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Advances in Chronic Kidney Disease Jul 2022Metabolic acidosis is common in people with chronic kidney disease and can contribute to functional decline, morbidity, and mortality. One avenue through which metabolic... (Review)
Review
Metabolic acidosis is common in people with chronic kidney disease and can contribute to functional decline, morbidity, and mortality. One avenue through which metabolic acidosis can result in these adverse clinical outcomes is by negatively impacting skeletal muscle; this can occur through several pathways. First, metabolic acidosis promotes protein degradation and impairs protein synthesis, which lead to muscle breakdown. Second, metabolic acidosis hinders mitochondrial function, which decreases oxidative phosphorylation and reduces energy production. Third, metabolic acidosis directly limits muscle contraction. The purpose of this review is to examine the specific mechanisms of each pathway through which metabolic acidosis affects muscle, the impact of metabolic acidosis on physical function, and the effect of treating metabolic acidosis on functional outcomes.
Topics: Acidosis; Humans; Muscles; Renal Insufficiency, Chronic
PubMed: 36175077
DOI: 10.1053/j.ackd.2022.04.010 -
The Journal of the Association of... Apr 2018Mortality associated with methanol has been of great concern time and again. The concurrence of cases from a particular area raises doubts about methanol as the culprit....
Mortality associated with methanol has been of great concern time and again. The concurrence of cases from a particular area raises doubts about methanol as the culprit. Knowledge of the patho-physiological changes that occur in the body after methanol consumption is essential for all practicing doctors. This article elucidates the clinical presentation and emergency management of these cases under the framework of basic physiological and biochemical phenomena after methanol exposure. Conversion of methanol to formaldehyde by hepatic enzyme alcohol dehydrogenase triggers the cascade of metabolic events. The manifestations begin as early as 30 minutes and progress to decompensated metabolic acidosis in about 12 hours, if left untreated. Seizures, hypoglycemia and blindness frequently complicate the picture. Acute kidney injury warrants urgent haemodialysis. Fundoscopic examination and arterial blood gas analysis are the key diagnostic elements. The management comprises of intravenous sodium bicarbonate, correction of dyselectrolytemia, ethanol, folic acid and haemodialysis, if necessary. The basic steps in approach must be carried out in the emergency department and followed-up with meticulous monitoring in the intensive care unit for salvage as well as prevention of long term sequelae.
Topics: Acidosis; Alcoholism; Ethanol; Humans; Methanol; Sodium Bicarbonate
PubMed: 30347953
DOI: No ID Found -
Advances in Chronic Kidney Disease Jul 2022The various mechanisms responsible for the development of metabolic acidosis are briefly reviewed, and the metabolic acidoses are categorized both by mechanism and by... (Review)
Review
The various mechanisms responsible for the development of metabolic acidosis are briefly reviewed, and the metabolic acidoses are categorized both by mechanism and by the presence or absence of an increased anion gap. When a diagnosis of metabolic acidosis is established, it becomes imperative to identify the primary causative etiology as quickly as possible. This is often readily apparent from the history and physical exam (ie, diabetic ketoacidosis when the glucose is very high in a patient with diabetes mellitus; lactic acidosis in a patient with sepsis and hypotension, etc.). However, when the etiology is not obvious, it is very helpful to determine if the metabolic acidosis is of the hyperchloremic or high-anion-gap type (or a combination of both). Once this categorization has been established, a stepwise consideration of each of the potential causative etiologies will usually direct the clinician to order the appropriate diagnostic studies.
Topics: Acid-Base Imbalance; Acidosis; Anions; Glucose; Humans; Physical Examination
PubMed: 36175073
DOI: 10.1053/j.ackd.2022.07.004 -
Annals of Hepatology 2022In addition to the kidneys and lungs, the liver also plays an important role in the regulation of the Acid-Base Equilibrium (ABE). The involvement of the liver in the... (Review)
Review
In addition to the kidneys and lungs, the liver also plays an important role in the regulation of the Acid-Base Equilibrium (ABE). The involvement of the liver in the regulation of ABE is crucial because of its role in lactic acid metabolism, urea production and in protein homeostasis. The main acid-base imbalance that occurs in patients with liver cirrhosis is Respiratory Alkalosis (RAlk). Due to the fact that in these patients additional pathophysiological mechanisms that affect the ABE are present, other disorders may appear which compensate or enhance the primary disorder. Conventional ABE reading models fail to identify and assess the underlying disorders in patients with liver cirrhosis. This weakness of the classical models led to the creation of new physicochemical mathematical models that take into account all the known parameters that develop and affect the ABE. In addition to the RAlk, in patients with liver cirrhosis, metabolic alkalosis (due to hypoalbuminemia), hyponatremic metabolic acidosis, hyperchloremic metabolic acidosis, lactic acidosis and metabolic alkalosis due to urea metabolism are some of the pathophysiological mechanisms that affect the ABE.
Topics: Acidosis; Alkalosis; Humans; Liver Cirrhosis; Liver Diseases; Urea
PubMed: 35074477
DOI: 10.1016/j.aohep.2022.100675 -
BMJ Case Reports Feb 2024Linezolid is a commonly prescribed antibiotic in clinical practice. Although thrombocytopenia and peripheral neuropathy are frequently encountered following prolonged...
Linezolid is a commonly prescribed antibiotic in clinical practice. Although thrombocytopenia and peripheral neuropathy are frequently encountered following prolonged administration of linezolid, lactic acidosis is a rare adverse drug reaction. We present the case of a patient on linezolid for disseminated multidrug-resistant tuberculosis who presented with vomiting, dyspnoea, hypotension and high anion gap metabolic acidosis. The initial presentation mimicked sepsis syndrome. Ketoacidosis and renal dysfunction were ruled out. There was no history of ingestion of toxins/toxic alcohols. Sepsis was unlikely because extensive radiological and microbiological testing could not identify an infection. Given the possibility of linezolid-induced lactic acidosis (LILA), linezolid was discontinued on admission. The patient's lactic acidosis resolved, and his overall condition improved. A retrospective diagnosis of LILA was thus established. LILA should be considered when patients on linezolid present with lactic acidosis and other causes for the lactic acidosis have been ruled out.
Topics: Humans; Linezolid; Acidosis, Lactic; Retrospective Studies; Anti-Bacterial Agents; Acidosis
PubMed: 38331448
DOI: 10.1136/bcr-2023-259335 -
Biomedicine & Pharmacotherapy =... Feb 2023Metabolic acidosis is frequent in chronic kidney disease (CKD) and is associated with accelerated progression of CKD, hypercatabolism, bone disease, hyperkalemia, and... (Review)
Review
Metabolic acidosis is frequent in chronic kidney disease (CKD) and is associated with accelerated progression of CKD, hypercatabolism, bone disease, hyperkalemia, and mortality. Clinical guidelines recommend a target serum bicarbonate ≥ 22 mmol/L, but metabolic acidosis frequently remains undiagnosed and untreated. Sodium zirconium cyclosilicate (SZC) binds potassium in the gut and is approved to treat hyperkalemia. In clinical trials with a primary endpoint of serum potassium, SZC increased serum bicarbonate, thus treating CKD-associated metabolic acidosis. The increase in serum bicarbonate was larger in patients with more severe pre-existent metabolic acidosis, was associated to decreased serum urea and was maintained for over a year of SZC therapy. SZC also decreased serum urea and increased serum bicarbonate after switching from a potassium-binding resin in normokalemic individuals. Mechanistically, these findings are consistent with SZC binding the ammonium ion (NH) generated from urea by gut microbial urease, preventing its absorption and, thus, preventing the liver regeneration of urea and promoting the fecal excretion of H. This mechanism of action may potentially result in benefits dependent on corrected metabolic acidosis (e.g., improved well-being, decreased catabolism, improved CKD mineral bone disorder, better control of serum phosphate, slower progression of CKD) and dependent on lower urea levels, such as decreased protein carbamylation. A roadmap is provided to guide research into the mechanisms and clinical consequences of the impact of SZC on serum bicarbonate and urate.
Topics: Humans; Hyperkalemia; Bicarbonates; Acidosis; Potassium; Renal Insufficiency, Chronic
PubMed: 36916426
DOI: 10.1016/j.biopha.2022.114197 -
Advances in Chronic Kidney Disease Jul 2022Eating a net acid-producing diet can produce an "acid stress" of severity proportional to the diet net acid load, as indexed by the steady-state renal net acid excretion... (Review)
Review
Eating a net acid-producing diet can produce an "acid stress" of severity proportional to the diet net acid load, as indexed by the steady-state renal net acid excretion rate. Depending on how much acid or base is ingested or produced from endogenous metabolic processes and how well our homeostatic mechanisms can buffer or eliminate the additional acids or bases, we can alter our systemic acid-base balance. With increasing age, the kidney's ability to excrete daily net acid loads declines (a condition similar to that of mild CKD), invoking increased utilization of potential base stores (eg, bone, skeletal muscle) on a daily basis to mitigate the acid accumulation, thereby contributing to development of osteoporosis, loss of muscle mass, and age-related renal insufficiency. Patients suffering from more advanced CKD often present with more severe acid stress or metabolic acidosis, as the kidney can no longer excrete the entire acid load. Alkaline diets based on fruits and vegetables may have a positive effect on long-term preservation of renal function while maintaining nutritional status. This chapter discusses the biochemistry of dietary precursors that affect acid or base production.
Topics: Acid-Base Equilibrium; Acidosis; Diet; Humans; Renal Insufficiency, Chronic; Vegetables
PubMed: 36175075
DOI: 10.1053/j.ackd.2022.03.008 -
Advances in Chronic Kidney Disease Jul 2022
Topics: Acidosis; Humans
PubMed: 36175069
DOI: 10.1053/j.ackd.2022.07.008 -
Clinical Journal of the American... Feb 2021
Topics: Acidosis; Ammonium Compounds; Animals; Bicarbonates; Citric Acid; Disease Progression; Humans; Hydrogen-Ion Concentration; Renal Insufficiency, Chronic
PubMed: 32769096
DOI: 10.2215/CJN.07990520 -
International Journal of Molecular... May 2024Metabolic acidosis is a frequent complication of chronic kidney disease and is associated with a number of adverse outcomes, including worsening kidney function, poor... (Review)
Review
Metabolic acidosis is a frequent complication of chronic kidney disease and is associated with a number of adverse outcomes, including worsening kidney function, poor musculoskeletal health, cardiovascular events, and death. Mechanisms that prevent metabolic acidosis detrimentally promote further kidney damage, creating a cycle between acid accumulation and acid-mediated kidney injury. Disrupting this cycle through the provision of alkali, most commonly using sodium bicarbonate, is hypothesized to preserve kidney function while also mitigating adverse effects of excess acid on bone and muscle. However, results from clinical trials have been conflicting. There is also significant interest to determine whether sodium bicarbonate might improve patient outcomes for those who do not have overt metabolic acidosis. Such individuals are hypothesized to be experiencing acid-mediated organ damage despite having a normal serum bicarbonate concentration, a state often referred to as subclinical metabolic acidosis. Results from small- to medium-sized trials in individuals with subclinical metabolic acidosis have also been inconclusive. Well-powered clinical trials to determine the efficacy and safety of sodium bicarbonate are necessary to determine if this intervention improves patient outcomes.
Topics: Humans; Acidosis; Renal Insufficiency, Chronic; Sodium Bicarbonate; Animals; Treatment Outcome
PubMed: 38791238
DOI: 10.3390/ijms25105187