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Does sodium bicarbonate infusion really have no effect on the incidence of acute kidney injury after cardiac surgery? A prospective observational trial.
Wetz, AJ, Bräuer, A, Quintel, M, Heise, D
Critical care (London, England). 2015;(1):183
Abstract
INTRODUCTION Postoperative acute kidney injury (AKI) is a frequently observed phenomenon after cardiac surgery with cardio-pulmonary bypass (CPB); this severe complication is associated with adverse patient outcomes. There are multiple mechanisms involved in AKI during cardiac surgery, including CPB-dependent hemolysis. An IV infusion of sodium bicarbonate, which leads to urine alkalization, may play a role in preventing AKI. Recently, several trials have investigated the effect of sodium bicarbonate and reported controversial results. The purpose of this investigation was to investigate the following question. Under what circumstances can sodium bicarbonate prevent postoperative AKI? METHODS We analyzed data from 342 patients undergoing CPB surgery at the University Hospital Goettingen, Germany. A total of 174 patients received a preemptive dose of sodium bicarbonate. Directly after the induction of anesthesia, the continuous infusion of 0.15 mmol/kg body weight/h was started and continued until 2 pm on the first postoperative day. Patients who were not treated with sodium bicarbonate formed the control group (n = 168). To verify the AKI risk configuration of each group, we surveyed risk factors and determined the commonly used clinical predictive score according to Thakar and colleagues. We recorded the concentration of free hemoglobin (fhb) to estimate the amount of CPB-dependent hemolysis. The definition of AKI was acquired by applying the AKI-network (AKIN) classification over the course of five postoperative days. RESULTS Patients who received the sodium bicarbonate infusion showed a significantly lower incidence (35.6 vs. 50%) of AKI than that of patients who did not receive the infusion (p = 0.01). AKIN levels 2 and 3 were also more frequent when sodium bicarbonate was not administered. Particularly, in the low-risk cohort (<3 Thakar points), the incidence of AKI was significantly reduced (26 vs. 46%) when patients received sodium bicarbonate (p = 0.01), whereas in the high-risk patients, no significant reduction was observed. CONCLUSION In this study, we observed that low-risk patients particularly benefited from the preventive treatment with sodium bicarbonate. The incidence of AKI was significantly reduced in low-risk patients while there was no statistically significant difference in the high-risk patient cohort. TRIAL REGISTRATION DRKS00007616, Registered 12 December 2014.
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Effect of sodium bicarbonate and Beta-alanine on repeated sprints during intermittent exercise performed in hypoxia.
Saunders, B, Sale, C, Harris, RC, Sunderland, C
International journal of sport nutrition and exercise metabolism. 2014;(2):196-205
Abstract
PURPOSE To investigate the separate and combined effects of sodium bicarbonate and beta-alanine supplementation on repeated sprints during simulated match play performed in hypoxia. METHODS Study A: 20 recreationally active participants performed two trials following acute supplementation with either sodium bicarbonate (0.3 g·kg-1BM) or placebo (maltodextrin). Study B: 16 recreationally active participants were supplemented with either a placebo or beta-alanine for 5 weeks (6.4 g·day-1 for 4 weeks, 3.2 g·day-1 for 1 week), and performed one trial before supplementation (with maltodextrin) and two following supplementation (with sodium bicarbonate and maltodextrin). Trials consisted of 3 sets of 5 × 6 s repeated sprints performed during a football specific intermittent treadmill protocol performed in hypoxia (15.5% O2). Mean (MPO) and peak (PPO) power output were recorded as the performance measures. RESULTS Study A: Overall MPO was lower with sodium bicarbonate than placebo (p = .02, 539.4 ± 84.5 vs. 554.0 ± 84.6 W), although there was no effect across sets (all p > .05). Study B: There was no effect of beta-alanine, or cosupplementation with sodium bicarbonate, on either parameter, although there was a trend toward higher MPO with sodium bicarbonate (p = .07). CONCLUSIONS The effect of sodium bicarbonate on repeated sprints was equivocal, although there was no effect of beta-alanine or cosupplementation with sodium bicarbonate. Individual variation may have contributed to differences in results with sodium bicarbonate, although the lack of an effect with beta-alanine suggests this type of exercise may not be influenced by increased buffering capacity.
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pH buffering does not influence BDNF responses to exercise.
Rojas Vega, S, Hollmann, W, Vera Wahrmann, B, Strüder, HK
International journal of sports medicine. 2012;(1):8-12
Abstract
The influence of acidosis on brain-derived neurotrophic factor (BDNF) was examined by buffering pH changes during 10 min of continuous low intensity (LIE) and following high intensity cycling exercise to exhaustion (HIE). 11 athletes participated in 2 trials separated by 1 week. Individuals received either a placebo infusion (isotonic saline) or an isotonic sodium bicarbonate infusion before and during exercise. Blood samples were drawn at rest, after LIE and after HIE, as well as 3, 6, 10 and 15 min post exercise. During placebo trial, HIE induced a profound decrease (p<0.01) of capillary blood bicarbonate concentration (HCO3-), pH, base excess (BE) and pCO2. Higher (p<0.01) HCO3-, pH and BE were found during bicarbonate infusion and post exercise in comparison to the placebo trial. Exercise induced an identical increase of blood lactate concentration in both trials. Serum BDNF concentration was increased (p<0.01) at the end of HIE and remained elevated until 3 min post exercise in both trials. The present study suggests that during HIE lactate might have an acidosis-independed impact on BDNF secretion because buffering of blood gases, that attenuate the fall of pH but not the accumulation of lactic acid, failed to alter the exercise-induced increase of BDNF.
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Sodium bicarbonate for the prevention of contrast-induced nephropathy: the efficacy of high concentration solution.
Tamai, N, Ito, S, Nakasuka, K, Morimoto, K, Miyata, K, Inomata, M, Yoshida, T, Suzuki, S, Murakami, Y, Sato, K
The Journal of invasive cardiology. 2012;(9):439-42
Abstract
BACKGROUND The appropriate dose of sodium bicarbonate to prevent contrast-induced nephropathy (CIN) has not been established. METHODS AND RESULTS To determine the efficacy of high-concentration sodium bicarbonate, 123 consecutive patients with renal dysfunction undergoing coronary angiography with/without intervention were administrated either high-concentration (group H: 833 mEq/L, n = 87) or low-concentration (group L: 160 mEq/L, n = 36) sodium bicarbonate at the rate of 3 mL/kg/h for 1 hour before the contrast exposure, and followed by 1 mL/kg/h for 7 hours. A total of 77 patients (group H, n = 54; group L, n = 23) without prophylactic continuous hemodiafiltration were analyzed in this study. Urine pH (n = 10 for each group and n = 5 for control) was increased by concentration and time-dependent manner in each group. Urine pH at 3 hours after administration of sodium bicarbonate was significantly higher in group H than group L and control (8.50 ± 0.94 vs 6.95 ± 1.17 vs 5.70 ± 0.97, respectively; P<.001). Incidence of CIN (0% vs 17.3%; P=.005) was lower in group H than group L. Percent change in creatinine within 48 hours was significantly lower in group H than group L (-2.65 ± 9.83% vs 9.14 ± 14.0%; P=.001). Percent change in estimated glomerular filtration rate within 48 hours was significantly higher in group H than group L (3.97 ± 11.8 vs -7.43 ± 13.3; P<.001). CONCLUSION Administration of a higher concentration of sodium bicarbonate was more effective for urine alkalization and prevention of CIN.
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Sodium bicarbonate versus sodium chloride and oral N-acetylcysteine for the prevention of contrast-induced nephropathy in advanced chronic kidney disease.
Shavit, L, Korenfeld, R, Lifschitz, M, Butnaru, A, Slotki, I
Journal of interventional cardiology. 2009;(6):556-63
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Abstract
INTRODUCTION Contrast-induced acute kidney injury (CI-AKI) is one of the leading causes of hospital-acquired acute kidney injury. Multiple clinical studies have proposed several preventive strategies. AIMS To examine the efficacy of sodium bicarbonate compared with sodium chloride and oral N-acetylcysteine (NAC) for preventive hydration after cardiac catheterization. METHODS We conducted a prospective, single-center trial. Patients with chronic kidney disease (CKD) stage III-IV undergoing cardiac catheterization were allocated to receive either an infusion of 0.9% sodium chloride and oral NAC or 154 mEq/L sodium bicarbonate. MAIN Outcome measure CI-AKI, defined as an increase of 25% or 0.3 mg/dL or more in plasma creatinine within 2 days of contrast administration. RESULTS Ninety-three patients were allocated to one of the two groups: 42 patients in the saline plus NAC group and 51 patients in the bicarbonate group. There were no statistically significant differences between the groups in the most important clinical and procedural characteristics. Baseline plasma creatinine levels, estimated glomerular filtration rate, incidence of diabetes mellitus, hypertension, congestive heart failure, and contrast medium volume were similar. Mean plasma creatinine concentration was 1.76 +/- 0.54 mg/dL in the saline and NAC group and 1.9 +/- 1 mg/dL in the bicarbonate group (P = 0.23). The rate of CI-AKI was 9.8% in the bicarbonate group and 8.4% in the saline plus NAC group. No patient required renal replacement therapy. CONCLUSION Hydration with sodium bicarbonate is not more effective than hydration with sodium chloride and oral NAC for prophylaxis of CI-AKI in patients with CKD stage III-IV undergoing cardiac catheterization.
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Preexercise metabolic alkalosis induced via bicarbonate ingestion accelerates Vo2 kinetics at the onset of a high-power-output exercise in humans.
Zoladz, JA, Szkutnik, Z, Duda, K, Majerczak, J, Korzeniewski, B
Journal of applied physiology (Bethesda, Md. : 1985). 2005;(3):895-904
Abstract
The present study investigated the effect of preexercise metabolic alkalosis on the primary component of oxygen uptake (Vo(2)) kinetics, characterized by tau(1). Seven healthy physically active nonsmoking men, aged 22.4 +/- 1.8 (mean +/- SD) yr, maximum Vo(2) (Vo(2 max)) 50.4 +/- 4 ml.min(-1).kg(-1), performed two bouts of cycling, corresponding to 40 and 87% of Vo(2 max), lasting 6 min each, separated by a 20-min pause, once as a control study and a few days later at approximately 90 min after ingestion of 3 mmol/kg body wt of NaHCO(3). Blood samples for measurements of bicarbonate concentration and hydrogen ion concentration were taken from antecubital vein via catheter. Pulmonary Vo(2) was measured continuously breath by breath. The values of tau(1) were calculated by using six various approaches published in the literature. Preexercise level of bicarbonate concentration after ingestion of NaHCO(3) was significantly elevated (P < 0.01) compared with the control study (28.96 +/- 2.11 vs. 24.84 +/- 1.18 mmol/l; P < 0.01), and [H(+)] was significantly (P < 0.01) reduced (42.79 +/- 3.38 nmol/l vs. 46.44 +/- 3.51 nmol/l). This shift (P < 0.01) was also present during both bouts of exercise. During cycling at 40% of Vo(2 max), no significant effect of the preexercise alkalosis on the magnitude of tau(1) was found. However, during cycling at 87% of Vo(2 max), the tau(1) calculated by all six approaches was significantly (P < 0.05) reduced, compared with the control study. The tau(1) calculated as in Borrani et al. (Borrani F, Candau R, Millet GY, Perrey S, Fuchsloscher J, and Rouillon JD. J Appl Physiol 90: 2212-2220, 2001) was reduced on average by 7.9 +/- 2.6 s, which was significantly different from zero with both the Student's t-test (P = 0.011) and the Wilcoxon's signed-ranks test (P = 0.014).
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Effects of sodium bicarbonate on VO2 kinetics during heavy exercise.
Kolkhorst, FW, Rezende, RS, Levy, SS, Buono, MJ
Medicine and science in sports and exercise. 2004;(11):1895-9
Abstract
PURPOSE Sodium bicarbonate was used to investigate the effect of blood pH on VO2 kinetics during heavy exercise. METHODS On separate days, 10 active subjects performed two 6-min cycling bouts (208 +/- 12 W) at 25 W above their ventilatory threshold. Each subject ingested 0.3 g x kg(-1) of sodium bicarbonate with approximately 1 L of water or water alone 1 h before exercise. VO2 kinetics were examined by means of a three-component mono-exponential model. RESULTS Bicarbonate ingestion caused a significant increase in the preexercise blood pH (7.512 +/- 0.009 vs 7.425 +/- 0.007; P < 0.001). In the bicarbonate trial, the time constant for the rapid component (27.9 +/- 3.5 s) was slower than the control trial (20.8 +/- 2.4 s; P = 0.017). The higher blood pH after bicarbonate ingestion would have diminished local blood flow and caused a leftward shift of the oxygen-hemoglobin dissociation curve both of which would slow oxygen delivery to working muscle. In addition, bicarbonate ingestion diminished the amplitude of the slow component 29% (463 +/- 43 vs 649 +/- 53 mL x min(-1); P = 0.040). The primary cause of the slow component during heavy exercise is fatigue of working fibers and an accompanying increase of motor unit recruitment. Elevated plasma bicarbonate concentration is reported to stimulate the efflux of H from muscle fibers and to increase intramuscular pH. CONCLUSIONS The slower time constant during the rapid component suggested that oxygen delivery is a limiting factor of VO2 kinetics during the onset of heavy exercise. Also, these results imply that bicarbonate ingestion diminished fatigue in working fibers during the slow component.
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Effects of sodium bicarbonate ingestion on prolonged intermittent exercise.
Price, M, Moss, P, Rance, S
Medicine and science in sports and exercise. 2003;(8):1303-8
Abstract
PURPOSE The aim of this study was to determine the effects of sodium bicarbonate ingestion on prolonged intermittent exercise and performance. METHODS Eight healthy male subjects (mean +/- SD: age 25.4 +/- 6.4 yr, mass 70.9 +/- 5.1 kg, height 179 +/- 7 cm, VO(2max) 4.21 +/- 0.51 L.min-1) volunteered for the study, which had received ethical approval. Subjects undertook two 30-min intermittent cycling trials (repeated 3-min blocks; 90 s at 40% VO(2max), 60 s at 60% VO(2max), 14-s maximal sprint, 16-s rest) after ingestion of either sodium bicarbonate (NaHCO(3); 0.3 g.kg-1) or sodium chloride (NaCl; 0.045 g x kg(-1). Expired air, blood lactate (BLa), bicarbonate (HCO(3)-), and pH were measured at rest, 30 and 60 min postingestion, and during the 40% VO(2max) component of exercise (4, 10, 16, and 29 min). RESULTS After ingestion, pH increased from rest to 7.46 +/- 0.03 and 7.40 +/- 0.01 for NaHCO(3) and NaCl, respectively (main effect for time and trial; P < 0.05). Values decreased at 15 min of exercise to 7.30 +/- 0.07 and 7.21 +/- 0.06, respectively, remaining at similar levels until the end of exercise. BLa peaked at 15 min (12.03 +/- 4.31 and 10.00 +/- 2.58 mmol.L-1, for NaHCO(3) and NaCl, respectively; P > 0.05) remaining elevated until the end of exercise (P < 0.05). Peak power expressed relative to sprint 1 demonstrated a significant main effect between trials (P < 0.05). Sprint 2 increased by 11.5 +/- 5% and 1.8 +/- 9.5% for NaHCO(3) and NaCl, respectively. During NaHCO(3), sprint 8 remained similar to sprint 1 (0.2 +/- 17%), whereas a decrease was observed during NaCl (-10.0 +/- 16.0%). CONCLUSION The results of this study suggest that ingestion of NaHCO(3) improves sprint performance during prolonged intermittent cycling.
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A comparison of the effects of potassium citrate and sodium bicarbonate in the alkalinization of urine in homozygous cystinuria.
Fjellstedt, E, Denneberg, T, Jeppsson, JO, Tiselius, HG
Urological research. 2001;(5):295-302
Abstract
For many years, urine alkalinization has been one of the cornerstones in the treatment of homozygous cystinuria. Because of the relationship found between the excretion of urinary sodium and cystine, potassium citrate has emerged as the preferred sodium-free alkalizing agent. To evaluate the usefulness of potassium citrate for urine alkalization in cystinuric patients, sodium bicarbonate and potassium citrate were compared in 14 patients (10 on tiopronin treatment and four without treatment with sulfhydryl compounds). The study started with 1 week without the use of any alkalizing agents (Period 0) followed by 2 weeks with sodium bicarbonate (Period 1) and 2 weeks with potassium citrate (Period 2). Urinary pH, volume, excretion of sodium, potassium, citrate and free cystine, as well as the plasma potassium concentration, were recorded. Potassium citrate was shown to be effective as an alkalizing agent and, in this respect, not significantly different from sodium bicarbonate. Even though a normal diet was used, a significant increase in urinary sodium excretion was observed with sodium bicarbonate (Period 1). Urinary potassium and citrate excretion increased with potassium citrate (Period 2). A significant correlation was found between urinary sodium and cystine in the tio-pronin-treated patients. No significant differences in cystine excretion were recorded in Periods 0, 1 and 2. Plasma potassium was significantly higher during Period 2, but only one patient developed a mild hyperkalemia (5.0 mmol/l). The use of potassium citrate for urine alkalization in homozygous cystinuria is effective and can be recommended in the absence of severe renal impairment.