Contrast-Induced Nephropathy Medication
- Author: Renu Bansal, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
NAC is acetylated L-cysteine, an amino acid. As previously mentioned, its sulfhydryl groups make it an excellent antioxidant and scavenger of free oxygen radicals. It also enhances the vasodilatory properties of nitric oxide. Twelve meta-analyses covering 29 randomized, controlled trials have been published on the effect of NAC therapy in CIN. They all suffer from significant heterogeneity. The standard oral NAC regimen consists of 600 mg twice daily for 24 hours before and on the day of the procedure. Higher doses of 1 g, 1200 mg, and 1500 mg twice daily have also been studied, with no significant dose-related or route-related (oral vs intravenous) difference. NAC has very low oral bioavailability; substantial interpatient variability and inconsistency between the available oral products obscure the picture further.[25, 33]
Used for prevention of contrast toxicity.
Used for prevention of contrast toxicity in susceptible individuals such as those with diabetes mellitus. May provide substrate for conjugation with toxic metabolites.
These agents are used for their favorable effects on endothelin and thrombus formation, plaque stabilization and anti-inflammatory properties by improving lipid profile.
Indicated for hyperlipoproteinemia (Type III). Inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA reductase), which in turn inhibit cholesterol synthesis, and increases cholesterol metabolism. Increase HDL cholesterol and decrease LDL-C, total-C, apolipoprotein B, VLDL cholesterol, and plasma triglycerides.
The most efficacious of the statins at high doses. Inhibits 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA reductase), which in turn inhibits cholesterol synthesis and increases cholesterol metabolism. Reports have shown as much as a 60% reduction in LDL-C. The Atorvastatin versus Revascularization Treatment study (AVERT) compared 80 mg atorvastatin daily to standard therapy and angioplasty in patients with CHD. While events at 18 mo were the same between both groups, the length of time until the first CHD event occurred was longer with aggressive LDL-C lowering. The half-life of atorvastatin and its active metabolites is longer than that of all the other statins (ie, approximately 48 h compared to 3-4 h).
May modestly elevate HDL-C levels. Clinically, reduced levels of circulating total cholesterol, LDL-C, and serum TGs are observed.
Before initiating therapy, patients should be placed on a cholesterol-lowering diet for 3-6 mo; the diet should be continued indefinitely.
Adjunct to dietary therapy in reducing serum cholesterol. Immediate-release (Mevacor) and extended-release (Altocor) are available.
Synthetically prepared HMG-CoA reductase inhibitor with some similarities to lovastatin, simvastatin, and pravastatin. However, structurally distinct and has different biopharmaceutical profile (eg, no active metabolites, extensive protein binding, minimal CSF penetration).
Used as an adjunct to dietary therapy in decreasing cholesterol levels.
Effective in reducing circulating lipid levels and improving the clinical and anatomic course of atherosclerosis.
HMG-CoA reductase inhibitor that in turn decreases cholesterol synthesis and increases cholesterol metabolism. Reduces total-C, LDL-C, and TG levels and increases HDL-C level. Used adjunctively with diet and exercise to treat hypercholesterolemia.
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|Class of Contrast Agent||Type of Contrast Agent||Iodine Dose
(cPs at 37°C)
(mOsm/kg H2 O)
|Molecular Weight (Da)|