Automated Contrast Injection and Targeted Renal Therapy: Strategies to Prevent Contrast-Induced Nephropathy (FULL TITLE BELOW)
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Automated Contrast Injection and Targeted Renal Therapy: Strategies to Prevent Contrast-Induced Nephropathy and to Treat Renal Insufficiency
It is currently estimated that in the United States there are 15–18 million patients with peripheral arterial disease (PAD), and 18–20 million with diabetes mellitus (DM).1,2 These incidences are increasing, along with the number of PAD patients revascularized with percutaneous peripheral interventions (PPI).2,3 Several factors are likely to increase the number of PPIs performed yearly and therefore, patient contrast exposure. The rapid adoption of multidetector computed tomography angiography (MDCTA) as a noninvasive modality in PAD diagnosis, treatment and follow-up will likely increase contrast exposure. A large number of patients with significant symptomatic and asymptomatic PAD who are currently undiagnosed and/or untreated will likely be diagnosed by MDCTA and become candidates for PPI. Additionally, PAD patients still require multiple PPIs and reinterventions secondary to the diffuse location of the disease and our current technology. These unique clinical dynamics of PAD underscore a need for contrast optimization and a better understanding of the role of prevention and treatment of contrast-induced nephropathy (CIN) in patients with PAD.
The definition of CIN varies, but in clinical trials CIN has been defined as an increase in serum creatinine (Cr) > 0.5 mg/dl or > 25% of baseline between 24–120 hours after contrast exposure, with peak levels reported between 3–5 days.4–6 The pathogenesis of CIN is complex and remains incompletely defined. The proposed mechanism of developing CIN results in a “vicious cycle” of events that culminates in critical renal medullary hypoxia and cell necrosis. This cycle includes a direct renal cellular cytotoxic effect, resulting in increased toxic oxygen-free radicals; intense renal medullary vasoconstriction and hypoxia mediated by multiple vasoconstrictors, including adenosine, vasopressin and prostaglandin E2;7,8 acute increase in renal osmolality, requiring increased renal cellular oxygen consumption; acute reduction of renal blood flow with endothelial dysfunction and decreased nitric oxide production resulting in renal medullary hypercoaguability, hyperviscosity, and worsening ischemia, leading to acute tubular necrosis (ATN). Once initiated, there are few therapeutic options to interrupt this cycle.
McCullough et al. described the clinical impact in percutaneous coronary intervention (PCI) and identified the significant increase in morbidity and mortality associated with CIN.9 CIN is the third leading cause of hospital-acquired acute renal failure (ARF). McCullough reported a 14% incidence of CIN in 1,826 PCI patients with a 7.1% in-hospital mortality in patients developing CIN not requiring dialysis, and 35.7% if requiring dialysis (p < 0.001).9 With dialysis, the patient has < 20% two-year survival.9 The in-hospital mortality was 0.7% without CIN. Gruberg et al. reported a 37% incidence of CIN (7.3% requiring dialysis) in 440 PCI patients with baseline renal insufficiency (RI) (Cr ? 1.8mg/dl) with three times higher in-hospital mortality (14.9% versus 4.9%) and two times higher 1-year mortality (37.7% versus 19.4%) in patients with CIN.10 Likewise, Levey et al. noted a 5.5-fold risk for increased mortality in patients undergoing diagnostic studies requiring contrast exposure who developed CIN.11 Clearly, the clinical impact of CIN in the PCI patient population is significant and unappreciated, and CIN potentially stands to have an even greater clinical impact on the treatment of PAD as compared to PCI.
The incidence and impact of CIN in PPI remains almost totally unknown and unexplored. Mehran et al. identified CIN predictors in PCI, including diabetes (DM), age > 75 years, female gender, contrast volume, Cr clearance (CRCL), congestive heart failure (CHF), hypotension, preprocedure renal insufficiency (RI) and anemia, and validated a CIN risk score prediction model.12 The incidences of these CIN predictors are usually greater in the older PPI versus PCI population. The individual incidences of DM and preprocedural RI in PCI trials was approximately 20%, but the incidence of DM and RI have been reported at a 50–80% incidence in PPI, especially for critical limb ischemia (CLI).13 This becomes significant when considering the combination of DM and preprocedure RI, shown by Parfey et al. to increase the incidence of CIN during PCI to 50%.14
Additionally, there are several significant clinical and periprocedural differences during PPI versus PCI that increase the risk of CIN. These include complex, longer PPI case durations with higher contrast use; higher rates of multiple procedures and secondary reinterventions; overall higher complication rates in PPI; more frequent MDCTA use, therefore, more contrast exposure; and a higher incidence of renal artery stenosis (RAS). A typical PAD patient would be a frail > 80-year-old female weighing 90 pounds, with CLI, hematocrit of 27.5%, serum Cr of 1.9 mg/dL and a calculated CrCL of < 30 mL/min. This typical patient is certainly at extreme risk for developing CIN. Strategies to prevent CIN are not only warranted, but are essential in treating patients with PAD.
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