Evaluation of different sodium bicarbonate regimens for the prevention of contrast medium-induced nephropathy

Abstract

IntroductionThe rapid decline in renal function caused by radiographic contrast agents usually is transient, but it can result in chronic kidney disease. The pathophysiology of contrast-induced nephropathy (CIN) is poorly understood, but it may include acute hypoxia-induced oxidative stress and free radicals generated within the acid environment of the renal medulla. Thus, the alkalization of urine by sodium bicarbonate has been regarded as resulting in the reduction of CIN. The aim of this study was to determine whether a long-duration sodium bicarbonate regimen is more effective than a short-duration regimen in reducing CIN.MethodsOne hundred patients were assigned randomly to treatment with sodium bicarbonate solution using either the short regimen (intravenous bolus 3 mL/kg/h of 166 mEq/L sodium bicarbonate for 1 hour immediately before radiocontrast) or the long regimen (initial intravenous bolus of 3 mL/kg/h of 166 mEq/L sodium bicarbonate for 6 hr). Patients with renal dysfunction (estimated glomerular filtration rate [eGFR], 60 mL/min/1.73 m2 or less) who underwent elective or emergent coronary angiography (CAG) with/without percutaneous coronary intervention (PCI) at Nephrology Department (Theodor Bilharz Research Institute) were enrolled in the study. Data were analyzed by SPSS version 12, using Kruskal Wallis, ANOVA, Chi square test and Spearman rank correlation coefficient.ResultsThere was a significant increase in serum creatinine and a decrease in eGFR 48 hr post-intervention in group 1 (short regimen) with no statically difference regarding those parameters group 2 (long regimen). Serum potassium clearly was decreased significantly post procedure in both groups.ConclusionsThe results of our study indicated that the long regimen of bicarbonate supplementation was a more effective strategy to prevent CIN than the short regimen.

Protective Effects of Salvianolate on Contrast-Induced Nephropathy after Primary Percutaneous Coronary Intervention: A Prospective Multicenter Randomized Controlled Trial

“…More and more studies have focused on finding new preventive measures. The protective effects of sodium bicarbonate, N-acetylcysteine, and high-dose statins on CIN have already been confirmed [30,31]. Salvianolate is a Danshen extract that has many pharmacological effects, such as scavenging oxygen-free radicals and improving microcirculation, and antioxidant, anti-inflammatory, anti-ischemic properties.…”

Prevention Strategies of Contrast Medium Induced Nephropathy (CIN): A Review of the Current Literature

“…To date, CIN is one of the most serious adverse reactions to iodinated CM. Since there is no specific therapy for CIN and the disease is iatrogenic, prevention is of paramount importance [45]. The patients at highest risk have a GFR below 60 ml/min.…”

“…Actually, CIN incidence has been significantly reduced with oral administration of 600 mg of NAC 24 hours before CM injection instead of hydration alone [47]. Another study proposed intravenous NAC 7 hours instead of 20 min before CM injection to prevent CIN after coronarography [45]. In a randomized study, Li et al compared pre-medication with probucol and hydration.…”

The Protective Effect of Short-term Infusion Regimens with Sodium Bicarbonate and Theophylline against Contrast Induced Nephropathy in Rats

“…ntravenous administration of contrast dye can lead to a contrast-induced nephropathy (CIN) that begins soon after its injection (Abouzeid and Mosbah, 2016;Lefel et al,2016).CIN remains the third most common cause of hospital-acquired acute renal failure (Yeganehkhah et al, 2014). It is associated with prolonged hospitalization, need for renal replacement therapy and increase in occurrence…”

“…The proposed mechanisms are outer-medullary hypoxia arising from an imbalance of local vasoconstrictive and vasodilatory influences which seems to be mediated partly by adenosine. High osmolarity contrast dye may also have a direct cytotoxic effect that operates through the generation of reactive oxygen species within the acid environment of the renal medulla (Barlak etal., 2010;Abouzeid and Mosbah ,2016).…”