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Metabolic Acidosis Review

Metabolic Acidosis In Hemodialysis Patients: A Review

Metabolic Acidosis In Hemodialysis Patients: A Review

Metabolic acidosis in hemodialysis patients: a 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. Keywords:acidosis; renal dialysis; bicarbonates End-stage renal disease (ESRD), which can be treated by either dialysis or transplantation, is a worldwide public health problem. Its incidence has increased in recent years, causing substantial economic burden to health care systems in the world. 1 , 2 Of note, the mortality of dialysis patients remains elevated compared to general population with approximately half of the patients dying from cardiovascular disease. 3 In Brazil, for example, according to the Brazilian Survey of Chronic Dialysis of 2014, the estimated total number of dialysis patients was 100,397. National estimates of the rates of prevalence and incidence of dialysis were 499 and 170 patients per million people, respectively. The annual rate of crude mortality was 17.9%. The absolute number of dialysis patients has increased 3% annually over the past three years. 4 The presence of metab Continue reading >>

Review. Perioperative Management Of Lactic Acidosis In End-stage Liver Disease Patient

Review. Perioperative Management Of Lactic Acidosis In End-stage Liver Disease Patient

Review. Perioperative Management of Lactic Acidosis in End-Stage Liver Disease Patient Lactic acidosis (LA) in end-stage liver disease (ESLD) patients has been recognized as one of the most complicated clinical problems and is associated with increased morbidity and mortality. Multiple-organ failure, associated with advanced stages of cirrhosis, exacerbates dysfunction of numerous parts of lactate metabolism cycle, which manifests as increased lactate production and impaired clearance, leading to severe LA-induced acidemia. These problems become especially prominent in ESLD patients, that undergo partial hepatectomy and, particularly, liver transplantation. Perioperative management of LA and associated severe acidemia is an inseparable part of anesthesia, post-operative and critical care for this category of patients, presenting a wide variety of challenges. In this review, lactic acidosis applied pathophysiology, clinical implications for ESLD patients, diagnosis, role of intraoperative factors, such as anesthesia- and surgery-related, vasoactive agents impact, and also current treatment options and modalities have been discussed. 1. Kreisberg RA. Lactate Homeostasis and Lactic Acidosis, Ann. of Int. Med. 1980;92: 227-237. 2. Gunnerson KJ1, Saul M, He S, Kellum JA. Lactate versus nonlactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients Crit Care 2006; 10:R22. 3. Cohen RD, Woods HF. Clinical and biochemical aspects of lactic acidosis. Blackwell Scientific Publication, Oxford, 1976 pp.46-64. 4. Kraut J., Madias N. Lactic Acidosis N Engl J Med. 2014 Dec 11;371:2309-19. 5. Jeppesen JB, Mortensen C, Bendtsen F, Mller S. Lactate metabolism in chronic liver disease. Scand J Clin Lab Invest Scand J Clin Lab Invest. 2013;73:293-9. 6. Bakker Continue reading >>

A Comprehensive Review Of Metabolic Acidosis

A Comprehensive Review Of Metabolic Acidosis

A comprehensive review of metabolic acidosis Summarized from Kraut J, Madias N. Metabolic acidosis: pathophysiology diagnosis and management. Nat Rev Nephrol 2010; 6: 274-85 Arterial blood gas analysis is used to assess and monitor patient acid-base status. Disturbance of acid-base balance is classified to one of four main types depending on the pH, pCO2(a) and bicarbonate results generated during blood gas analysis; the four types are respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis. A recent review article focuses on one of these disturbances, metabolic acidosis, which is characterized by primary decrease in bicarbonate and compensatory decrease in pCO2(a). pH may be either reduced (if compensation is incomplete) or normal (if compensation is complete). This wide-ranging, comprehensive review includes discussion of epidemiology, pathophysiology, clinical consequences and management of metabolic acidosis. The authors distinguish acute metabolic acidosis (lasting hours/days) from the much less common, chronic metabolic acidosis, which can last for years. Acute metabolic acidosis is a common feature of serious illness; a study quoted in the review suggests it affects around two thirds of all patients admitted to intensive care. In broad terms metabolic acidosis arises as a result of net loss of bicarbonate or excessive addition of acid. Discussion of pathophysiology includes detailed consideration of the role of the kidney in regulating acid-base balance, focusing particularly on mechanisms involved in the maintenance of sufficient bicarbonate in blood to buffer metabolic acids. Distinguishing pure metabolic acidosis from a mixed respiratory/metabolic acidosis on the basis of the hypoventilatory response (i.e. magnitude of the redu Continue reading >>

Metabolic Acidosis Nclex Review Notes

Metabolic Acidosis Nclex Review Notes

Are you studying metabolic acidosis and need to know a mnemonic on how to remember the causes? This article will give you a clever mnemonic and simplify the signs and symptoms and nursing interventions on how to remember metabolic acidosis for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate metabolic acidosis from metabolic alkalosis. Don’t forget to take the metabolic acidosis and metabolic alkalosis quiz. This article will cover: Metabolic acidosis simplified Lab values expected with metabolic acidosis Causes of metabolic acidosis Signs and symptoms of metabolic acidosis Nursing interventions for metabolic acidosis Lecture on Metabolic Acidosis Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: increased acid production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: HCO3: decreased <22 Blood pH: decreased <7.35 CO2: <35 or normal (may be normal b Continue reading >>

Anion Gap Metabolic Acidosis Archives - Roshreview.com

Anion Gap Metabolic Acidosis Archives - Roshreview.com

Published: September 27, 2017 | Author: Nachi Gupta, M.D., Ph.D., and Jeff Nusbaum, M.D. | Category: Blog , Podcasts | Tagged: a lines , aggressive cooling , agitation , anion gap metabolic acidosis , apnea , b lines , benzodiazepine , bilious projectile vomiting , bradycardia , confusion , deer mice , deferoxamine , dehydration , dermacentor , double decimal sign , doxycycline , ecmo , ecstasy , fever , fundal height , gestational sac , hantavirus , hemoperitoneum , hemorrhagic fever , hydration , hypertension , hypochloremic hypokalemic metabolic alkalosis , infectious diseases , iron overdose , Lung sliding , mdma , Mississippi river , neurology , obstetrics , operating room , pediatrics , photophobia , Pneumonia , Pneumothorax , pregnany , pubic symphysis , pulmonary edema , pulmonology , pyloric stenosis , resuscitation , rocky mountain spotted fever , serotonin syndrome , severe headache , shock , tachycardia , toxicology , Ultrasound , umbilicus , upper gi series , vagus nerve , xiphoid process , yolk sac | Read more Somewhere, something incredible is waiting to be known. -Sharon Begley Welcome back to Roshcast Episode 32! We are returning to our regular format letting the question back randomly generate this weeks material. We will have another collaborative episode with the EM Clerkship podcast soon.We start this episode off with another rapid review based on [] Continue reading >>

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Review Metformin-associated Lactic Acidosis: Current Perspectives On Causes And Risk

Abstract Although metformin has become a drug of choice for the treatment of type 2 diabetes mellitus, some patients may not receive it owing to the risk of lactic acidosis. Metformin, along with other drugs in the biguanide class, increases plasma lactate levels in a plasma concentration-dependent manner by inhibiting mitochondrial respiration predominantly in the liver. Elevated plasma metformin concentrations (as occur in individuals with renal impairment) and a secondary event or condition that further disrupts lactate production or clearance (e.g., cirrhosis, sepsis, or hypoperfusion), are typically necessary to cause metformin-associated lactic acidosis (MALA). As these secondary events may be unpredictable and the mortality rate for MALA approaches 50%, metformin has been contraindicated in moderate and severe renal impairment since its FDA approval in patients with normal renal function or mild renal insufficiency to minimize the potential for toxic metformin levels and MALA. However, the reported incidence of lactic acidosis in clinical practice has proved to be very low (< 10 cases per 100,000 patient-years). Several groups have suggested that current renal function cutoffs for metformin are too conservative, thus depriving a substantial number of type 2 diabetes patients from the potential benefit of metformin therapy. On the other hand, the success of metformin as the first-line diabetes therapy may be a direct consequence of conservative labeling, the absence of which could have led to excess patient risk and eventual withdrawal from the market, as happened with earlier biguanide therapies. An investigational delayed-release metformin currently under development could potentially provide a treatment option for patients with renal impairment pending the resu Continue reading >>

A Review Article: Sevelamer Hydrochloride And Metabolic Acidosis In Dialysis Patients

A Review Article: Sevelamer Hydrochloride And Metabolic Acidosis In Dialysis Patients

A Review Article: Sevelamer Hydrochloride and Metabolic Acidosis in Dialysis Patients Author(s): Yoshinari Oka , Masashi Miyazaki , Shigeko Takatsu , Toshiaki Oohara , Keisuke Toda , Futoshi Uno , Hiroaki Matsuda . Department of Surgery, Saiwai- cho Memorial Hospital, 3-57 Oomotoekimae, Okayama, Japan 700- 0903. Journal Name: Cardiovascular & Hematological Disorders-Drug Targets Sevelamer hydrochloride is a phosphate binder and its effectiveness to reduce the cardiovascular mortality of dialysis patients has been tested. Sevelamer hydrochloride also contains chlorine, so a decrease in bicarbonate due to chlorine load was anticipated and metabolic acidosis thought to associate with sevelamer hydrochloride has been reported in some papers. We reported that sevelamer hydrochloride exacerbated metabolic acidosis in hemodialysis patients, depending on the dosage. Also a Japanese nationwide survey suggested that sevelamer hydrochloride usage potentially aggravates acidosis in dialysis patients. A multi-institute research study by Edmung et al. has shown that metabolic acidosis, with serum CO2 below 17.5 mmol/L, is by itself associated with increased risk of death in dialysis patients. Furthermore, the Dialysis Outcomes and Practice Patterns Study (DOPPS) revealed that both high ( > 27 mmol/L) and low ( < or % 17 mmol/L) serum bicarbonate (total CO2) levels were associated with increased risk for mortality and hospitalization. There has not been any significant evidence to show that sevelamer hydrochloride has reduced the cardiovascular mortality of dialysis patients compared with calcium-based binder. Clinicians should check not only the level of chlorine but also the level of total CO2 or bicarbonate during the treatment with sevelamer hydrochloride, and control metabolic a Continue reading >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Increased Anion Gap Metabolic Acidosis As A Result Of 5-oxoproline (pyroglutamic Acid): A Role For Acetaminophen

Increased Anion Gap Metabolic Acidosis As A Result Of 5-oxoproline (pyroglutamic Acid): A Role For Acetaminophen

Increased Anion Gap Metabolic Acidosis as a Result of 5-Oxoproline (Pyroglutamic Acid): A Role for Acetaminophen *Department of Internal Medicine; Metabolic Disease Center, BRI Baylor University Medical Center, Dallas, Texas Dr. Andrew Z. Fenves, Nephrology Division, Baylor University Medical Center, 3500 Gaston, Dallas, TX 75246. Phone: 214-820-2350; Fax: 214-820-7367; E-mail: fenvesa{at}dneph.com The endogenous organic acid metabolic acidoses that occur commonly in adults include lactic acidosis; ketoacidosis; acidosis that results from the ingestion of toxic substances such as methanol, ethylene glycol, or paraldehyde; and a component of the acidosis of kidney failure. Another rare but underdiagnosed cause of severe, high anion gap metabolic acidosis in adults is that due to accumulation of 5-oxoproline (pyroglutamic acid). Reported are four patients with this syndrome, and reviewed are 18 adult patients who were reported previously in the literature. Twenty-one patients had major exposure to acetaminophen (one only acute exposure). Eighteen (82%) of the 22 patients were women. Most of the patients were malnourished as a result of multiple medical comorbidities, and most had some degree of kidney dysfunction or overt failure. The chronic ingestion of acetaminophen, especially by malnourished women, may generate high anion gap metabolic acidosis. This undoubtedly is an underdiagnosed condition because measurements of serum and/or urinary 5-oxoproline levels are not readily available. The endogenous organic acid metabolic acidoses that occur most frequently in adults are lactic acidosis and ketoacidosis. Other organic acidoses that are encountered in adult patients are those that are caused by the metabolism of toxic substances such as methanol to formaldehyde or ethy Continue reading >>

Metabolic Acidosis In Emergency Medicine

Metabolic Acidosis In Emergency Medicine

Author: Antonia Quinn, DO; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. This article discusses the differential diagnosis of metabolic acidosis and presents a scheme for identifying the underlying cause of acidosis by using laboratory tests that are available in the emergency department. Clinical strategies for treating metabolic acidosis are also reviewed. There are 3 approaches to understanding acid/base balance: A qualitative approach using the Henderson/Hasselbalch equation, a semiqualitative approach with base excess, and the Strong Ion Theory. The 3 theories are reviewed below. Henderson-Hasselbalch approach to acid/base physiology The Henderson-Hasselbalch equation describes the relationship between blood pH and the components of the H2 CO3 buffering system. This qualitative description of acid/base physiology allows the metabolic component to be separated from the respiratory components of acid/base balance. Bicarbonate (HCO3) is in equilibrium with the metabolic components. Acid production from endogenous or exogenous sources Carbonic acid (H2 CO3) is in equilibrium with the respiratory component, as shown by the below equation: Metabolic acidosis can be caused by the following: Increase in the generation of H + from endogenous (eg, lactate, ketones) or exogenous acids (eg, salicylate, ethylene glycol, methanol) Inability of the kidneys to excrete the hydrogen from dietary protein intake (type I, IV renal tubular acidosis) The loss of bicarbonate (HCO 3) due to wasting through the kidney (type Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Jeffrey A. Kraut, MD is Chief of Dialysis in the Division of Nephrology at the Greater Los Angeles Veterans Administration Healthcare System, Professor of Medicine at the David Geffen School of Medicine at UCLA, and an investigator at the UCLA Membrane Biology Laboratory, Los Angeles, CA, USA. He completed his nephrology training at the TuftsNew England Medical Center where he performed basic research examining the mechanisms regulating acid excretion by the kidney. His present research is focused on delineating the mechanisms contributing to cellular damage with various acidbase disturbances, including metabolic acidosis, with the goal of developing newer treatment strategies. Nicolaos E. Madias, MD is Chairman of the Department of Medicine at St. Elizabeth's Medical Center in Boston, and Maurice S. Segal, MD Professor of Medicine at Tufts University School of Medicine, Boston, MA, USA. He completed his nephrology training at TuftsNew England Medical Center. He has previously served as Chief of the Division of Nephrology at TuftsNew England Medical Center, Established Investigator of the American Heart Association, member of the Internal Medicine and Nephrology Boards of the American Board of Internal Medicine, and Executive Academic Dean and Dean ad interim of Tufts University School of Medicine. His research interests are focused on acidbase and electrolyte physiology and pathophysiology. Nature Reviews Nephrology volume 6, pages 274285 (2010) Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of 1 mmHg for every 1 mmol/l fall in serum HCO3 concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chro Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Metabolic Acidosis: Pathophysiology, Diagnosis And Management

Abstract | Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO3 concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO2) of ~1 mmHg for concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum ] + [Cl]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the administration of base for the treatment of chronic metabolic acidosis is associated with improved cellular Kraut, J. A. & Madias, N. E. Nat. Rev. Nephrol. 6, 274285 (2010); publshed online 23 March 2010; doi:10.1038/nrneph.2010.33 Metabolic acidosis is characterized by a primary reduc- tion in the serum concentration of bicarbonate (HCO3 a secon dary decrease in the arterial partial pre Continue reading >>

Review Of The Diagnostic Evaluation Of Normal Anion Gap Metabolic Acidosis

Review Of The Diagnostic Evaluation Of Normal Anion Gap Metabolic Acidosis

Acid-Base, Electrolyte and Fluid Alterations: Review Review of the Diagnostic Evaluation of Normal Anion Gap Metabolic Acidosis I have read the Karger Terms and Conditions and agree. I have read the Karger Terms and Conditions and agree. Buy a Karger Article Bundle (KAB) and profit from a discount! If you would like to redeem your KAB credit, please log in . Save over 20% compared to the individual article price. Buy Cloud Access for unlimited viewing via different devices Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use * The final prices may differ from the prices shown due to specifics of VAT rules. For additional information: Background: Normal anion gap metabolic acidosis is a common but often misdiagnosed clinical condition associated with diarrhea and renal tubular acidosis (RTA). Early identification of RTA remains challenging for inexperienced physicians, and diagnosis and treatment are often delayed. Summary: The presence of RTA should be considered in any patient with a high chloride level when the CL-/Na+ ratio is above 0.79, if the patient does not have diarrhea. In patients with significant hyperkalemia one should evaluate for RTA type 4, especially in diabetic patients, with a relatively conserved renal function. A still growing list of medications can produce RTA. Key Messages: This review highlights practical aspects concerning normal anion gap metabolic acidosis. Berend K, de Vries AP, Gans RO: Physiological approach to assessment of acid-base disturbances. N Engl J Med 2015;372:195. Kraut JA, Madias NE: Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol 2007;2:162-174. Roberts WL Continue reading >>

Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Metabolic Acidosis: Pathophysiology, Diagnosis And Management.

Nat Rev Nephrol. 2010 May;6(5):274-85. doi: 10.1038/nrneph.2010.33. Epub 2010 Mar 23. Metabolic acidosis: pathophysiology, diagnosis and management. Division of Nephrology, Veterans Administration Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. Metabolic acidosis is characterized by a primary reduction in serum bicarbonate (HCO(3)(-)) concentration, a secondary decrease in the arterial partial pressure of carbon dioxide (PaCO(2)) of approximately 1 mmHg for every 1 mmol/l fall in serum HCO(3)(-) concentration, and a reduction in blood pH. Acute forms (lasting minutes to several days) and chronic forms (lasting weeks to years) of the disorder can occur, for which the underlying cause/s and resulting adverse effects may differ. Acute forms of metabolic acidosis most frequently result from the overproduction of organic acids such as ketoacids or lactic acid; by contrast, chronic metabolic acidosis often reflects bicarbonate wasting and/or impaired renal acidification. The calculation of the serum anion gap, calculated as [Na(+)] - ([HCO(3)(-)] + [Cl(-)]), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the ad Continue reading >>

Nutrients | Free Full-text | Diet-induced Low-grade Metabolic Acidosis And Clinical Outcomes: A Review

Nutrients | Free Full-text | Diet-induced Low-grade Metabolic Acidosis And Clinical Outcomes: A Review

Nutrients 2017, 9(6), 538; Diet-Induced Low-Grade Metabolic Acidosis and Clinical Outcomes: A Review VP Research Institute, 287, Carlos Petit St, So Paulo 04110-000, Brazil Departament of Food Science and Technology, Federal University of Santa Maria, Rio Grande do Sul 97105-900, Brazil Author to whom correspondence should be addressed. Received: 27 March 2017 / Revised: 5 May 2017 / Accepted: 17 May 2017 / Published: 25 May 2017 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 sou Continue reading >>

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