-
International Journal of Molecular... Feb 2024Diets can influence the body's acid-base status because specific food components yield acids, bases, or neither when metabolized. Animal-sourced foods yield acids and... (Review)
Review
Diets can influence the body's acid-base status because specific food components yield acids, bases, or neither when metabolized. Animal-sourced foods yield acids and plant-sourced food, particularly fruits and vegetables, generally yield bases when metabolized. Modern diets proportionately contain more animal-sourced than plant-sourced foods, are, thereby, generally net acid-producing, and so constitute an ongoing acid challenge. Acid accumulation severe enough to reduce serum bicarbonate concentration, i.e., manifesting as chronic metabolic acidosis, the most extreme end of the continuum of "acid stress", harms bones and muscles and appears to enhance the progression of chronic kidney disease (CKD). Progressive acid accumulation that does not achieve the threshold amount necessary to cause chronic metabolic acidosis also appears to have deleterious effects. Specifically, identifiable acid retention without reduced serum bicarbonate concentration, which, in this review, we will call "covert acidosis", appears to cause kidney injury and exacerbate CKD progression. Furthermore, the chronic engagement of mechanisms to mitigate the ongoing acid challenge of modern diets also appears to threaten health, including kidney health. This review describes the full continuum of "acid stress" to which modern diets contribute and the mechanisms by which acid stress challenges health. Ongoing research will develop clinically useful tools to identify stages of acid stress earlier than metabolic acidosis and determine if dietary acid reduction lowers or eliminates the threats to health that these diets appear to cause.
Topics: Animals; Bicarbonates; Acid-Base Equilibrium; Diet; Acidosis; Renal Insufficiency, Chronic
PubMed: 38397012
DOI: 10.3390/ijms25042336 -
Praxis 2018CME: Ethylene Glycol Intoxication Abstract. Ethylene glycol is a sweet-tasting alcohol used in common antifreeze and other industrial solutions. Without appropriate... (Review)
Review
CME: Ethylene Glycol Intoxication Abstract. Ethylene glycol is a sweet-tasting alcohol used in common antifreeze and other industrial solutions. Without appropriate therapy, intoxication with ethylene glycol can result in severe metabolic acidosis, acute renal failure, and in death. After gastrointestinal resorption, hepatic metabolism starts with oxidation by alcohol dehydrogenase and results in severe anion gap metabolic acidosis. Other metabolic products are calcium oxalate crystals, which can deposit in several tissues like the kidneys and lead to acute tubular necrosis with reversible renal failure. The crucial therapeutic step is rapid inhibition of alcohol dehydrogenase with fomepizole or ethanol to avoid the formation of toxic metabolites. Additionally, haemodialysis is the most effective way to eliminate ethylene glycol as well as its toxic metabolites. If therapy is initiated rapidly, prognosis is favorable.
Topics: Acid-Base Equilibrium; Acidosis; Acute Kidney Injury; Adult; Combined Modality Therapy; Critical Care; Diagnosis, Differential; Early Diagnosis; Early Medical Intervention; Emergency Service, Hospital; Ethylene Glycol; Humans; Kidney Cortex Necrosis; Male; Renal Dialysis; Suicide, Attempted
PubMed: 30278847
DOI: 10.1024/1661-8157/a003071 -
Jornal Brasileiro de Nefrologia 2017Metabolic acidosis is highly prevalent in hemodialysis patients. The disorder is associated with increased mortality and its deleterious effects are already present in... (Review)
Review
Metabolic acidosis is highly prevalent in hemodialysis patients. The disorder is associated with increased mortality and its deleterious effects are already present in the predialysis phase of chronic kidney disease. Metabolic acidosis has been linked to progression of chronic kidney disease, changes in protein and glucose metabolism, bone and muscle disorders and cardiovascular disease. At present, the control of metabolic acidosis in hemodialysis is mainly focused on the supply of bicarbonate during dialysis session, but further studies are needed to set the optimum target serum bicarbonate and the best concentration of the bicarbonate dialysate. The present study reviews pathophysiological and epidemiological aspects of metabolic acidosis in hemodialysis patients and also addresses its adverse effects and treatment.
Topics: Acidosis; Humans; Kidney Failure, Chronic; Renal Dialysis
PubMed: 29044339
DOI: 10.5935/0101-2800.20170053 -
Journal of the American Society of... Mar 2015Metabolic acidosis was one of the earliest complications to be recognized and explained pathologically in patients with CKD. Despite the accumulated evidence of... (Review)
Review
Metabolic acidosis was one of the earliest complications to be recognized and explained pathologically in patients with CKD. Despite the accumulated evidence of deleterious effects of acidosis, treatment of acidosis has been tested very little, especially with respect to standard clinical outcomes. On the basis of fundamental research and small alkali supplementation trials, correcting metabolic acidosis has a strikingly broad array of potential benefits. This review summarizes the published evidence on the association between serum bicarbonate and clinical outcomes. We discuss the role of alkali supplementation in CKD as it relates to retarding kidney disease progression, improving metabolic and musculoskeletal complications.
Topics: Acidosis; Alkalies; Animals; Bicarbonates; Cardiovascular Diseases; Dietary Supplements; Humans; Renal Insufficiency, Chronic
PubMed: 25150154
DOI: 10.1681/ASN.2014020205 -
Nutrients May 2017Low-grade metabolic acidosis is a condition characterized by a slight decrease in blood pH, within the range considered normal, and feeding is one of the main factors... (Review)
Review
Low-grade metabolic acidosis is a condition characterized by a slight decrease in blood pH, within the range considered normal, and feeding is one of the main factors that may influence the occurrence of such a condition. The excessive consumption of acid precursor foods (sources of phosphorus and proteins), to the detriment of those precursors of bases (sources of potassium, calcium, and magnesium), leads to acid-base balance volubility. If this condition occurs in a prolonged, chronic way, low-grade metabolic acidosis can become significant and predispose to metabolic imbalances such as kidney stone formation, increased bone resorption, reduced bone mineral density, and the loss of muscle mass, as well as the increased risk of chronic diseases such as type 2 diabetes mellitus, hypertension, and non-alcoholic hepatic steatosis. Considering the increase in the number of studies investigating the influence of diet-induced metabolic acidosis on clinical outcomes, this review gathers the available evidence evaluating the association of this disturbance and metabolic imbalances, as well as related mechanisms. It is necessary to look at the western dietary pattern of most countries and the increasing incidence of non-comunicable diseases for the balance between fruit and vegetable intake and the appropriate supply of protein, mainly from animal sources, so that it does not exceed the daily recommendations.
Topics: Acidosis; Diet; Humans; Noncommunicable Diseases
PubMed: 28587067
DOI: 10.3390/nu9060538 -
The Journal of Surgical Research Apr 2018Acid-base disorders are frequently present in critically ill patients. Metabolic acidosis is associated with increased mortality, but it is unclear whether as a marker... (Review)
Review
Acid-base disorders are frequently present in critically ill patients. Metabolic acidosis is associated with increased mortality, but it is unclear whether as a marker of the severity of the disease process or as a direct effector. The understanding of the metabolic component of acid-base derangements has evolved over time, and several theories and models for precise quantification and interpretation have been postulated during the last century. Unmeasured anions are the footprints of dissociated fixed acids and may be responsible for a significant component of metabolic acidosis. Their nature, origin, and prognostic value are incompletely understood. This review provides a historical overview of how the understanding of the metabolic component of acid-base disorders has evolved over time and describes the theoretical models and their corresponding tools applicable to clinical practice, with an emphasis on the role of unmeasured anions in general and several specific settings.
Topics: Acidosis; Adult; Anions; Critical Illness; Humans; Intensive Care Units; Prognosis; Wounds and Injuries
PubMed: 29506851
DOI: 10.1016/j.jss.2017.11.013 -
Nephrology, Dialysis, Transplantation :... May 2023Guidelines recommend treatment of metabolic acidosis (MA) in patients with chronic kidney disease (CKD), but the diagnosis and treatment rates in real-world settings are...
BACKGROUND
Guidelines recommend treatment of metabolic acidosis (MA) in patients with chronic kidney disease (CKD), but the diagnosis and treatment rates in real-world settings are unknown. We investigated the frequency of MA treatment and diagnosis in patients with CKD.
METHODS
In this retrospective cohort study, we examined administrative health data from two US databases [Optum's de-identified Integrated Claims + Clinical Electronic Health Record Database (US EMR cohort; 1 January 2007 to 30 June 2019) and Symphony Health Solutions IDV® (US claims cohort; 1 May 2016 to 30 April 2019)] and population-level databases from Manitoba, Canada (1 April 2006 to 31 March 2018). Patients who met laboratory criteria indicative of CKD and chronic MA were included: two consecutive estimated glomerular filtration results <60 mL/min/1.73 m2 and two serum bicarbonate results 12 to <22 mEq/L over 28-365 days. Outcomes included treatment of MA (defined as a prescription for oral sodium bicarbonate) and a diagnosis of MA (defined using administrative records). Outcomes were assessed over a 3-year period (1 year pre-index, 2 years post-index).
RESULTS
A total of 96 184 patients were included: US EMR, 6179; Manitoba, 3223; US Claims, 86 782. Sodium bicarbonate treatment was prescribed for 17.6%, 8.7% and 15.3% of patients, and a diagnosis was found for 44.7%, 20.9% and 20.9% of patients, for the US EMR, Manitoba and US Claims cohorts, respectively.
CONCLUSIONS
This analysis of 96 184 patients with laboratory-confirmed MA from three independent cohorts of patients with CKD and MA highlights an important diagnosis and treatment gap for this disease-modifying complication.
Topics: Humans; Sodium Bicarbonate; Retrospective Studies; Acidosis; Renal Insufficiency, Chronic; Bicarbonates
PubMed: 36323446
DOI: 10.1093/ndt/gfac299 -
American Journal of Kidney Diseases :... Feb 2016The kidney has the principal role in the maintenance of acid-base balance. Therefore, a decrease in renal ammonium excretion and a positive acid balance often leading to... (Review)
Review
The kidney has the principal role in the maintenance of acid-base balance. Therefore, a decrease in renal ammonium excretion and a positive acid balance often leading to a reduction in serum bicarbonate concentration are observed in the course of chronic kidney disease (CKD). The decrease in serum bicarbonate concentration is usually absent until glomerular filtration rate decreases to <20 to 25mL/min/1.73 m(2), although it can develop with lesser degrees of decreased kidney function. Non-anion gap acidosis, high-anion gap acidosis, or both can be found at all stages of CKD. The acidosis can be associated with muscle wasting, bone disease, hypoalbuminemia, inflammation, progression of CKD, and increased mortality. Administration of base may decrease muscle wasting, improve bone disease, and slow the progression of CKD. Base is suggested when serum bicarbonate concentration is <22 mEq/L, but the target serum bicarbonate concentration is unclear. Evidence that increments in serum bicarbonate concentration > 24 mEq/L might be associated with worsening of cardiovascular disease adds complexity to treatment decisions. Further study of the mechanisms through which metabolic acidosis contributes to the progression of CKD, as well as the pathways involved in mediating the benefits and complications of base therapy, is warranted.
Topics: Acid-Base Equilibrium; Acidosis; Animals; Bicarbonates; Disease Progression; Glomerular Filtration Rate; Humans; Kidney; Renal Insufficiency, Chronic
PubMed: 26477665
DOI: 10.1053/j.ajkd.2015.08.028 -
Kidney & Blood Pressure Research 2020Metabolic acidosis may be diagnosed as chronic (cMA) if it persists for at least 5 days, although an exact definition has not been provided by any guidelines yet. The... (Review)
Review
BACKGROUND
Metabolic acidosis may be diagnosed as chronic (cMA) if it persists for at least 5 days, although an exact definition has not been provided by any guidelines yet. The most common cause is CKD; numerous less-known diseases can also account for cMA.
SUMMARY
In recent years, CKD-associated cMA has been proposed to induce several clinical complications. The aim of the article was to assess the current clinical evidence for complications and the respective management of CKD-associated cMA. In summary, cMA in CKD most likely promotes protein degradation and loss of bone mineral density. It aggravates CKD progression as indicated by experimental and (partly) clinical data. Therefore, cMA control must be recommended. Besides oral bicarbonate, dietary interventions potentially offer an alternative. Veverimer is a future option for cMA control; further systematic data are needed.
CONCLUSIONS
The most common cause of cMA is CKD. CKD-associated cMA most likely induces a negative protein balance; the exact role on bone metabolism remains uncertain. It presumably aggravates CKD progression. cMA control is recommendable; the serum bicarbonate target level should range around 24 mEq/L. Veverimer may be established as future option for cMA control; further systematic data are needed.
Topics: Acidosis; Animals; Bicarbonates; Bone Density; Chronic Disease; Diet Therapy; Disease Management; Humans; Polymers; Proteolysis; Renal Insufficiency, Chronic
PubMed: 33264780
DOI: 10.1159/000510829 -
The Veterinary Clinics of North... Mar 2017Metabolic acidosis results from an increase in the concentration of a strong anion. Metabolic acidosis is divided into hyperchloremic metabolic acidosis and high anion... (Review)
Review
Metabolic acidosis results from an increase in the concentration of a strong anion. Metabolic acidosis is divided into hyperchloremic metabolic acidosis and high anion gap acidosis based on the changes in the anion gap. Hyperchloremic metabolic acidosis is the result of chloride retention, excessive loss of sodium relative to chloride, or excessive gain of chloride relative to sodium. Clinical signs are related to the underlying disease that accompanies the metabolic acidosis. Treatment of hyperchloremic acidosis is based on addressing the underlying disease process.
Topics: Acid-Base Equilibrium; Acidosis; Animals; Chlorides; Renal Insufficiency, Chronic
PubMed: 28017409
DOI: 10.1016/j.cvsm.2016.11.001