Context Contrast-induced nephropathy remains a common complication of radiographic procedures. Pretreatment with sodium bicarbonate is more protective than sodium chloride in animal models of acute ischemic renal failure. Acute renal failure from both ischemia and contrast are postulated to occur from free-radical injury. However, no studies in humans or animals have evaluated the efficacy of sodium bicarbonate for prophylaxis against contrast-induced nephropathy. Objective To examine the efficacy of sodium bicarbonate compared with sodium chloride for preventive hydration before and after radiographic contrast. Design, Setting, and Patients A prospective, single-center, randomized trial conducted from September 16, 2002, to June 17, 2003, of 119 patients with stable serum creatinine levels of at least 1.1 mg/dL (Ն97.2 µmol/L) who were randomized to receive a 154-mEq/L infusion of either sodium chloride (n=59) or sodium bicarbonate (n=60) before and after iopamidol administration (370 mg iodine/mL). Serum creatinine levels were measured at baseline and 1 and 2 days after contrast.

Contrast-induced nephropathy has continued to plague interventional cardiology as an all-too-frequent complication of diagnostic and therapeutic procedures. We present an evidence-based protocol for prevention of this complication that uses infusion of NaHCO3 to effect urinary alkalinization and possibly decrease free-radical renal injury resulting from contrast exposure.

Nephropathy following contrast media (CM) exposure is reduced by administration before, during, and after the contrast procedure of either isotonic sodium chloride solution (Saline) or isotonic sodium bicarbonate solution (IsoBicarb). The reasons for this reduction are not well established for either sodium salt; probable mechanisms are discussed in this paper. For Saline, the mechanism for the decrease in CIN is likely related primarily to the increased tubular flow rates produced by volume expansion and therefore a decreased concentration of the filtered CM during transit through the kidney tubules. Furthermore, increased tubular flow rates produce a slight increase in tubular pH resulting from a fixed acid excretion in an increased tubular volume. The mechanism for the decreased CIN associated with sodium bicarbonate includes the same mechanisms listed for Saline in addition to a renal pH effect. Increased filtered bicarbonate anion raises both tubular pH and tubular bicarbonate anion levels toward blood physiologic levels, thus providing increased buffer for reactive oxygen species (ROS) formed in the tubules as a result of exposure to CM in renal tubular fluid.

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The fixed bed microcatalytic system reported earlier (Chen and Lucki, 1971) has been modified and automated. The automated system is used to do repeated cycles of crackinghegeneration. Thus, the cyclic nature of the catalytic cracking process can be simulated by this unit. The test procedure is programmed by an electric timer to actuate six control circuits over a 60-min cycle allowing unit operation substantially unattended. The circuit is particularly suited for studies of long term stability of cracking catalysts.