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Management of acute metabolic acidosis in the ICU: sodium bicarbonate and renal replacement therapy.
Yagi, K, Fujii, T
Critical care (London, England). 2021;(1):314
Abstract
This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2021. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2021 . Further information about the Annual Update in Intensive Care and Emergency Medicine is available from https://link.springer.com/bookseries/8901 .
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Sodium Bicarbonate in Different Critically Ill Conditions: From Physiology to Clinical Practice.
Coppola, S, Caccioppola, A, Froio, S, Chiumello, D
Anesthesiology. 2021;(5):774-783
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Advances in management of chronic metabolic acidosis in chronic kidney disease.
Chen, W, Abramowitz, MK
Current opinion in nephrology and hypertension. 2019;(5):409-416
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PURPOSE OF REVIEW Chronic metabolic acidosis is a common complication of chronic kidney disease (CKD) and is associated with adverse consequences, such as CKD progression and muscle wasting. We review the findings from recent clinical trials that have examined the effects of sodium bicarbonate therapy and veverimer in patients with CKD and chronic metabolic acidosis. RECENT FINDINGS There are four recent clinical trials on chronic metabolic acidosis of CKD. In a pilot, cross-over study, 6 weeks of sodium bicarbonate therapy improved vascular endothelial function, measured by brachial artery flow-mediated dilation. In a single-center, randomized, open-label study, 6 months of sodium bicarbonate therapy increased muscle mass and lean body mass, and preserved kidney function. The other two clinical trials (phase 1/2 and phase 3 studies) examined the effects of veverimer, which is a hydrochloric acid binder. The phase 3 study showed that 12-weeks of veverimer increased serum bicarbonate levels and might improve physical function. The effects of veverimer on CKD progression, physical function and cardiovascular endpoints as well as its long-term safety are yet to be determined. SUMMARY Recent studies suggest that sodium bicarbonate therapy may improve vascular endothelial function and muscle mass, and preserve renal function. Veverimer increases serum bicarbonate level and could be a potential new therapeutic option for treating chronic metabolic acidosis.
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Tolerance to Sodium in Patients With CKD-Induced Metabolic Acidosis: Does the Accompanying Anion Matter?
Bushinsky, DA
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2019;(6):858-865
Abstract
Patients with chronic kidney disease (CKD) continue to produce endogenous acids but have a reduction in net acid excretion, resulting in a primary decrease in serum bicarbonate concentration, which is termed chronic metabolic acidosis. Recent prospective studies, along with retrospective cohort analyses, demonstrate a higher risk for CKD progression with untreated metabolic acidosis. To normalize serum bicarbonate levels, acidemic patients are often treated with sodium bicarbonate (NaHCO3) or sodium citrate, which have been shown to slow the progression of CKD. However, studies using this approach have routinely excluded patients with common sodium-sensitive comorbid conditions, such as poorly controlled hypertension, congestive heart failure, volume overload, or edema. This article examines the effect of the anion that accompanies sodium delivered with these therapies. Do the negative effects on blood pressure (BP) and sodium retention, as measured by an increase in edema, weight gain, and congestive heart failure, observed with oral administration of sodium chloride (NaCl) differ when a similar amount of sodium is given with bicarbonate or citrate in this patient population? A review of the literature suggests that NaHCO3 does not increase BP or sodium retention when administered to patients with CKD during a concurrent severe NaCl dietary restriction (∼10 mEq/d). However, this degree of NaCl restriction is feasible only under strict control in clinical research environments. In contrast, when NaHCO3 is given to patients without severe dietary NaCl restriction, there is an increase in BP and sodium retention. Thus, unless patients with CKD can tolerate a diet virtually devoid of NaCl, additional sodium, regardless of the accompanying anion, appears to increase BP and sodium retention.
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Distal renal tubular acidosis and severe hypokalemia: a case report and review of the literature.
Vasquez-Rios, G, Westrich, DJ, Philip, I, Edwards, JC, Shieh, S
Journal of medical case reports. 2019;(1):103
Abstract
BACKGROUND Distal renal tubular acidosis is a relatively infrequent condition with complex pathophysiology that can present with life-threatening electrolyte abnormalities. CASE PRESENTATION We describe a case of a 57-year-old Caucasian woman with previous episodes of hypokalemia, severe muscle weakness, and fatigue. Upon further questioning, symptoms of dry eye and dry mouth became evident. Initial evaluation revealed hyperchloremic metabolic acidosis, severe hypokalemia, persistent alkaline urine, and a positive urinary anion gap, suggestive of distal renal tubular acidosis. Additional laboratory workup and renal biopsy led to the diagnosis of primary Sjögren's syndrome with associated acute tubulointerstitial nephritis. After potassium and bicarbonate supplementation, immunomodulatory therapy with hydroxychloroquine, azathioprine, and prednisone was started. Nonetheless, her renal function failed to improve and remained steady with an estimated glomerular filtration rate of 42 ml/min/1.73 m2. The literature on this topic was reviewed. CONCLUSIONS Cases of renal tubular acidosis should be carefully evaluated to prevent adverse complications, uncover a potentially treatable condition, and prevent the progression to chronic kidney disease. Repeated episodes of unexplained hypokalemia could be an important clue for diagnosis.
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Evidence for biofilm acid neutralization by baking soda.
Zero, DT
Journal of the American Dental Association (1939). 2017;(11S):S10-S14
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BACKGROUND The generating of acids from the microbial metabolism of dietary sugars and the subsequent decrease in biofilm pH below the pH at which tooth mineral begins to demineralize (critical pH) are the key elements of the dental caries process. Caries preventive strategies that rapidly neutralize biofilm acids can prevent demineralization and favor remineralization and may help prevent the development of sugar-induced dysbiosis that shifts the biofilm toward increased cariogenic potential. Although the neutralizing ability of sodium bicarbonate (baking soda) has been known for many years, its anticaries potential as an additive to fluoride dentifrice has received only limited investigation. TYPES OF STUDIES REVIEWED There is evidence that baking soda rapidly can reverse the biofilm pH decrease after a sugar challenge; however, the timing of when it is used in relation to a dietary sugar exposure is critical in that the sooner its used the greater the benefit in preventing a sustained biofilm pH decrease and subsequent demineralization. Furthermore, the effectiveness of baking soda in elevating biofilm pH appears to depend on concentration. Thus, the concentration of baking soda in marketed dentifrice products, which ranges from 10% to 65%, may affect their biofilm pH neutralizing performance. People with hyposalivation particularly may benefit from using fluoride dentifrice containing baking soda because of their diminished ability to clear dietary sugars and buffer biofilm acids. CONCLUSIONS Although promising, there is the need for more evidence that strategies that modify the oral ecology, such as baking soda, can alter the cariogenic (acidogenic and aciduric) properties of biofilm microorganisms. PRACTICAL IMPLICATIONS The acid neutralization of dental biofilm by using fluoride dentifrice that contains baking soda has potential for helping counteract modern high-sugar diets by rapidly neutralizing biofilm-generated acid, especially in people with hyposalivation.
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Meta-Analysis of Individual Patient Data of Sodium Bicarbonate and Sodium Chloride for All-Cause Mortality After Coronary Angiography.
Brown, JR, Pearlman, DM, Marshall, EJ, Alam, SS, MacKenzie, TA, Recio-Mayoral, A, Gomes, VO, Kim, B, Jensen, LO, Mueller, C, et al
The American journal of cardiology. 2016;(10):1473-1479
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We sought to examine the relation between sodium bicarbonate prophylaxis for contrast-associated nephropathy (CAN) and mortality. We conducted an individual patient data meta-analysis from multiple randomized controlled trials. We obtained individual patient data sets for 7 of 10 eligible trials (2,292 of 2,764 participants). For the remaining 3 trials, time-to-event data were imputed based on follow-up periods described in their original reports. We included all trials that compared periprocedural intravenous sodium bicarbonate to periprocedural intravenous sodium chloride in patients undergoing coronary angiography or other intra-arterial interventions. Included trials were determined by consensus according to predefined eligibility criteria. The primary outcome was all-cause mortality hazard, defined as time from randomization to death. In 10 trials with a total of 2,764 participants, sodium bicarbonate was associated with lower mortality hazard than sodium chloride at 1 year (hazard ratio 0.61, 95% confidence interval [CI] 0.41 to 0.89, p = 0.011). Although periprocedural sodium bicarbonate was associated with a reduction in the incidence of CAN (relative risk 0.75, 95% CI 0.62 to 0.91, p = 0.003), there exists a statistically significant interaction between the effect on mortality and the occurrence of CAN (hazard ratio 5.65, 95% CI 3.58 to 8.92, p <0.001) for up to 1-year mortality. Periprocedural intravenous sodium bicarbonate seems to be associated with a reduction in long-term mortality in patients undergoing coronary angiography or other intra-arterial interventions.
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A Brief Review on Toxic Alcohols: Management Strategies.
Hassanian-Moghaddam, H, Zamani, N
Iranian journal of kidney diseases. 2016;(6):344-350
Abstract
The information on burden of alcohol abuse in Iran is scarce. However, the available data show that mortality rates and frequency of its use have increased in the Iranian community. In particular, Iran occupies the 1st rank in the number of outbreak incidents and victims of toxic alcohols such as methanol in the Middle East. Mortality and morbidity of toxic alcohols are high if prompt diagnosis and treatment are not initiated rapidly. On-time diagnosis, proper case finding, and standard treatment have an essential role to reduce mortality and morbidity of toxic alcohols particularly blindness and other physical and psychological disabilities. This review focuses on intoxication with methanol, ethylene glycol, and isopropanol, and their treatment.
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How Strong Is the Evidence for Sodium Bicarbonate to Prevent Contrast-Induced Acute Kidney Injury After Coronary Angiography and Percutaneous Coronary Intervention?
Dong, Y, Zhang, B, Liang, L, Lian, Z, Liu, J, Liang, C, Zhang, S
Medicine. 2016;(7):e2715
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Hydration with sodium bicarbonate is one of the strategies to prevent contrast-induced acute kidney injury (CI-AKI). The purpose of this study was to determine how strong is the evidence for sodium bicarbonate to prevent CI-AKI after coronary angiography (CAG) and/or percutaneous coronary intervention (PCI).We conducted PubMed, EMBASE, and CENTRAL databases to search for randomized controlled trials (RCTs) comparing the efficacy of sodium bicarbonate with sodium chloride to prevent CI-AKI after CAG and/or PCI. Relative risk (RR), standardized mean difference (SMD), or weighted mean difference (WMD) with 95% confidence intervals (CIs) was calculated. Heterogeneity, publication bias, and study quality were evaluated, sensitivity analyses, cumulative analyses, and subgroup analyses were performed. The risk of random errors was assessed by trial sequential analysis (TSA).Sixteen RCTs (3537 patients) met the eligibility criteria. Hydration with sodium bicarbonate showed significant beneficial effects in preventing CI-AKI (RR 0.67; 95% CI: 0.47-0.96, P = 0.029), decreasing the change in serum creatinine (SCr) (SMD -0.31 95% CI: -0.55 to -0.07, P = 0.011) and estimated glomerular filtration rate (eGFR) (SMD -0.17 95% CI: -0.30 to -0.04, P = 0.013). But no significant differences were observed in the requirement for dialysis (RR 1.11; 95% CI: 0.60-2.07, P = 0.729), mortality (RR 0.71; 95% CI: 0.41-1.21, P = 0.204) and reducing the length of hospital stay (LHS) (WMD -1.47; 95% CI: -4.14 to 1.20, P = 0.279). The result of TSA on incidence of CI-AKI showed the required information size (RIS = 6614) was not reached and cumulative z curve did not cross TSA boundary. The result of TSA on the requirement for dialysis and mortality demonstrated the required information sizes (RIS = 170,510 and 19,516, respectively) were not reached, and the cumulative z-curve did not cross any boundaries.The evidence that sodium bicarbonate reduces the incidence of CI-AKI is encouraging but more well-designed randomized controlled trails are required to allow definitive firm conclusion to be drawn.
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Sodium bicarbonate versus isotonic saline solution to prevent contrast-induced nephropathy : a systematic review and meta-analysis.
Zapata-Chica, CA, Bello Marquez, D, Serna-Higuita, LM, Nieto-Ríos, JF, Casas-Arroyave, FD, Donado-Gómez, JH
Colombia medica (Cali, Colombia). 2015;(3):90-103
Abstract
INTRODUCTION Contrast-induced nephropathy is one of the main causes of acute kidney injury and increased hospital-acquired morbidity and mortality. The use of sodium bicarbonate for nephroprotection has emerged as a preventative strategy; however, its efficacy is controversial compared to other strategies, such as hydration using 0.9% saline solution. OBJECTIVE To compare the effectiveness of sodium bicarbonate vs. hydration using 0.9% saline solution to prevent contrast-induced acute kidney injury. METHODS A systematic review of studies registered in the COCHRANE, PUBMED, MEDLINE, LILACS, SCIELO and EMBASE databases was conducted. Randomized controlled studies that evaluated the use of 0.9% saline solution vs. sodium bicarbonate to prevent contrast-induced nephropathy were included. RESULTS A total of 22 studies (5,686 patients) were included. Sodium bicarbonate did not decrease the risk of contrast-induced nephropathy (RD= 0.00; 95% CI= -0.02 to 0.03; p= 0.83; I(2)= 0%). No significant differences were found in the demand for renal replacement therapy (RD= 0.00; 95% CI= -0.01 to 0-01; I(2)= 0%; p= 0.99) or in mortality (RD= -0.00; 95% CI= -0.001 to 0.001; I(2)= 0%; p= 0.51). CONCLUSIONS Sodium bicarbonate administration is not superior to the use of 0.9% saline solution for preventing contrast-induced nephropathy in patients with risk factors, nor is it better at reducing mortality or the need for renal replacement therapy.