No prophylaxis is non-inferior and cost-saving to prophylactic intravenous hydration in preventing contrast-induced nephropathy on requiring iodinated contrast material administration

Abstract

J Thorac Dis 2017;9(6):1440-1442 jtd.amegroups.com intravenous hydration as proposed by the guidelines to no prophylaxis in the high-risk population targeted by the guidelines. CIN incidences found in the AMACING trial were low (2.6-2.7%), and no haemodialysis or related deaths occurred within 35 days. The AMACING study found no prophylaxis to be non-inferior to prophylactic intravenous hydration in the prevention of CIN, as well as cost-saving. We often have worried about the development of CIN and subsequent haemodialysis in CKD patients on use of iodinated contrast material administration (5). Based on these results, withholding prophylaxis for high-risk patients with eGFR higher than 29 mL/min/1.73 m 2 might be considered without compromising patient safety. On the other hand, this study excluded the patients with eGFR lower than 30 mL/min/1.73 m 2 , emergencies and intensive care patients with higher contrast volume or haemodynamic instability. Although the difference in risk of CIN between hydrated and non-hydrated groups is small within the subgroup analysis regarding interventional versus diagnostic procedure, these results cannot be generalised to include such patients with acute myocardial infarction where some benefit of hydration has been found (6,7). In addition, patients undergoing emergent percutaneous coronary intervention (PCI) are at high risk for CIN because of hemodynamic instability and infeasibility of adequate prophylaxis (8,9). There were only three clinical trials on the prevention of CIN including a randomly assigned group not receiving prophylaxis (Table 1) (6,7,10). Two were done in patients with ST-elevation myocardial infarction, most of whom had normal renal function, and both found prophylaxis superior which might be explained by other factors such as higher contrast volume, haemodynamic instability and nephrotoxic treatments inherent to this population (6,7). James et al. performed a large meta-analysis and systematic review of mortality associated with CIN (11). They found that after adjustment for variables other than CIN that could contribute to the mortality, there was a significant reduction in the association between CIN and mortality. In the future, large clinical trials will provide further insight into the potential strengths of these results whether giving no prophylaxis is non-inferior to standard care prophylactic hydration on undergoing an elective procedure requiring iodinated contrast material administration. AcknowledgementsNone. Footnote Conflicts of Interest:The authors have no conflicts of interest to declare.

Safety of a rapid outpatient hydration protocol for patients with renal impairment requiring intravenous iodinated contrast media for computed tomography

“…Further, no complications of fluid overload from hydration were observed. Although complication from intravenous hydration has been cited elsewhere, (13,14) it was not observed in our patients, who were all outpatients and may have fasted up to three hours beforehand, rendering them relatively under-hydrated.…”

“…(3) Intravenous physiological saline is the established prophylaxis for CIN in patients with CKD. (5,9,(13)(14)(15) A popular regimen is normal saline infused at 1 mL/kg/h for 6-12 hours before the procedure and continued for 6-12 hours afterwards. (3) Another possible protocol would be 0.9% saline at 100 mL/h, beginning 6-12 hours before and continuing 4-12 hours after the procedure, but this is practical only in the inpatient setting.…”

Contrast-Induced Nephropathy: Update on the Use of Crystalloids and Pharmacological Measures

“…To repeat the trial with a higher number of individuals has been discussed as unethical and should, also in our opinion, be avoided. Some of these issues have been addressed in a recent commentary by Sato et al [ 29 ].…”

Contrast-associated acute kidney injury, new findings and old believes

“…Various mechanisms like direct toxicity of contrast agents to the tubular epithelial cells, running to apoptosis and necrosis of epithelial cells and finally dysfunction of tubules. Accordingly, an indirect mechanism of contrast-induced nephropathy is vasomotor alteration in kidney due to vasoactive substances like endothelin, nitric oxide and prostaglandins, which leads to ischemic injury (3)(4)(5). Then ischemic injury directs to intra-renal vasoconstriction and diminution of glomerular blood flow.…”