Contrast-induced nephropathy (CIN) is defined as an acute decrease in renal function
after intravascular administration of iodinated contrast media (CM) in absence of
other direct causes. Physicians working in critical care wards are very much familiar
with this entity. It increases the burden on hospital resources.[1] In addition, it has been linked to increased length of hospital stay and long-term
mortality.[2]
[3] It is the third leading cause of hospital-acquired acute kidney injury.[4] Although its incidence in most studies has been found to be low (1 to 2%) in general
patient population, in high-risk patients it has been calculated to be more than 20
to 30%.[5]
Various interventional neuroradiological procedures (e.g., carotid artery stenting
[CAS], carotid angioplasty, carotid angiogram, and embolization of vascular lesions)
have made substantial advancement in the past couple of decades. All these procedures
expose neurologically sick patients to iodinated radiocontrast media. Many of these
patients are elderly with associated comorbidities. The vessels are imaged with iodinated
contrast that has not only deleterious hemodynamic effects but is also injurious to
the renal tubular cells mainly in the outer medulla.[6] Although literature is replete with epidemiology of CIN in percutaneous coronary
intervention, not much is published of the risks of CIN in patients undergoing interventional
procedures for neurological conditions. More importantly, there are scant reports
on prospective controlled data for neurointerventional field. Neuroradiological procedures
differ from cardiac radiology endovascular procedures in respect of CM dose, injection
technique, types of patients, and moreover, they are not on antiedema therapy.
Several risk factors that predispose a patient to CIN have been described, including
chronic kidney disease, diabetes mellitus, hypertension, old age, use of nephrotoxic
medications, such as nonsteroidal anti-inflammatory drugs, dehydration, large contrast
volume, and repeated exposure to CM within 72 hours.[2]
[7]
[8] Many neurological patients of stroke, CAS, and even aneurysmal subarachnoid hemorrhage
patients fall in this high-risk category. In addition to the aforementioned risk factors,
certain risk factors are unique to this patient population such as mannitol administration.
Although potential renal protective properties of mannitol given after CM administration
have been discussed in literature, they were not confirmed by Solomon et al[9] who observed higher rate of CIN after the administration of saline and mannitol,
as compared to saline alone. Additionally, the general beneficial role of mannitol
in neurosurgical patients came under a cloud, when it was found to be an independent
risk factor for acute kidney injury after cerebral trauma.[10] Secondly, with mannitol administration, the volume of the infused fluid for hydration
could be insufficient to prevent patients from post-contrast nephropathy. Therefore,
mannitol is not recommended before or following contrast administration.
Kato et al[11] observed 8.8% incidence of CIN in patients undergoing CAS. In the group that developed
CIN, prolonged carotid sinus reflex (CSR) during the procedure was found to be in
57.1% of the cases. Neither preoperative renal function contrast volume nor history
was related to the incidence of CIN, while on multivariate analysis, prolonged CSR
was found to be an independent risk factor for CIN. Hemodynamic depression after CAS
and carotid endarterectomy is caused by the manipulation of carotid sinus, leading
to development of CIN in this group of patients. The frequency of development of prolonged
CSR during CAS implantation varies from 11 to 42%.[12] Donahue et al[13] too observed that in the presence of pre-existing chronic kidney disease, persistent
hemodynamic depression (decrease in systolic pressure below 90 mm Hg or mean arterial
pressure below 60 mm Hg) was more common in patients who developed acute kidney injury,
and only a brief episode of 2.5 min of hypotension was the threshold of hemodynamic
depression. Thus, according to them, hemodynamic depression and not the contrast volume
represents an independent predictor of acute kidney injury.
Tao et al observed increasing age, proteinuria, estimated glomerular filtration rate
of less than 60 mL/min/1.73 M,[2] high National Institutes of Health Stroke Scale score and anemia to be independent
risk factors for CIN in patients with stroke undergoing cerebral angiography with
or without CAS implantation. In their study, multivariate regression analysis revealed
that even after adjusting for potential confounding risk factors, patients with proteinuria
still had fivefold higher risk of CIN than patients without. However, some established
factors for CIN in coronary angiography, such as age and diabetes, were not seen as
risk factors in this study owing to lower proportion of elderly and patients with
diabetes mellitus.[14] However, various nonrandomized evidence suggests that computed tomography (CT) angiogram
and CT perfusion studies are not associated with statistically significant increase
in risk of acute kidney injury in patients of stroke, even those with chronic kidney
disease.[15]
Aneurysmal subarachnoid hemorrhage (aSAH) patients require multiple contrast studies
for carotid angiogram and coil embolization. Lee et al identified contrast-induced
acute kidney injury in 7.3% patients undergoing coil embolization. They remarked CIN
to be an independent predictor of the overall outcome of aSAH after endovascular treatment.[16] Furthermore, they also evaluated the impact of GCS on CIN in aSAH patients and concluded
that it was the low initial GCS that was responsible for the CIN in them without the
negative influence of other factors (e.g., volume of contrast, type of contrast, duration
of procedure and size of aneurysm, age, and diabetes mellitus). However, Prasad et
al[17] observed that CIN in these patients may be the result of administration of large
volume of CM (> 250 mL). Although the direct association between CIN and contrast
agent usage has not been proven, reducing the total amount of CM used in the diagnosis
and treatment of aSAH is important. However, some authors claim that only age more
than 75 years is a predisposing factor for CIN development in this neurological condition.[18]
A plethora of therapies for the prevention of CIN have been suggested of which, the
most beneficial is good hydration of the patient with normal saline.[19] Volume expansion maintains satisfactory blood pressure, good renal blood flow, and
nitric oxide production. All these factors prevent medullary ischemia and enhance
contrast excretion.
Though most of the studies do not conclude that the incidence of CIN as well as factors
leading to occurrence of CIN is different in neurologically sick patients compared
with non-neurological patients, probably additional unique factors do play a role
in etiology in them. Clearly, our knowledge in this context is limited owing to lack
of large, high-quality, multicenter randomized controlled trials. Until we have results
from such trials, we have to accept the observations from retrospective data, albeit,
with a pinch of salt.
