Key words
contrast agents - acute kidney injury - preventive measures - clinical practice guideline
Background
Administrating contrast agents for medical purposes has a long history. It dates back
to the early 1920 s when syphilis was still treated with iodine-salts and iodine was
accidentally discovered to be a contrast agent [1]. The usefulness of this radio-opacity effect is illustrated in the widespread use
of iodinated contrast material: an estimated 75 million iodinated contrast injections
were administered worldwide in 2005, in diagnostic/interventional procedures such
as CT scans, coronary angiographies and interventions, peripheral angioplasties and
stenting, etc. [2]. Assuming a continuing 9 % increase a year, the number of injections will be closer
to 250 million in 2020. Fortunately contrast media are no longer extremely toxic,
cell-invading salts, but have since undergone a rapid evolution to become relatively
inert complex benzene molecules [3].
Despite the tremendous improvement in molecular properties, there may still be systemic
and hemodynamic consequences of intravascular iodinated contrast material injection,
especially for the kidneys. Over 99 % of iodinated contrast material is eliminated
from the body by the kidneys (possibly < 1 % via liver, gallbladder, intestines, transpiration,
tears, saliva) [4].
The first report of post-iodinated contrast administration acute renal failure was
published in 1954 [5]. After a period of controversy, the groups at risk were recognized [6]
[7]: kidney injury after iodinated contrast administration seldom occurs in patients
whose kidney function is normal. Rather, acute kidney injury occurs when other insults
are already present, particularly those leading to reduced perfusion of the kidneys
[8]
[9]. Diabetes mellitus, advanced age, cardiovascular disease, reduction in effective
intravascular volume (due to liver cirrhosis, congestive heart failure or dehydration
for example), and nephrotoxic medication are all compounding risk factors [10]. However, the main characteristic of high-risk patients is pre-existing renal insufficiency.
Iodinated Contrast Administration and Acute Kidney Injury
Iodinated Contrast Administration and Acute Kidney Injury
There are two main probable reasons why pre-existing renal insufficiency may predispose
to acute kidney injury after contrast administration. First, diseased kidneys are
less efficient with regard to excretion. Consequently, exposure to contrast after
an injection is prolonged, exacerbating any toxic effects. The actual transit times
will vary per individual dosage and specific contrast used. With relatively normal
kidney function, contrast is probably eliminated from the body with a 2.5 hour half-life,
while this half-life may be 10 hours or longer in the case of advanced renal insufficiency
[11]
[12]. Second, diseased kidneys by definition already have fewer functioning nephrons,
possibly chronic ischemic areas, and diminished renal adaptation mechanisms. Chronically
injured kidneys therefore do not have the renal reserve to preserve glomerular filtration
rate (GFR) in the event of contrast-induced injury.
Although much research has been done to elucidate the physiological pathway through
which iodinated contrast materials may cause acute kidney injury, it remains unclear.
Two main plausible effects through which contrast may cause kidney injury have been
proposed: the first centers on the hemodynamic effects of iodinated contrast materials,
alterations in blood flow and/or viscosity, which may cause reduced blood flow through
the kidneys and renal ischemia; the second proposed effect is contrast toxicity to
cells [13]. Most information on the effects of contrast on cells and organs comes from in vitro
and animal studies. Toxic effects may be overestimated due to confounding variables
such as contrast dilution and mixing with blood before reaching the kidney; animals
with normal renal function seem to tolerate extremely high iodinated contrast material
volumes without any effect on renal function [14]. A recent promising study combining an in vitro, mice model and clinical data suggests
a multi-step mechanism in which activation of the immune system resident in the kidney
plays an important role [15]. However, the association between intravascular iodinated contrast administration
and acute kidney injury is still primarily a temporal one.
From Contrast-Induced Nephropathy to Post-Contrast Acute Serum Creatinine Increase
From Contrast-Induced Nephropathy to Post-Contrast Acute Serum Creatinine Increase
Serum creatinine is used to estimate GFR in clinical practice [16]. There is continual production of creatinine as a by-product of muscle metabolism,
and continual excretion of it in the urine. Because the total body content of muscle
creatine is fairly constant, serum creatinine levels largely depend on the rate of
clearance through the kidneys.
An acute increase in serum creatinine is taken as an indication of acute kidney injury,
and this is the basis for the definition of contrast-induced acute kidney injury,
primarily a biochemical diagnosis. Historically the term used for this phenomenon
is contrast-induced nephropathy (CIN), defined as an increase in serum creatinine
> 25 % or > 44 µmol/l from baseline within a few days after contrast exposure. It
is the definition still most widely found in the literature. However, over the last
years there has been some debate as to the meaning, terminology, and optimal definition
for the phenomenon [17]
[18]
[19].
Currently most agree that there is no reason why the definition for acute kidney injury
occurring after contrast exposure should differ from that of acute kidney injury in
general. The current consensus therefore is to use the criteria established in the
2012 Kidney Disease Improving Global Outcome (KDIGO) guidelines [20]: a serum creatinine increase from baseline ≥ 26.5 μmol/L within 48 h, or a factor
of ≥ 1.5 within the previous 7 days, or urine output reduced to < 0.5 mL/kg/h during
6 hours [18]
[19]
[21]. In clinical practice, especially in the outpatient setting, the more feasible serum
creatinine criteria are most often used.
Part of the definition, which is often overlooked, is that the acute rise in serum
creatinine is diagnosed as contrast-induced acute kidney injury only if occurring
“in absence of another etiology”. However, in practice it is hard to discern the correct
etiology. Indeed, serum creatinine is a sensitive but non-specific surrogate indicator
of renal function.
Despite its limitations and extensive research into alternate markers, serum creatinine
remains the main indicator of (changes in) renal function used in clinical practice.
When used as the basis for the estimation of GFR, formulas are used to correct for
age, sex, and race [16]. However, serum creatinine is influenced by muscle mass, diet, hydration, and activity;
it shows diurnal and seasonal fluctuations; and it is often unstable in patients with
health issues [22]
[23]
[24]. Furthermore, sustained vasoconstriction (hours to days) observed after contrast
administration [13] may be sufficient to temporarily reduce the filtration rate in the absence of acute
kidney injury.
Because of the many confounding factors and uncertainties, the true implications of
the often-transient post-contrast rise in serum creatinine are unclear. On the one
hand, iodinated contrast injections have consistently been associated with an acute
rise in serum creatinine indicating acute kidney injury [5]
[6]
[7]
[9]
[10]
[12]
[17]
[18]
[25]. Furthermore, although serum creatinine usually returns to baseline values within
one to two weeks, it may progress to continued deterioration of renal function, a
requirement of dialysis, and mortality [25], and several studies have shown correlations between post-contrast rise in serum
creatinine and increased morbidity and mortality risk [10]
[11]
[25]. On the other hand, several retrospective studies have shown that serum creatinine
fluctuations equal to those indicating contrast-induced acute kidney injury are seen
without contrast administration, in incidences equal to or greater than reported incidences
after contrast [26]
[27]
[28]
[29]
[30]. It may be that measuring post-contrast change in serum creatinine yields mostly
noise, with only a few instances of acute kidney injury. However, given the persistent
reports and correlations, an acute increase in serum creatinine, at the very least,
is a marker and predictor of poor outcome.
Recent changes in terminology reflect the growing uncertainties surrounding the phenomenon.
Until about 5 years ago, CIN was the term most widely used in the literature to refer
to acute kidney injury after iodinated contrast administration ([Fig. 1]). More recently it was argued that the term CIN is misleading: “Contrast-Induced”
implies a causal link which has not been established in the clinical setting, mostly
because studies on incidences of acute kidney injury after iodinated contrast administration
lack a control group. “Contrast-Associated Nephropathy” (CAN) has been used by some
instead. However, it was also argued that “Nephropathy” indicates a disease or damage
to the kidney, whereas the context of intravascular iodinated contrast administration
implies acute renal insult, leading to the use of the term Contrast-Induced Acute
Kidney Injury (CI-AKI). Recently terms addressing both the temporal link with contrast
administration and the acute nature of the phenomenon have been introduced: Contrast-Associated
Acute Kidney Injury (CA-AKI), and the term recommended in current clinical practice
guidelines, Post-Contrast Acute Kidney Injury (PC-AKI) ([Fig. 1]) [18]
[19].
Fig. 1 Number of publications using the terms CIN, CI-AKI, CAN, CA-AKI, or PC-AKI to denote
an increase in serum creatinine after iodinated contrast administration (PubMed search
done on February 4th, 2020).
Abb. 1 Anzahl der Publikationen mit den Suchbegriffen CIN, CI-AKI, CAN, CA-AKI oder PC-AKI
mit Erwähnung eines Anstiegs des Serumkreatinins nach Gabe jodhaltiger Kontrastmittel
(PubMed-Suche am 4. Februar 2020).
In practice, there is no certainty that an acute post-contrast increase in serum creatinine
greater than a predefined threshold equals acute kidney injury. In other words, post-contrast
acute increase in serum creatinine (PC-ASCI) may include but does not equal contrast-induced
AKI.
In the rest of this paper two terms will be used: in deference to the recommendation
in updated guidelines, PC-AKI will be used to denote acute injury to the kidneys occurring
after iodinated contrast material, and PC-ASCI to denote a post-contrast acute rise
in serum creatinine, > 25 % or > 44 µmol/l from baseline, as measured in clinical
practice and most trials to date.
Guidelines for the Prevention of Post-Contrast Acute Kidney Injury
Guidelines for the Prevention of Post-Contrast Acute Kidney Injury
Once acute kidney injury has occurred, no known treatment is available to mitigate
possible effects. As a consequence, the focus in clinical practice is on prevention.
The identification of high-risk patients around the 1980 s enabled a more structured
approach and standardization of preventive measures, and several radiological committees
were formed in the 1990 s to that end. Around the year 2000, national and umbrella
radiologic societies began issuing guidelines on the safe use of intravascular iodinated
contrast material. Examples of umbrella organizations are ESUR for Europe, ACR for
the United States of America, and RANZCR for New Zealand and Australia [31]
[32]
[33]. Many countries have their own guidelines, such as the United Kingdom [34] and the Netherlands [18]. Germany does not have a national guideline for the prevention of PC-AKI, and it
is assumed the European ESUR guideline is followed.
Clinical practice guidelines are defined as “systematically developed statements to
assist practitioner and patient decisions about appropriate health care for specific
clinical circumstances” (The Institute of Medicine). They include concise instructions
on patient selection, diagnostic/screening tests, medical/surgical procedures, and
other clinical practice details. They are regularly updated, incorporating systematic
literature reviews, and thus reflect current evidence-based knowledge in the field.
Guidelines for the prevention of PC-AKI specify how to identify at-risk patients and
how best to prevent PC-AKI in these patients [18]
[31]
[32]
[33]
[34]. Patients at risk of PC-AKI have specific risk factors, mainly pre-existing renal
insufficiency or, in other words, patients with chronic kidney disease (CKD). Procedure-related
risk factors are contrast type (e. g. dimer > monomer; high > low osmolality) and
volume (iodine dose); administration route (first pass renal exposure > intra-arterial
> intravenous); and repeated contrast injections. To reduce procedure-related risks,
optimal contrast administration is stressed, such as using a contrast volume that
is as low as feasible. Aiming for clinical euvolemia and withholding medication such
as metformin, NSAIDs, and ACE inhibitors in high-risk patients are recommended to
reduce patient-related risk factors.
Guidelines agree that no medicinal prophylaxes studied to date (e. g. statins, NAC)
have been shown to consistently protect against PC-AKI. The prophylaxis universally
recommended to prevent PC-AKI is intravenous hydration.
To Hydrate or Not To Hydrate? Intravenous Prophylactic Hydration
To Hydrate or Not To Hydrate? Intravenous Prophylactic Hydration
Intravenous hydration as prophylaxis for PC-AKI was first introduced in the literature
in 1981 [35]. Since then peri-procedural intravenous hydration has been strongly recommended,
and it is still the cornerstone treatment for PC-AKI prevention today.
The pathophysiological pathway through which intravenous hydration protects renal
function is unclear, mainly because the physiological pathway of PC-AKI is unclear.
However, there is consensus among experts that administering intravenous fluids before
and after contrast exposure may mitigate some of the hemodynamic effects of contrast
material by reducing blood osmolality and viscosity. It has been shown that contrast
is rapidly filtered and excreted in the urine of euvolemic mice, whereas it is reabsorbed
and accumulates in the tubules during volume depletion [15]. The main mechanism by which intravenous hydration is thought to work is by producing
an infusion rate-dependent increase in tubular fluid volume [36].
Water infusion alone could reduce intra-tubular contrast concentration. In recommended
prophylaxis protocols, sodium chloride or sodium bicarbonate is added. Sodium chloride
may induce a tubular reaction to increase salt and water excretion, which may theoretically
promote contrast excretion. Furthermore, increased salt excretion may cause a slight
reduction in tubular acidity. The acid handled by a kidney is relatively constant
over limited periods of time, therefore increasing volume in the tubuli through infusion
will reduce acid concentration. Apoptosis (programmed cell death) after free radical
generation has been shown to be accelerated in an acid environment in vitro: by increasing
tubular pH, physiological sodium chloride solution may attenuate free radical-induced
damage. Intravenous hydration with 1.4 % sodium bicarbonate theoretically has all
the same beneficial influences as normal saline, with the added potential benefits
of substantial renal tubule alkalinization and free radical clearing [36].
For the prevention of PC-AKI, intravenous hydration with normal saline is considered
the absolute gold standard. However, evidence for effectiveness is scarce [25]
[37]. It has not been conclusively shown that this prophylaxis mitigates PC-AKI risk,
let alone whether it reduces the risks of dialysis and mortality in the long term.
Clinical trials evaluating strategies to prevent PC-AKI mostly focus on a comparison
of two or more variations of intravenous prophylaxis and lack a control group not
receiving any prophylaxis. Only relatively recently were trials incorporating such
a control group published.
Two trials, published in 2014 and 2015, included patients with normal GFR and CKD
patients and evaluated intravenous hydration with normal saline versus no prophylaxis
[38]
[39]. Two found lower PC-ASCI incidences after prophylaxis (22/108 vs. 38/108 [38] and 22/204 vs. 43/204 [39]). Less in-hospital mortality for the prophylaxis group was reported in one trial
(3/108 vs. 10/108) [38], but no difference between groups was reported in the other [39]. However, both trials were set in acute care (primary percutaneous intervention
for ST-elevation myocardial infarction), where hemodynamic instability and other factors
play a role.
Several trials were done in computed tomography (CT) comparing 1-hour 1.4 % sodium
bicarbonate intravenous hydration before contrast administration to no prophylaxis.
Among the included normal and CKD patients, no difference in efficacy was found (PC-ASCI
3/43 vs. 4/44) [40]. The sample size was very small, however, and the included patients with estimated
GFR (eGFR) ≥ 60 mL/min/1.73 m2 are not considered at risk. A second small trial was done in patients suspected of
pulmonary embolism; all patients had CKD. No prophylaxis was found non-inferior (PC-ASCI
5/70 vs. 6/65) [41]. This year a similar but larger study was published: the multi-center KOMPAS study
included all CKD outpatients undergoing elective contrast-enhanced CT. Again, no prophylaxis
was found non-inferior (PC-ASCI 7/262 vs. 4/261, no instances of dialysis and similar
incidences of mortality at one-year follow-up) [42]. These three trials appear to indicate no benefit of prophylactic intravenous hydration
in the elective setting of computed tomography. However, hydration protocols in these
studies deviate from traditionally recommended protocols. First, sodium bicarbonate
was used instead of the more widely accepted normal saline, but this may not be a
major issue since no notable differences between pre- and post-contrast prophylaxis
with sodium chloride and sodium bicarbonate have been reported in the literature [e. g.
43]. Second, considering the plausible mechanisms of PC-AKI, the preventive effect
of intravenous fluids is probably rate-dependent [36]. In other words, in order to be fully effective, intravenous hydration must probably
be continued for the time it takes the kidneys to filter out the contrast material.
The possibility that 1-hour pre-hydration is simply not enough to make a difference
therefore cannot be excluded. It must also be noted that several retrospective studies
question the risk of intravenous contrast administration [e. g. 44].
The only trial to date comparing intravenous prophylactic pre- and post-hydration
with normal saline in elective CKD patients receiving intravenous or intraarterial
iodinated contrast is the AMACING trial [45]
[46]. All referrals for elective procedures with iodinated contrast were included in
screening for patients that were at risk according to current at the time of the trial
Dutch and European guidelines. Non-inferiority of no prophylaxis to standard prophylaxis
in the prevention of PC-AKI was shown: PC-ASCI 8/296 (2.7 %) vs. 8/307 (2.6 %); no
dialysis or related deaths at one month; no clinically relevant differences in one-year
dialysis, mortality, change in serum creatinine, or renal events. In short, no benefits
of prophylactic intravenous hydration could be discerned. On the other hand, prophylaxis
is not without risk (complications of intravenous hydration occurred in 5.5 % of hydrated
patients), requires extra hospitalization of patients, and incurs considerable costs.
These findings led to the conclusion that standard prophylaxis can be safely withheld
for patients like those included in the AMACING trial.
eGFR < 30 mL/min/1.73 m2 patients: what do we know?
eGFR < 30 mL/min/1.73 m2 patients: what do we know?
The available evidence from controlled trials for the effectiveness of prophylactic
intravenous hydration is limited, and pertains to patients with eGFR ≥ 30 mL/min/1.73 m2 only. The AMACING trial, for example, included elective patients with eGFR 30–59 mL/min/1.73 m2 combined with the risk factors diabetes, cardiovascular disease, age > 75, anemia,
or nephrotoxic medication. eGFR < 30 mL/min/1.73 m2 patients (i. e., CKD stages 4 & 5) were excluded. These patients represent only a
small fraction of all patients receiving intravascular iodinated contrast.
In the general population, the prevalence of stages 4 & 5 CKD is 0.4 % to 0.5 %. In
the setting of elective intravascular iodinated contrast administration, the prevalence
is even lower, 0.06 % to 0.5 % [47]. Consequently, very few trials manage to include even a few cases, and little is
known about PC-AKI and prophylaxis in these patients. Worldwide, however, based on
the prevalence and estimated number of contrast procedures, at least 375 000 and up
to 1.25 million patients with this severe level of CKD will be confronted with the
risks of contrast administration each year [2]
[47].
A retrospective analysis comparing the excluded eGFR < 30 mL/min/1.73 m2 patients from the AMACING trial to enrolled patients (with eGFR 30–59 mL/min/1.73 m2) found the former to be at significantly higher risk [47]: PC-ASCI 13.6 % vs. 2.7 % (p = 0.0019); dialysis at 1 month 0.9 % vs. 0.0 % (p = 0.2646);
and mortality at 1 month 9.2 % vs. 0.0 % (p < 0.0001).
A much larger, 4-year retrospective observational study of elective procedures in
eGFR < 30 mL/min/1.73 m2 patients with intravascular iodinated contrast administration, found that prophylactic
intravenous hydration might confer some benefit for renal function [48]. Results did not reach statistical significance, but point estimates indicated a
protective trend compared to patients without prophylaxis (PC-ASCI, GFR decline and
1-month dialysis all yielded adjusted odds ratios < 1). On the other hand, analyses
of 1-month all-cause mortality yielded adjusted odds ratios > 1, indicating a trend
toward higher short-term mortality risk for prophylaxis patients. Confounding by indication
may play a part in the latter observation, but prophylaxis complications contributed
to the observed higher mortality risk. Amongst the 281 eGFR < 30 mL/min/1.73 m2 prophylaxis patients studied, 18 (6.4 %) serious complications occurred: 3 arrhythmias,
and 15 heart failures. The latter included 5 deaths. Of all deaths observed in prophylaxis
patients, 24 % (5/21) were adjudicated as related to intravenous prophylactic hydration.
The study incorporated a comparison of baseline characteristics between patients who
had suffered serious complications and those who had not. The results suggested that
evaluating individual cardiac function parameters before prescribing prophylaxis for
high-risk patients with eGFR < 30 mL/min/1.73 m2 may help to identify those prone to serious complications [48].
Recommendations for Current Clinical Practice
Recommendations for Current Clinical Practice
PC-AKI prevention guidelines have drastically changed in recent years. Optimal contrast
administration, adhering to the ALARA (As Low As Reasonably Achievable) principle,
remains perhaps the most important prerequisite for patient safety. On the subject
of PC-AKI and prophylaxis, however, many questions remain unanswered and evidence
is still lacking. There is no evidence, for example, for an optimal prophylactic protocol.
At this time pre- and post-contrast intravenous hydration with normal saline seems
to be the preferred protocol ([Table 1]).
Table 1
Current recommendations in recently updated guidelines for the prevention of PC-AKI.
Tab. 1 Heutige Empfehlungen auf Basis der jüngst revidierten Richtlinien zur Prävention
einer PC-AKI.
|
guideline
|
update
|
definition used
|
patient-related risk factors
|
recommended prophylactic treatment for high-risk patients
|
|
NVvR (NL)
|
2017
|
KDIGO criterion 1 or 2 measure at 2–7 d
|
eGFR < 30 mL/min/1.73 m2
|
iv 1.4 % NaHCO3
1 h pre-CM at 3 mL/kg/h (or 250 ml)
or 1 h pre-CM at 3 mL/kg/h (or 250 ml) and 6 h post-CM at 1 mL/kg/h (or 500 ml)
|
|
ESUR (Europe)
|
2018
|
KDIGO criterion 1 or 2 within 48–72 h
|
eGFR < 30 mL/min/1.73 m2
eGFR < 45 mL/min/1.73 m2 before 1st pass renal exposure or in ICU patients
|
iv 0.9 % NaCl
3–4 h pre-CM at 1 mL/kg/h and 4–6 h post-CM at 1 mL/kg/h
or iv 1.4 % NaHCO3
(or 154 mmol/l in dextrose 5 % water)
1 h pre-CM at 3 mL/kg/h; for 1st pass renal exposure also 4–6 h post-CM at 1 mL/kg/h
• The clinician responsible for patient care should individualize preventive hydration
in patients with severe congestive heart failure or patients with end-stage renal
failure
|
|
RANZCR (Oceania)
|
2018
|
None – refer to NICE guideline
within 48 h or 7 d
|
eGFR < 30 mL/min/1.73 m2
eGFR < 45 mL/min/1.73 m2 in deteriorating renal function
|
iv 0.9 % NaCl
“There is no evidence to support a specific volume or duration... A practical protocol
… is 1.0–1.5 mL/kg/h, for at least 6 h before and after …”
• Exact administration protocols depend on, amongst other things, the patient’s pre-test
risk of cardiac failure/pulmonary oedema
|
|
ACR (America)
|
2020
|
AKIN criteria
within 48 h
|
eGFR < 30 mL/min/1.73 m2
|
iv 0.9 % NaCl (or Lactated Ringer’s)
“The ideal infusion rate and volume is unknown... One possible protocol would be …
100 mL/h, beginning 6 to 12 h before and continuing 4 to 12 h after...”
|
|
NKF-ACR statement
(America)
|
2020
|
KDIGO criteria
within 48 h
|
eGFR < 30 mL/min/1.73 m2
eGFR < 45 mL/min/1.73 m2 in “individual high-risk circumstances”
|
iv 0.9 % NaCl (“iv 1.4 % NaHCO3 is not preferred”)
“The ideal timing, volume, and rate of volume expansion is uncertain. Typical … regimens
begin 1 h before and continue 3–12 h after … with typical doses ranging from fixed
(e. g., 500 mL before and after) to weight-based volumes (1–3 mL/kg/h)”
• Risk of prophylaxis should be considered before initiation
|
NVvR = Radiological Society of the Netherlands; ESUR = European Society of Urogenital
Radiology; RANZCR = Royal Australian and New Zealand College of Radiologists; ACR = American
College of Radiology; NKF = National Kidney Foundation (America).
KDIGO = Kidney Disease Improving Global Outcomes (International); NICE = National
Institute for Health and Care Excellence (United Kingdom); AKIN = Acute Kidney Injury
Network (international); RIFLE = Risk, Injury, Failure, Loss of kidney function, and
End-stage kidney disease classification by the Acute Dialysis Quality Initiative (ADQI)
group (international).
CI-AKI = Contrast-Induced Acute Kidney Injury; PC-AKI = Post-Contrast Acute Kidney
Injury; h = hours; d = days; eGFR = estimated Glomerular Filtration Rate; CM = Contrast
Material injection.
(PC-)AKI definitions: KDIGO (a combination of RIFLE and AKIN) = a serum creatinine increase from baseline 1.
≥ 0.3 mg/dL (> 26.4 μmol/L) within 48 h, or 2. ≥ 50 % (≥ 1.5-fold) within the prior
7 days, or 3. urine output < 0.5 mL/kg/h for 6 h; AKIN (only considered after an adequate status of hydration is achieved) = a serum creatinine
increase (in two consecutive samples) 1. ≥ 0.3 mg/dL (≥ 26.5 μmol/L), or 2. ≥ 50 %
(≥ 1.5-fold above baseline) within 48 h, or 3. urine output reduced to ≤ 0.5 mL/kg/hour
for at least 6 h; NICE (in line with RIFLE, AKIN or KDIGO) = a serum creatinine increase 1. > 26 μmol/L
within 48 hours, or 2. > 50 % known or presumed to have occurred within the past 7
days, or 3. urine output reduced to < 0.5 mL/kg/h for more than 6 h in adults and
more than 8 h in children and young people, or 4. ≥ 25 % fall in eGFR in children
and young people within the past 7 days.
Aiming for a euvolemic state in all patients before a procedure is an integral part
of optimal contrast administration. Dehydrated patients are at higher risk of acute
kidney injury and should therefore be re-hydrated before contrast administration irrespective
of renal function. However, standard prophylactic intravenous hydration is no longer recommended in eGFR ≥ 30 mL/min/1.73 m2 patients. Elective patients with eGFR 30–59 mL/min/1.73 m2 combined with the risk factors diabetes, anemia, cardiovascular disease, or nephrotoxic
medication have been relegated from the ‘high-risk’ to the ‘low to intermediate-risk’
group, and the standard prophylaxis threshold is now set at eGFR < 30 mL/min/1.73 m2 ([Table 1]). This does indeed appear to better define the high-risk population [47]
[48]
[49].
This change in recommendations has already had an enormous beneficial impact on current
clinical practice of guideline-adhering medical centers, enormously reducing complications,
hospitalizations, and costs [50]. Another welcome change is that most guidelines now specifically mention the risk
of intravenous hydration. This previously unrecognized but important aspect of safe
iodinated contrast material administration is especially relevant for eGFR < 30 mL/min/1.73 m2 patients [49]. An appropriate dual screening process, including both renal and cardiac parameters
(see example in [Fig. 2]), will minimize the risk of prophylactic hydration in this high-risk population.
Fig. 2 Clinical practice flowchart for the prevention of PC-AKI (according to our internal
Maastricht UMC+ standard operating procedure).
Abb. 2 Klinisches Screening-Diagramm zur Vermeidung einer PC-AKI (standardisierte interne
Vorgehensweise (Maastricht UMC+)).
