intravascular administration of iodinated contrast material.p

Third most common cause of acute renal failure in hospitalized patients.

Between six and 10% of patients undergoing coronary angiography or percutaneous coronary intervention experience acute kidney injury.

The incidence of CN is 13% in an unselected population and can be as much as 57% in patients with poor kidney function and congestive heart failure.

Mechanism probably related to renal vascular vasoconstriction resulting in medullary ischemia or direct nephrotoxicity.

Iodine contrast media induced nephropathy common cause of renal failure associated with prolonged hospitalization with an incidence of 2% on low-risk patients and as high as 50% in patients with high risk factors.

A 25% increase in serum creatinine or an absolute increase of 0.5 mg/dL 2-7 days following the administration of contrast.

Contrast-associated acute kidney injury, defined by small decrements in kidney function, is associated with increased mortality.

The development of CN after percutaneous coronary intervention is independently associated with an increased risk of short- and long-term ischemic and hemorrhagic events.

Contrast-associated acute kidney injury is also correlated with accelerated progression of underlying chronic kidney disease.

Criteria: include absolute increase in serum creatinine of 0.3 mg/dL from baseline, a 50% increase in serum creatinine from baseline, or urine output less than 0.5 mL/Kg/hour for at least 6 hours.

Renal function deterioration is usually identified within 48-72 hours after exposure to contrast medium.

The threshold baseline renal insufficiency is not exact: the three most common serum creatinine thresholds for avoiding iodinated contrast are 1.5, 1.7, and 2.0 mg/dL, used by 35%, 27%and 31% of radiologists.

The estimated GFR provides the best level of evidence for risk stratification of contrast induced nephropathy and suggests iodinated contrast can be safely adminstered in patients with eGFR above 30 mL/min/1.73m.

Contrast-induced nephropathy may occasionally be reversible.

Recent studies suggest the incidence and severity of contrast induced nephropathy have been overestimated by previous uncontrolled studies.

In a study of 6902 patients the rates of acute kidney insufficiency, emergent dialysis and mortality were not significantly higher in an intravenous contrast group than a noncontrast group in either chronic kidney subgroup ( McDonald JS et al).

In the above studies finding suggests ministration of intravenous contrast material does not increase the risk of acute kidney injury, emergent dialysis, and mortality, even among those patients who have substantially compromised renal function.

Toxicity appears as acute tubular necrosis with creatinine peaking in 4 to 5 days.

Most important risk factor is renal insufficiency but any clinical condition associated with decreased in renal blood flow such as congestive heart failure, hyopovolemia, liver disease, multiple myeloma, pre-existing renal disease, diuretic use and diabetes mellitus increase the risk of contrast nephropathy.

Agents that can impair renal response such as angiotensin II receptor blockers, ACE inhibitors, diuretics, and nuns there are non anti-inflammatory drugs should be withdrawn at the time of the procedure, if possible.

High contrast medium osmolality and large volumes of contrast medium should be avoided.

High contrast osmolality media in patients with renal dysfunction, demonstrates greater nephrotoxicity compared to low osmolality contrast media.

Associated with the use of intra-aortic pump, advanced age, hypertension, hypotension, anemia, and left ventricular ejections fraction under 40%.

Contrast induced nephropathy may be associated with prolonged hospitalizations, need for dialysis, and an increased risk of death.

One study reports increase in serum creatinine of 25% or more in 14.5% of patients who underwent coronary angiogram.

If acute renal insufficiency results after cardiac catheterization an in-hospital mortality rate of 20% can occur in unselective patients, while a 1-year mortality of up to 66% is possible in patients following myocardial infarction and preexisting renal dysfunction.

Patients over the age of 60 years are at risk for contrast nephropathy.

Severe nephropathy is uncommon unless the dose of the contrast agent exceeds 100 ml.

One study revealed that in the absence of renal disease only 8% of patients with baseline serum creatinine level below 1.5 mg per deciliter have an increase in their serum creatinine of 0.5 mg per deciliter and none have an increase of 1.0 mg per deciliter after contrast media studies.

Intravenous hydration at the time of the procedure has proven to be superior to oral hydration in preventing nephropathy.

Intravenous hydration should be part of any mitigation protocol for at risk patients receiving iodinated contrast.

Hydration with saline 0.9% is superior to IV hydration with 0.45% saline in preventing nephropathy

N-acetylcysteine 600 mg twice daily on the day before and the day of radiocontrast administration may decrease the risk of nephropathy although meta-analyses have reached conflicting results.

Orally administered acetylcysteine acts as a scavenger of oxygen-derived free radicals.

Despite conflicting data, it is reasonable to use oral N-cetylcysteine because of its low cost and safety profile.

Isotonic sodium bicarbonate administered at 3 mL/kg per hour 1 hour before and 1 mL/kg per hour for 6 hours after radiocontrast exposure reduces risk to 2% of patients exposed.

The Cardiac Angiography in Renally Impaired Patients (CARE) trial, a randomized comparison of 2 contrast media with participants receiving periprocedural hydration with sodium bicarbonate the incidence of contrast induced nephropathy was 10.6% in the group receiving sodium bicarbonate only and 11.9% in the group receiving sodium bicarbonate and N-acetylcysteine.

Volume expansion with sodium bicarbonate has most recently been shown to have no benefit over sodium chloride infusions and, can be harmful in some populations (Zoungas S et al).

In a randomized controlled, single blind study of patients undergoing coronary angiography receiving sodium chloride or sodium bicarbonate revealed no difference in the prevention of contrast induced nephropathy in patients with chronic renal disease (Brar).

Recent studies have suggested that the risk of acute kidney injury due to contrast material is overestimated.

Therefore, angiographic procedures may be underused in patients with chronic kidney disease who present with conditions such as acute coronary syndromes, presumably because of concern about precipitating acute kidney injury.

Contrast agents are directly toxic to tubular epithelial cells.

Such agents lead to loss of function, apoptosis and necrosis.

Indirect mechanisms are related to ischemic injury due to vasomotor changes mediated by vasoactive substances makes the medulla particularly susceptible to the hemodynamic effects of contrast material.

The decline in kidney function after the intravascular administration of iodinated contrast material is defined as an increase in the plasma creatinine level of at least 0.5 mg per deciliter or at least a 25% increase from the baseline level within 2 to 5 days after exposure to contrast material.

The risk of acute kidney injury after the administration of contrast material is also influenced by preexisting chronic kidney disease.

The strongest patient-related risk factor for contrast associated kidney injury is lower levels of kidney function.

Severe chronic kidney disease is the strongest independent risk factor for contrast-associated acute kidney injury.

Diabetes mellitus increases susceptibility in patients with underlying chronic kidney disease, rather than being an independent risk factor. for contrast associated acute kidney injury.

Any drug which inhibits the CYP1A2 enzyme pathway, enzyme is likely to precipitate the toxicity of pirfenidone.

Use of contrast medium at a high volume or repeated administration within 72 hours after initial administration has been shown to be associated with an increased risk.

Patients with ST-segment elevation myocardial infarction who undergo PCI have a particularly high risk of contrast-associated kidney injury.

Arteriography is associated with a higher risk of contrast associated kidney disease than computed tomography (CT), due to delivery of more concentrated contrast material to the kidneys with arteriographic procedures.

There have been been no clinical trials showing that prevention of contrast-associated acute kidney injury results in a survival benefit.

Patients with chronic kidney disease are less likely to undergo coronary angiography and revascularization than patients who do not have chronic kidney disease.

A meta-analysis of 25,950 patients revealed no significant difference in the risk of acute kidney injury between patients who underwent procedures with intravenous administration of iodinated contrast material and those who underwent procedures without it: 6.4% and 6.5%, respectively (McDonald).

Another meta-analysis showed a lower risk of acute kidney injury among patients with acute ischemic stroke who underwent CT with intravenous administration of contrast material, as compared with patients who underwent CT without the use of contrast material .

These studies uniformly concluded that intravascular administration of iodinated contrast material does not appear to be associated with an increased risk of acute kidney injury.

The nominal increments in plasma creatinine levels that are used to define acute kidney injury are not uncommon in patients who have undergone contrast-enhanced procedures, nor are such increases uncommon among hospitalized patients in general.

The incidence of severe acute kidney injury, however, due to contrast material is quite low.

In a study that assessed the development of contrast-associated acute kidney injury among patients with chronic kidney disease who were undergoing nonemergency coronary angiography showed that 1.2% of the patients had a postprocedure increase in plasma creatinine level that was 50% or more of the baseline value, and none had an increase of 100% or more or required dialysis.

In a meta-analysis of studies involving patients who underwent contrast-enhanced CT, the rate of post-procedure dialysis was just 0.3%.

Severe acute kidney injury characterized by substantial decrements in kidney function, the need for renal replacement therapy, or both appears to be very infrequent after intravascular contrast administration.

Providing periprocedural intravenous crystalloid is the primary intervention to mitigate risk of contrast-associated acute kidney injury.

Observational studies have shown a protective effect of intravenous fluids.

However, evidence from randomized clinical trials is relatively sparse.

The American College of Radiology guidelines on the administration of contrast material recommend the use of intravenous isotonic saline at an infusion rate of 100 ml per hour for 6 to 12 hours before and 4 to 12 hours after angiography.

The European Society of Cardiology guidelines on myocardial revascularization recommend intravenous isotonic saline at a rate of 1 to 1.5 ml per kilogram per hour for 12 hours before and up to 24 hours after the procedure.

For outpatients and those undergoing urgent procedures, a shorter protocol that is more practical for outpatients comprises an intravenous infusion of isotonic saline for 1 to 3 hours before and 6 hours after the procedure.

In a noninferiority trial challenged the tenet that intravenous fluids are effective: randomly assigned 660 patients undergoing contrast-enhanced procedures to receive either periprocedural intravenous isotonic saline or no intravenous fluids, there was no significant difference in the incidence of acute kidney injury between the hydration group and the no-hydration group2.7% and 2.6%, respectively.

However, it is premature to conclude that intravenous fluids are ineffective or unnecessary on the basis of the results of this trial because inadequate numbers.

The volume of intravenous fluid necessary for the prevention of acute kidney injury in patients undergoing contrast-enhanced imaging procedures, including those with underlying heart failure, is unknown.

Multiple trials have compared intravenous isotonic sodium bicarbonate with isotonic sodium chloride for the prevention of contrast-associated acute kidney injury.

It was hypothesized that urinary alkalinization would reduce contrast-induced generation of injurious oxygen free radicals.

The highly divergent results of these trials and resultant clinical equipoise formed the basis for

The Prevention of Serious Adverse Events Following Angiography (PRESERVE) study assigned 5177 high-risk patients undergoing nonemergency angiography to receive intravenous isotonic sodium bicarbonate or intravenous isotonic saline, as well as oral acetylcysteine or oral placebo, for the prevention of a primary 90-day composite end point comprising death, need for dialysis, or persistent impairment in kidney function.

The trial showed no significant difference in the incidence of the primary outcome, 4.4% with bicarbonate and 4.7% with saline, or in the incidence of contrast-associated acute kidney injury, which was a secondary end point, 9.5% with bicarbonate and 8.3% with saline.

The conclusion is that isotonic sodium bicarbonate provides no benefit relative to isotonic saline.

Clinical trials have investigated the role of acetylcysteine for the prevention of contrast-associated acute kidney injury.

In trials acetylcysteine administered at a dose of 1200 mg twice daily for 5 days, beginning on the day of angiography.

As compared with placebo, acetylcysteine was not associated with reductions in the rate of death, need for dialysis, or the rate of persistent impairment in kidney function at 90 days or in the rate of contrast-associated acute kidney injury.

The routine administration of acetylcysteine is not recommended for the prevention of acute kidney injury or longer-term adverse events after angiographic procedures.

The Prevention of Radiocontrast Medium–Induced Nephropathy Using Short-Term High-Dose Simvastatin in Patients with Renal Insufficiency Undergoing Coronary Angiography trial failed to show a difference between simvastatin and placebo with respect to the mean peak increase in the plasma creatinine level within 48 hours after angiography in patients with chronic kidney disease.

Conversely, the PRATO-ACS (Protective Effect of Rosuvastatin and Antiplatelet Therapy on Contrast-Induced Acute Kidney Injury and Myocardial Damage in Patients with Acute Coronary Syndrome) trial showed a significant reduction in rates of acute kidney injury and 30-day cardiovascular and renal events after PCI in patients treated with high-dose rosuvastatin.

Several studies have documented a benefit of prophylactic statins in patients undergoing PCI, it these trials have methodologic limitations.

Recommendations for patients identified as high risk, using the lowest necessary total dose of low-osmolality or iso-osmolality contrast medium is advisable.

A specific threshold definitively associated with contrast-associated acute kidney injury has not yet been determined.

Insufficient data exists support discontinuation of diuretics, angiotensin-converting–enzyme inhibitors, or angiotensin-receptor blockers.

Stopping potentially nephrotoxic agents, including nonsteroidal antiinflammatory medications, is appropriate to prevent contrast associated kidney injury.

Temporarily halting of metformin therapy has been advocated, out of concern about the development of lactic acidosis, should severe acute kidney injury occur.

Additional data are needed before firm, evidence-based recommendations can be provided regarding the discontinuation of metformin in patients undergoing contrast-enhanced procedures.

The reliance of findings based on small increments in the plasma creatinine level, which are frequently transient and nonspecific for contrast-induced damage, coupled with observational studies showing an association with serious, adverse outcomes without known cause, has limited meaningful progress in determining the clinical importance of contrast associated kidney injury.

Studies have shown that the increase in creatinine levels is similar in patients who receive contrast media and those who do not: serum creatinine is subject to natural fluctuations in the absence of any contrast media, is a poor marker of kidney injury.

A meta-analysis of more than 100,000 patients involved in controlled studies showed that there are no significant associations between contrast-enhanced CT and kidney injury, the need for renal replacement therapy, or all-cause mortality.

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