What Gfr Is Safe For Iv Contrast – If you wish to reuse any or all of this article, please use the link below, which will take you to the Copyright Clearance Center RightsLink. You can get quick pricing and quick permission to reuse your content in a variety of ways.
Contrast-induced nephropathy (CIN), also known as contrast-induced acute kidney injury, is an iatrogenic renal injury that occurs after intravenous administration of radiopaque contrast agents (CA) in unsuspected individuals. CIN was first described in the 1950s in reports of fatal acute renal failure after intravenous pyelography in patients with renal disease arising from multiple myeloma.1,2 Despite technological advances, CIN is responsible for one-third of all hospital-acquired acute illnesses. Kidney injury (KI)3,4 and affects high-risk subgroups in 1% to 2% of the general population and up to 50% after coronary angiography (CA) or percutaneous coronary intervention (PCI).
What Gfr Is Safe For Iv Contrast
Prevalence of imaging modalities and interventional procedures involving intravascular CM administration in both non-cardiac modalities (eg, CT vascular angiography and interventional vascular angiography) and established (eg, CA and PCI) and emerging cardiac modalities (eg, CT coronary angiography). (CTCA) and transcatheter aortic valve implantation (TAVI) have significantly increased the number of patients undergoing CM and thus the number of patients at risk of CIN. Widespread use of primary PCI to treat acute myocardial infarction (AMI) has increased the incidence of CIN due to inherent difficulties in rapid assessment of CIN risk, initiation of preventive measures, hemodynamic disturbances, and contrast enhancement, despite significant improvements in cardiovascular outcomes. . volumes, are all risk factors for the development of CIN.6 Despite several therapeutic approaches, the increasing age and frequency of comorbidities in the broad group of cardiac patients receiving CM have made CIN prevention remain an important clinical problem.7
Contrast Associated Acute Kidney Injury
As discussed in the following sections, an individual’s risk of developing CIN can be assessed using known clinical and periprocedural factors consistent with proposed pathologic mechanisms of CIN. Stage III pre-existing chronic kidney disease (CKD), estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m
More than 3 months, the most frequently identified risk factor for CIN; However, CIN can occur in the absence of underlying VAT if there are many other risk factors. 5 Risk scoring systems have been developed from cohort studies8,9 that have allowed clinicians to predict the likelihood of CIN occurrence and allow targeted use. Preventive treatment. The highly iatrogenic and predictable nature of CIN makes it an ideal area for cardiovascular and nephrology research, focusing on pathophysiological mechanisms as well as new risk assessment, preventive, diagnostic and therapeutic interventions.
The generally accepted definition of CIN is a 25% relative increase in serum creatinine (SCr) or an absolute increase of 0.5 mg/dL (44 μmol/L) within 72 h of contrast exposure in the absence of an alternative explanation.10 Criticism This definition is unpopular, with a slight increase in SCr. Insensitivity to growth has been shown to be associated with events, 11 ,12 a combination of relative and absolute SCr changes and lack of functional assessment such as changes in urinary output as used in the RIFLE, 13 AKIN14 and KDIGO15 classification systems. However, this definition has the advantage of being widely used as an end point in many CIN studies, and it correlates well with negative clinical end points.
16 aimed to classify CIN according to three grades related to three relative and absolute creatinine elevation thresholds, including a group with minor elevation (<25% or 0.5 mg/dL), which is also associated with adverse long-term outcomes (Table) . 1)
Groups Publish Statements On Ct Contrast Use In Patients With Kidney Disease
An important problem with SCr is its relative insensitivity to the rapid changes in GFR seen in AKI, particularly in patients with normal renal function. , thereby reducing its usefulness as an AKI marker. However, early and mild stage changes in SCr may be a useful marker for CIN; A recent clinical trial by Ribicini
, 18 , including 216 at-risk patients undergoing CA, showed that a 5% increase in SCr from baseline at 12 h was a sensitive (75%) and specific (72%) marker of CIN at 48 h and persistent deterioration of renal function. . 30 days.
Several new renal biomarkers, including NGAL, 19 cystatin C, 20 urinary Kim-121, and interleukin-1822, have been proposed to detect CIN minutes to hours after renal injury. Unfortunately, to date, these biomarkers have not yet progressed beyond clinical trials; There is a clear clinical need for large trial validation of their use for early detection and intervention of AKI.
In clinical practice, CIN is often considered a transient phenomenon; In 80% of cases, SCr levels return to normal after approximately 1–3 weeks.23 Although CIN is of clinical importance, several clinical studies have shown that it exhibits several short-term and long-term adverse events. 24 After adjustment for comorbidities, observational studies have shown that in-hospital mortality in patients with HF is approximately five times higher than in patients with unrecognized CM, 25 and mortality at 1 and 5 years is approximately four times higher, 26 with some 20%12 and 1-year mortality rates in the range of 38%. 27 In other observational studies, approximately 20% of those who developed CIN had permanent deterioration of renal function after exposure to CM, 28 between renal replacement therapy. 0.7% in 25 and 7% in 27 patients with CIN (Table 2). Thus, the additional health care costs associated with CIN are estimated to be substantial.12
Renal Function–based Contrast Threshold Predicts Kidney Injury In Transcatheter Aortic Valve Replacement
However, it is important to note that a direct causal relationship between CIN and mortality was not established in these observational studies. The onset of CIN is more likely to occur in the presence of severe cardiac damage or disease, which alone portends a poor prognosis. Therefore, CIN may be a marker of adverse cardiovascular outcomes rather than an independent risk factor. A recent meta-analysis by James
, 29 reviewed 39 observational studies that examined cardiovascular outcomes in individuals with CIN and increased risk of death, cardiovascular events, renal failure, and long-term hospitalization. However, baseline clinical characteristics that simultaneously predispose to CIN and mortality have been found to be strong confounders, particularly in unadjusted studies. Even after making appropriate adjustments for co-morbidity, the authors recommend that any definitive conclusion about causation be interpreted with caution.
However, there are several potential pathophysiological mechanisms that may explain the direct association between CIN and major adverse cardiac events (MACE). In the short term, acute CIN involves severe volume overload, electrolyte disturbances, uremia, or hemodialysis (HD). Chronic MACE is increased in individuals with permanent kidney damage because of the cardiovascular risk associated with progressive CKD and its many pathological manifestations, including progressive atherosclerosis, vascular calcification, and left ventricular (LV) hypertrophy. Minor or transient changes in renal function increase the risk of MACE.
Large randomized controlled trials (RCTs) are needed to demonstrate a clear causal relationship between CIN and MACE, to demonstrate that effective CIN prevention strategies using adjunctive therapies can reduce both short-term and long-term MACE. Cardiovascular risk reduction benefits. Because of the similarities between kidney and cardiovascular diseases and their respective treatments, this is unlikely. Because of the many serious confounders associated with MACE, CIN clinical trials have focused only on clinically significant renal outcomes such as persistent worsening of renal function, new-onset proteinuria, and progression to end-stage renal disease (ESRF). Skipping any spurious correlations found with MACE correlations.
Prophylactic Hydration To Protect Renal Function From Intravascular Iodinated Contrast Material In Patients At High Risk Of Contrast Induced Nephropathy (amacing): A Prospective, Randomised, Phase 3, Controlled, Open Label, Non Inferiority Trial
Although there is no evidence to support any direct causal effect on MACE, the onset of CIN after cardiac procedures remains an alarming event that requires additional clinical vigilance and early intervention.
Intravenous CM is a concentrated triiodinated benzene compound that is radiopaque due to binding of iodine moieties. All CM agents are cytotoxic, and this may be attributed to the ionic strength, osmolarity, or viscosity of each particular agent. However, these agents have been found to be highly nephrotoxic and are now rarely used. 32 Therefore, safer agents have been developed, including nonionic “low osmolar” (LOCM) or “iso-osmolar” (IOCM) solutions. These compositions are significantly more viscous than blood plasma, with viscosity inversely related to osmolality (Table 3). In addition to direct vasoactive and cytotoxic effects, these two physicochemical properties of SM are believed to be related to the pathogenesis of CIN.34
The kidney is particularly susceptible to ischemic damage because it is under high metabolic and osmotic stress and is supplied by a complex microvascular circulation that is sensitive to local and systemic hypoperfusion. Oxygen demand is high due to active sodium reabsorption in the loop of Henle and the partial pressure of oxygen is approximately 20 mmHg. Approximately less.35 This is relative ischemia