How do you manage contrast-induced nephropathy?
Contrast-Induced Nephropathy Treatment & ManagementApproach Considerations.Hydration Therapy.Statins.Bicarbonate Therapy.N-acetylcysteine.Renal Replacement Therapy.Other Therapies.Deterrence and Prevention.
How can contrast-induced acute kidney injury be prevented?
Adequate hydration before the procedure (such as that based on the targeted hydration trials) would still be a key to reduce the risk of CI-AKI. Use of short-term high-intensity statins is supported by this network meta-analysis and by the guidelines; however, more data are needed in patients with CKD stage 3 or worse.
What are the drugs that can prevent contrast-induced nephropathy?
Medication Summary Hydration therapy, typically with intravenous isotonic saline, is the cornerstone of contrast-induced nephropathy (CIN) prevention. However, other agents have have demonstrated some benefit in prevention of CIN, including N-acetylcysteine (NAC) and statins.
What steps can be taken to ensure that the risk of contrast-induced nephropathy is Minimised?
A key preventive measure is to 1) assess renal function and 2) identify high-risk patients, in order to 3) adopt preventive strategies. These are to 1) prescribe intensive hydration prior to the procedure, 2) reduce the contrast volume injected to a minimum, and 3) use iso- or low-osmolarity contrast agents.
What are risk factors for contrast-induced nephropathy?
Several scoring systems have been developed to predict contrast-induced kidney injury and the following are the risk factors:Use of an intra-aortic balloon pump.Congestive heart failure (CHF)Hypotension.Elevated creatinine (More than 1.5)Age greater than 75.Diabetes.Anemia.Use of contrast volume more than 100 ml.
What is contrast-induced nephropathy?
Contrast-induced nephropathy (CIN) is defined as the impairment of kidney function—measured as either a 25% increase in serum creatinine (SCr) from baseline or a 0.5 mg/dL (44 µmol/L) increase in absolute SCr value—within 48-72 hours after intravenous contrast administration.
What medications should be stopped before CT with contrast?
Two Weeks Before ProcedureAspirin or aspirin-containing compounds – Stop taking five days before your procedure.Plavix – Stop taking five days before your procedure.Coumadin (warfarin) – Please obtain a laboratory test (INR) before your procedure to determine the exact time to stop the medication.More items...
What medication should be held if receiving contrast dye?
In patients with cardiovascular disease, kidney disease, and/or diabetes, renin-angiotensin system blockers, non-steroidal anti-inflammatory drugs, diuretics, and metformin can increase the risk of CI-AKI when undergoing contrast imaging.
What medication should be held before contrast dye?
Most clinical guidelines recommend holding renin-angiotensin system (RAS) blockers (angiotensin- converting enzyme inhibitors [ACEI], angiotensin receptor blockers [ARB], and mineralocorticoid antagonists), non- steroidal anti-inflammatory drugs (NSAIDs), diuretic, and metformin in patients with diabetes, kidney ...
Is kidney damage from contrast dye reversible?
The symptoms can be similar to those of kidney disease, which include feeling more tired, poor appetite, swelling in the feet and ankles, puffiness around the eyes, or dry and itchy skin. In many cases, CIN is reversible and people can recover.
How long does it take kidneys to recover from contrast dye?
As stated previously, the decrease in renal function is typically noted within the first 24-48 hours, peaks at 3-5 days, and returns to baseline by about 10-14 days following contrast administration.
Is CT scan with contrast hard on kidneys?
CT contrast materials do rarely cause kidney damage and a skin disorder called nephrogenic systemic fibrosis (NSF) can be caused by the MRI contrast agents. Patients with poor kidney function are the people at risk for these side effects.
Why is it important to assess renal function before injection of contrast medium?
It is important to assess renal function before injection of contrast medium to ensure that appropriate measures to reduce the risk are taken. Since serum creatinine alone does not provide a reliable measure of renal function, calculation of estimated glomerular filtration rate is advisable (see Figure 1 for calculations) (7).
What is contrast induced acute kidney injury?
Contrast-induced acute kidney injury is an important complication of iodinated contrast media. The most commonly used definition in clinical trials is an increase in serum creatinine (Cr) by > 0,5 mg/dl or > 25% assessed at 48h after the intravascular administration of contrast medium, without any other plausible aetiology (1).
What is the risk of CIN?
The risk of CIN is increased in patients with an estimated glomerular filtration rate (eGFR) < 60 ml/min/1,73 m2 (stage 3 to 5 of Chronic Kidney Disease), as is described in reports describing risk factors for CIN. In critically ill patients, renal function may be temporarily impaired (cardiogenic shock, heart failure, drug-induced injury), making the risk even greater. Table 1 summarises the main risk factors for developing CIN.
What is iodinated contrast media injection?
Iodinated contrast media injection is an inherent part of invasive cardiac procedures but it carries the risk of contrast-induced nephropathy (CIN). This important complication prolongs hospitalisation and increases morbimortality and health care costs.
How long before contrast exposure should I take anti-inflammatory drugs?
While there are no studies in this area, it seems reasonable to withhold nonsteroidal anti-inflammatory drugs, calcineurin inhibitors, high-dose loop diuretics, aminoglycosides and other nephrotoxic agents if possible for several days before contrast exposure.
Which contrast agent has the lowest risk of CIN?
Low osmolality and isosmolal agents, compared to high osmolality, have shown a significant reduction in the risk of CIN. Iodixanol, a isosmolal contrast agent, has been shown to have the lowest risk for CIN in patients with chronic kidney disease and diabetes.
Is contrast induced nephropathy a serious complication?
Contrast-induced nephropathy is a common and potentially serious complication after the administration of contrast media in patients at risk for acute renal injury (chronic kidney disease with eGFR< 60 ml/min/1,73 m2, particularly when diabetes is present).
How long before contrast induced nephropathy?
Patients suffering from contrast-induced nephropathy usually have a preceding history of contrast administration, 24-48 hours before the presentation, while undergoing a diagnostic or therapeutic procedure, such as percutaneous coronary intervention. Acute kidney injury is mostly nonoliguric.
Why do we need a physical exam for nephropathy?
A physical examination is helpful in ruling out other possible causes of acute nephropathies, for instance, cholesterol emboli (pathognomonic findings of which are blue toes and livedo reticularis) or interstitial nephritis secondary to drugs (that typically involves a rash). There may be signs of volume depletion or there could be decompensated heart failure.
What is the third leading cause of iatrogenic acute kidney injury?
Contrast-induced nephropathy is the third leading cause of iatrogenic acute kidney injury. The commonest cause is hypoperfusion of the kidneys causing either prerenal injury or acute tubular necrosis.[10] Moreover, the number and the type of risk factors directly affect the incidence of renal impairment. The incidence rate also depends on the procedure, with reports in the literature varying from 1.6-2.3% for diagnostic investigations to 14.5% overall in coronary intervention. [11]
What is CIN in contrast?
Currently, the understanding of CIN is that it is the impairment of renal function gauged as either a 25% rise in serum creatinine from baseline or an increase of 0.5 mg/dL (44 µmol/L) in absolute serum creatinine value within 48-72 hours following intravenous contrast administration.[1]
Why is iodine used in cardiac procedures?
Because of an increasing number of coronary angiography and coronary interventional procedures, the increasing use of contrast media, and the increasing number of invasive cardiac procedures being performed in high-risk patients with chronic kidney disease, diabetes mellitus, hypertension, and kidney failure due to contrast-induced nephropathy remains a growing concern. A sudden change in kidney function is a common complication of coronary angiography, and percutaneous coronary intervention, primarily because of contrast-induced acute kidney injury or contrast-induced nephropathy. This activity reviews the pathophysiology of contrast-induced nephropathy and highlights the role of the interprofessional team in its management and prevention.
How long does it take for renal impairment to return to baseline after contrast?
A temporal link is thus implied.[2] Post-contrast exposure, serum creatinine levels peak between two and five days and usually return to baseline in 14 days.
How long does it take for creatinine to rise after contrast?
In contrast-induced nephropathy, serum creatinine usually begins to rise within 24 hours after the administration of contrast media, peaks between 3 and 5 days, and comes back to baseline in 7-10 days. A surrogate marker of renal function, serum cystatin C, is increased in patients with contrast-induced nephropathy.
Why do we need a physical exam for nephropathy?from ncbi.nlm.nih.gov
A physical examination is helpful in ruling out other possible causes of acute nephropathies, for instance, cholesterol emboli (pathognomonic findings of which are blue toes and livedo reticularis) or interstitial nephritis secondary to drugs (that typically involves a rash). There may be signs of volume depletion or there could be decompensated heart failure.
How long does it take for renal impairment to return to baseline after contrast?from ncbi.nlm.nih.gov
A temporal link is thus implied.[2] Post-contrast exposure, serum creatinine levels peak between two and five days and usually return to baseline in 14 days.
What are the best tools to protect patients from unnecessary risk for CIN?from pubmed.ncbi.nlm.nih.gov
At present, the best tools to protect patients from unnecessary risk for CIN are careful assessment of renal function, judicious use of procedures that utilize contrast media, and adequate hydration with …
What is the third leading cause of iatrogenic acute kidney injury?from ncbi.nlm.nih.gov
Contrast-induced nephropathy is the third leading cause of iatrogenic acute kidney injury. The commonest cause is hypoperfusion of the kidneys causing either prerenal injury or acute tubular necrosis.[10] Moreover, the number and the type of risk factors directly affect the incidence of renal impairment. The incidence rate also depends on the procedure, with reports in the literature varying from 1.6-2.3% for diagnostic investigations to 14.5% overall in coronary intervention. [11]
What is CIN in contrast?from ncbi.nlm.nih.gov
Currently, the understanding of CIN is that it is the impairment of renal function gauged as either a 25% rise in serum creatinine from baseline or an increase of 0.5 mg/dL (44 µmol/L) in absolute serum creatinine value within 48-72 hours following intravenous contrast administration.[1]
What are the risk factors for CIN?from hopkinsmedicine.org
The risk factors for CIN include baseline renal insufficiency (defined by a creatinine of >1.5, or a glomerular filtration rate of < 60 ml/min), diabetic nephropathy, other conditions that lead to reduced renal perfusion, and receiving a high total dose of contrast (<5 mL/kg, > 100 mL). You may remember that the patient in this case was diabetic, had peripheral vascular disease, received a diuretic, and received over 100 ml of contrast in a short period of time.
Why is iodine used in cardiac procedures?from ncbi.nlm.nih.gov
Because of an increasing number of coronary angiography and coronary interventional procedures, the increasing use of contrast media, and the increasing number of invasive cardiac procedures being performed in high-risk patients with chronic kidney disease, diabetes mellitus, hypertension, and kidney failure due to contrast-induced nephropathy remains a growing concern. A sudden change in kidney function is a common complication of coronary angiography, and percutaneous coronary intervention, primarily because of contrast-induced acute kidney injury or contrast-induced nephropathy. This activity reviews the pathophysiology of contrast-induced nephropathy and highlights the role of the interprofessional team in its management and prevention.
What is CIN in a nephropathy?
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.
How long does it take for creatinine to change after contrast exposure?
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
What are the factors that increase the risk of CIN?
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]
What is the treatment for CIN?
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.
What is the key diagnostic criteria after excluding other causes?
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]
What causes renal medullary hypoxia?
Renal medullary hypoxia due to either a decrease in vasodilators (nitric oxide or prostaglandins), or an increase in vasoconstrictors (adenosine and endothelin).
Is a slight elevation in a post PCI scr prognostic?
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]
Why are contrast media no longer used?
Ionic, high osmolar (HOCM) contrast media (five to eight times the osmolality of plasma, or greater than 1500 mOsm/kg) are no longer used due to their nephrotoxicity. LOCM and IOCM are now used in clinical practice instead.
What is CIN in nephropathy?
Contrast induced nephropathy (CIN) is defined as impairment of renal function, an increase in serum creatinine levels by more than 25 percent or 0.5 mg/dL, occurring within 3 days after intravascular administration of contrast media in the absence of an alternative etiology. If renal function returns to normal, it usually does so within 7 to 10 days after contrast medium administration. 1 However, sometimes CIN progresses to acute kidney injury (AKI), which can be defined as a two-fold increase in the serum creatinine or a 50 percent decreased in glomerular filtration rate (GFR) or urine output less than 0.5 mL/kg per hour for 12 hours. Various types of imaging studies or procedures use intravascular contrast media including, intravenous (IV) pyelograms, brain or head and neck or body or coronary computed tomograms (CT), cerebral or cardiac or peripheral vascular angiograms, and radiologic therapeutic procedures. Contrast is injected IV for computed tomography and intra-arteriorly (IA) for angiograms and related interventional procedures. More than 62 million CT studies were performed in the United States in 2006 and the use of CT has tripled between 1996 and 2010, from 52 studies per 1000 patients to 149 studies per 1000 patients. 2
What is the best way to prevent CIN?
Numerous strategies to prevent CIN have been used, including: oral hydration; volume expansion with sodium chloride or bicarbonate or a combination of both ; administration of N-acetylcysteine (NAC); withdrawal of metformin, ACE (angiotensin-converting-enzyme) inhibitors, angiotensin II receptor blockers, or non-steroidal anti-inflammatory drugs; hemofiltration or hemodialysis; use of low osmolar, non-ionic, contrast media; and reducing the volume of contrast media administered.
What type of imaging is used for intravascular contrast?
Various types of imaging studies or procedures use intravascular contrast media including, intravenous (IV) pyelograms, brain or head and neck or body or coronary computed tomograms (CT ), cerebral or cardiac or peripheral vascular angiograms, and radiologic therapeutic procedures.
Does theophylline help with AKI?
Theophylline treatment significantly reduced the incidence of contrast-induced AKI and had a modest improvement on kidney function after contrast exposure. However, beneficial effects of theophylline were not observed in patients with high baseline creatinine values (serum creatinine 1.5 mg/dL).
How Long Does It Take To Recover From Contrast-induced Nephropathy?
There is no set answer to this question as it depends on the individual case. However, it is generally agreed that it takes around two weeks for the kidneys to recover from the effects of contrast-induced nephropathy. In some cases, it may take longer if the individual has underlying kidney problems.
How Common Is Contrast-induced Nephropathy?
Complications of contrast media administration (CM) are one of the most serious consequences of angiographic procedures. The third most common cause of acute renal injury in hospitals, this condition affects about 12% of patients.
Who Is Most At Risk For Contrast-induced Nephropathy?
Preexisting renal impairment is the most serious risk factor for developing nephropathy after exposure to iodinated contrast media. A person with chronic kidney disease is more likely to develop CIN if they have a high rate of filtration of the blood (e.g., 60 mL/min per 1.73 m (2)).
Contrast-induced Nephropathy Treatment
There is no specific treatment for contrast-induced nephropathy. Treatment focuses on addressing the underlying cause and managing the symptoms. If the underlying cause is resolved, the nephropathy typically resolves on its own. In some cases, kidney function may improve with time even if the underlying cause is not resolved.
Description
- Eligible patients were randomly assigned in a 1:1:1 ratio to receive N-acetylcysteine at a standard dose (standard-dose group), N-acetylcysteine at a double dose (high-dose group), or placebo (control group). Computer-generated random numbers determined randomization. Patients in the standard-dose group received an intravenous bolus of 600 mg of N-acetylcysteine (Fluimucil, Za…
Prevention
- Patients with risk factors for CIN should be educated about the necessity of follow-up care with their physicians with a postprocedure SCr estimation, especially if the initial procedure was done on an outpatient basis. Prevention centers around avoiding volume depletion. This has led to trials and practices using oral hydration, volume expansion with IV fluids and bicarbonate, and both h…
- The risk of contrast-mediuminduced nephropathy after primary angioplasty extends not only to patients with preexisting renal failure but also to those with normal baseline function. Therefore, in an era in which primary angioplasty is the preferred reperfusion treatment, prophylactic interventions against contrast-mediuminduced nephropathy are warranted. The objective is to fu…
Treatment
- A lack of consensus exists regarding the definition and treatment of CIN. Studies differ in regard to the marker used for renal function (SCr versus estimated glomerular filtration rate [eGFR]), the day of initial measurement and remeasurement of the marker, and the percentage increase used to define CIN. This makes it difficult to compare studies, especially in terms of the efficacy of vari…
- Primary angioplasty was performed according to standard clinical practice. Patients in the coronary care unit received a bolus of 5000 U of heparin, followed by additional intraprocedural boluses to maintain the activated clotting time of 300 seconds or more (or 200 to 250 seconds when abciximab was used). A nonionic, low-osmolality contrast agent, iohexol (350 mg of iodin…
Prognosis
- There is a complicated relationship between CIN, comorbidity, and mortality. Most patients who develop CIN do not die from renal failure. [4] Death, if it does occur, is more commonly from either a pre-existing nonrenal complication or a procedural complication.
- Overall, in-hospital mortality was 5.9 percent and, as previously reported,7 was significantly higher in patients with contrast-mediuminduced nephropathy than in those without (26 percent vs. 1.4 percent, P<0.001). In-hospital mortality was significantly reduced by N-acetylcysteine. The odds ratio of in-hospital death in the control group, as compared with the standard-dose and high-dos…
Risks
- Many physicians who refer patients for contrast procedures and some who perform the procedure themselves are not fully informed about the risk of CIN. A survey found that fewer than half of referring physicians were aware of potential risk factors, including ischemic heart disease and diabetes mellitus. [5] (See DDx.) The reported incidence of CIN might be an underestimation. S…
- Table 2 shows in-hospital complications and deaths in the three groups. One patient in the standard-dose N-acetylcysteine group had a transient systemic rash, probably a side effect of N-acetylcysteine. The rate of contrast-mediuminduced nephropathy was 33 percent in the control group, 15 percent in the standard-dose N-acetylcysteine group, and 8 percent in the high-dose …
Background
- Between February 20, 2003, and May 1, 2005, we screened all consecutive patients admitted to the coronary care unit at our institution, Centro Cardiologico Monzino in Milan, for ST-segment elevation acute myocardial infarction who underwent primary angioplasty. Patients were asked to be in the study if they presented within 12 hours (18 hours in cases of cardiogenic shock) after th…
Results
- In conclusion, we found that N-acetylcysteine reduced the severity of contrast-mediuminduced nephropathy in patients with acute myocardial infarction treated with primary angioplasty. The effect appears to be dose-dependent and is accompanied by a significantly improved in-hospital outcome. The mechanisms underlying the improvement in the in-hospital clinical outcome have …
Research
Diagnosis
- For renal insufficiency to be attributable to contrast administration, it should be acute, usually occurring within 2-3 days (although it has been suggested that renal insufficiency developing up to 7 days postcontrast administration be considered CIN); it should also not be attributable to any other identifiable cause of renal failure. A temporal link is thus implied. [2] Following contrast exp…
Definition
- Contrast-induced nephropathy (CIN) is defined as the impairment of renal functionmeasured as either a 25% increase in serum creatinine (SCr) from baseline or a 0.5 mg/dL (44 µmol/L) increase in absolute SCr valuewithin 48-72 hours after intravenous contrast administration. [1]