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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 -
Actas Urologicas Espanolas May 2023Urine contact with the mucosa of the urinary diversion (UD) after radical cystectomy (RC) produces different ion exchanges that favor the development of metabolic... (Review)
Review
Urine contact with the mucosa of the urinary diversion (UD) after radical cystectomy (RC) produces different ion exchanges that favor the development of metabolic acidosis (MA). This phenomenon is a frequent cause of hospital readmission and short/long-term complications. We performed a systematic review of MA in RCs with ileal UD, analyzing its prevalence, diagnosis, risk factors and treatment. We systematically searched Pubmed® and Cochrane Library for original articles published before May 2022 according to PRISMA guidelines. A total of 421 articles were identified. We selected 25 studies that met the inclusion criteria involving 5811 patients. Obtaining precise data on the prevalence of MA is difficult, largely due to the heterogeneity of the diagnostic criteria used given the diversity of studies analyzed. Development of MA is multifactorial. In the early period, MA is more prevalent in patients with UD with longer ileal segments, better urinary continence, and impaired renal function. Age and diabetes are risk factors associated with MA in later periods. MA is the most common cause of second or more hospital readmissions. Prophylaxis with oral bicarbonate for three months in patients at risk could improve these results. Although MA after ileal UD is a well-known condition, this review highlights the need to implement homogeneous criteria for the diagnosis, follow-up, and treatment, in addition to protocolizing prevention/prophylaxis strategies in patients at risk.
Topics: Humans; Cystectomy; Urinary Bladder Neoplasms; Urinary Bladder; Urinary Diversion; Acidosis
PubMed: 36427800
DOI: 10.1016/j.acuroe.2022.11.005 -
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 -
Jornal de Pediatria May 2007To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related... (Review)
Review
OBJECTIVES
To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies.
SOURCES
Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines.
SUMMARY OF THE FINDINGS
There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies.
CONCLUSIONS
Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease and the mechanisms generating metabolic acidemia. Other promising treatment alternatives have been proposed; however, the side effects and absence of controlled studies with pediatric populations translate into lack of evidence to support the routine use of such treatments.
Topics: Acidosis; Acidosis, Lactic; Cardiopulmonary Resuscitation; Child; Diabetic Ketoacidosis; Humans; Randomized Controlled Trials as Topic; Sodium Bicarbonate
PubMed: 17508091
DOI: 10.2223/JPED.1616 -
Clinical Journal of the American... Jan 2023Acid-base disorders are common in the intensive care unit. By utilizing a systematic approach to their diagnosis, it is easy to identify both simple and mixed...
Acid-base disorders are common in the intensive care unit. By utilizing a systematic approach to their diagnosis, it is easy to identify both simple and mixed disturbances. These disorders are divided into four major categories: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Metabolic acidosis is subdivided into anion gap and non-gap acidosis. Distinguishing between these is helpful in establishing the cause of the acidosis. Anion gap acidosis, caused by the accumulation of organic anions from sepsis, diabetes, alcohol use, and numerous drugs and toxins, is usually present on admission to the intensive care unit. Lactic acidosis from decreased delivery or utilization of oxygen is associated with increased mortality. This is likely secondary to the disease process, as opposed to the degree of acidemia. Treatment of an anion gap acidosis is aimed at the underlying disease or removal of the toxin. The use of therapy to normalize the pH is controversial. Non-gap acidoses result from disorders of renal tubular H + transport, decreased renal ammonia secretion, gastrointestinal and kidney losses of bicarbonate, dilution of serum bicarbonate from excessive intravenous fluid administration, or addition of hydrochloric acid. Metabolic alkalosis is the most common acid-base disorder found in patients who are critically ill, and most often occurs after admission to the intensive care unit. Its etiology is most often secondary to the aggressive therapeutic interventions used to treat shock, acidemia, volume overload, severe coagulopathy, respiratory failure, and AKI. Treatment consists of volume resuscitation and repletion of potassium deficits. Aggressive lowering of the pH is usually not necessary. Respiratory disorders are caused by either decreased or increased minute ventilation. The use of permissive hypercapnia to prevent barotrauma has become the standard of care. The use of bicarbonate to correct the acidemia is not recommended. In patients at the extreme, the use of extracorporeal therapies to remove CO 2 can be considered.
Topics: Humans; Bicarbonates; Critical Illness; Acidosis; Acid-Base Equilibrium; Acid-Base Imbalance; Alkalosis
PubMed: 35998977
DOI: 10.2215/CJN.04500422 -
Advances in Chronic Kidney Disease Sep 2017Subjects with CKD and reduced glomerular filtration rate are at risk for chronic metabolic acidosis, and CKD is its most common cause. Untreated metabolic acidosis, even... (Review)
Review
Subjects with CKD and reduced glomerular filtration rate are at risk for chronic metabolic acidosis, and CKD is its most common cause. Untreated metabolic acidosis, even in its mildest forms, is associated with increased mortality and morbidity and should therefore be treated. If reduced glomerular filtration rate or the tubule abnormality causing chronic metabolic acidosis cannot be corrected, it is typically treated with dietary acid (H) reduction using Na-based alkali, usually NaHCO. Dietary H reduction can also be accomplished with the addition of base-producing foods such as fruits and vegetables and limiting intake of H-producing foods like animal-sourced protein. The optimal dose of Na-based alkali that prevents the untoward effects of metabolic acidosis while minimizing adverse effects and the appropriate combination of this traditional therapy with dietary strategies remain to be determined by ongoing studies. Recent emerging evidence supports a phenomenon of H retention, which precedes the development of metabolic acidosis by plasma acid-base parameters, but further studies will be needed to determine how best to identify patients with this phenomenon and whether they too should be treated with dietary H reduction.
Topics: Acid-Base Equilibrium; Acidosis; Acidosis, Renal Tubular; Animals; Bicarbonates; Diet; Dietary Proteins; Fruit; Glomerular Filtration Rate; Humans; Renal Insufficiency, Chronic; Sodium Bicarbonate; Vegetables
PubMed: 29031356
DOI: 10.1053/j.ackd.2017.06.006 -
Current Opinion in Critical Care Aug 2003Metabolic acidosis is characterized by a decrease of the blood pH associated with a decrease in the bicarbonate concentration. This may be secondary to a decrease in the... (Review)
Review
Metabolic acidosis is characterized by a decrease of the blood pH associated with a decrease in the bicarbonate concentration. This may be secondary to a decrease in the strong ion difference or to an increase in the weak acids concentration, mainly the inorganic phosphorus. From a conceptual point of view, two types of nontoxic metabolic acidosis must be differentiated: the mineral metabolic acidosis that reveals the presence of an excess of nonmetabolizable anions, and the organic metabolic acidosis that reveals an excess of metabolizable anions. Significance and consequences of these two types of acidosis are radically different. Mineral acidosis is not caused by a failure in the energy metabolic pathways, and its treatment is mainly symptomatic by correcting the blood pH (alkali therapy) or accelerating the elimination of excessive mineral anions (renal replacement therapy). On the other hand, organic acidosis gives evidence that a severe underlying metabolic distress is in process. No reliable argument exists to prove that this acidosis is harmful under these conditions in humans. Experimental data even show that hypoxic cells are able to survive only if the medium is kept acidic. The management of an acute organic metabolic acidosis is therefore primarily based on the cause of the acidosis, and no scientific argument exists to justify the correction of the acid-base imbalance in this context.
Topics: Acidosis; Acute Disease; Bicarbonates; Critical Care; Humans; Hydrogen-Ion Concentration
PubMed: 12883279
DOI: 10.1097/00075198-200308000-00002 -
Advances in Chronic Kidney Disease Jul 2022Chronic kidney disease (CKD) is a major global epidemic associated with increased morbidity and mortality. Despite the effectiveness of kidney protection strategies of... (Review)
Review
Chronic kidney disease (CKD) is a major global epidemic associated with increased morbidity and mortality. Despite the effectiveness of kidney protection strategies of hypertension, diabetes, and lipid control and use of newer hypoglycemic agents and anti-angiotensin II drugs, the nephropathy in CKD continues unabated toward irreversible kidney failure. Thus, interventions targeting modifiable risk factors in CKD such as metabolic acidosis (MA) are needed. Acid reduction with sodium-based alkali has been shown to be an effective kidney-protection strategy for patients with CKD and reduced glomerular filtration rate (GFR). Small-scale studies reveal diets emphasizing ingestion of plant-sourced over animal-sourced protein reduce dietary acid, improve MA, and slow further nephropathy progression in patients with CKD and reduced GFR. Additionally, veverimer, an investigational, nonabsorbed polymer that binds and removes gastrointestinal hydrochloric acid, is being developed as a novel treatment for MA. As further studies define how to best use these interventions for kidney protection, clinicians must become aware of their potential utility in the management of patients with CKD. The aim of the present review is to explore the various intervention strategies that increase or normalize serum [HCO] in patients with CKD-associated MA or low normal serum [HCO] that may further slow progression of CKD.
Topics: Acidosis; Alkalies; Animals; Humans; Hydrochloric Acid; Hypoglycemic Agents; Lipids; Renal Insufficiency; Renal Insufficiency, Chronic; Sodium
PubMed: 36175079
DOI: 10.1053/j.ackd.2022.02.011 -
Deutsche Medizinische Wochenschrift... Nov 2020Acid-base disorders due to different etiologies are frequently encountered in daily clinical practice and may result in life-threatening situations. Basic knowledge of...
Acid-base disorders due to different etiologies are frequently encountered in daily clinical practice and may result in life-threatening situations. Basic knowledge of the diagnostic and therapeutic approach of acid-base disorders is therefore essential for every clinician. Acid-base disorders should be treated according to their underlying etiology. Therefore, diagnosis of the underlying etiology is the critical step in the process of care for patients with acid-base disorders. Undirected buffering with HCO should be avoided, since the application of HCO might lead to severe side effects. A strict diagnostic pathway for the diagnosis of acid-base disorders is required, which should be vigorously applied:- analysis of the pH to classify acidemia or alkalemia- analysis of pCO and HCO to classify the primary acid base disorder- analysis of the adequate regulation in order to detect additional acid-base disorders- analysis of the anion gap and the relationship of the anion gap vs. the change in HCO to detect further metabolic disordersMetabolic acidosis can be divided into two main etiologies:- acidosis with addition of acid with increased anion gap,- acidosis with loss of HCO with normal anion gap.
Topics: Acid-Base Equilibrium; Acidosis; Bicarbonates; Humans
PubMed: 33142331
DOI: 10.1055/a-0670-6038 -
Der Urologe. Ausg. A May 2021In cystectomy patients who underwent neobladder creation, the intestinal mucosa of the neobladder is in constant contact with urine, which may result in chronic... (Review)
Review
BACKGROUND
In cystectomy patients who underwent neobladder creation, the intestinal mucosa of the neobladder is in constant contact with urine, which may result in chronic metabolic acidosis (CMA) due to specific absorption capabilities of the intestinal mucosa. Despite being a prevalent comorbidity, the risk factors for CMA and its diagnostic parameters are poorly understood.
OBJECTIVES
This review examines the risk factors associated with the development of CMA and their prevalence in patients with a neobladder.
MATERIALS AND METHODS
We conducted a systematic literature search using the PubMed database to detect studies about the topics CMA and neobladder that were published between 2000 and 2020. The prevalence and risk factors for CMA in neobladder patients were assessed by reviewing 23 studies.
RESULTS
Acidosis is most prevalent during the first year after surgery (25-70%). Risk factors are renal failure, high continence, old age and diabetes mellitus.
CONCLUSIONS
The prevalence of CMA is at its highest during the early postoperative period for neobladder patients, so for this time period, weekly diagnostic investigations are recommended according to the German S3-guidelines for the "Früherkennung, Diagnose, Therapie und Nachsorge des Harnblasenkarzinomsent für Neoblasepatienten". Blood gas tests should not only be used to analyze the pH value but also to detect and counteract acid-base imbalance issues in time. The recommended normalization of serum bicarbonate levels with oral bicarbonate follows patient-specific therapy strategies.
Topics: Acidosis; Bicarbonates; Cystectomy; Humans; Risk Factors; Urinary Bladder Neoplasms; Urinary Diversion
PubMed: 33884463
DOI: 10.1007/s00120-021-01523-7