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Consequences Of Metabolic Acidosis

Consequences And Therapy Of The Metabolic Acidosis Of Chronic Kidney Disease

Consequences And Therapy Of The Metabolic Acidosis Of Chronic Kidney Disease

Metabolic acidosis is common in patients with chronic kidney disease (CKD), particularly once the glomerular filtration rate (GFR) falls below 25ml/min/1.73m2. It is usually mild to moderate in magnitude with the serum bicarbonate concentration ([HCO 3 ]) ranging from 12 to 23mEq/l. Even so, it can have substantial adverse effects, including development or exacerbation of bone disease, growth retardation in children, increased muscle degradation with muscle wasting, reduced albumin synthesis with a predisposition to hypoalbuminemia, resistance to the effects of insulin with impaired glucose tolerance, acceleration of the progression of CKD, stimulation of inflammation, and augmentation of 2-microglobulin production. Also, its presence is associated with increased mortality. The administration of base to patients prior to or after initiation of dialysis leads to improvement in many of these adverse effects. The present recommendation by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) is to raise serum [HCO 3 ] to 22mEq/l, whereas Caring for Australians with Renal Impairment (CARI) recommends raising serum [HCO 3 ] to >22mEq/l. Base administration can potentially contribute to volume overload and exacerbation of hypertension as well as to metastatic calcium precipitation in tissues. However, sodium retention is less when given as sodium bicarbonate and sodium chloride intake is concomitantly restricted. Results from various studies suggest that enhanced metastatic calcification is unlikely with the pH values achieved during conservative base administration, but the clinician should be careful not to raise serum [HCO 3 ] to values outside the normal range. Continue reading >>

Metabolic Acidosis: Causes, Symptoms, And Treatment

Metabolic Acidosis: Causes, Symptoms, And Treatment

The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th Continue reading >>

Acidosis

Acidosis

When your body fluids contain too much acid, it’s known as acidosis. Acidosis occurs when your kidneys and lungs can’t keep your body’s pH in balance. Many of the body’s processes produce acid. Your lungs and kidneys can usually compensate for slight pH imbalances, but problems with these organs can lead to excess acid accumulating in your body. The acidity of your blood is measured by determining its pH. A lower pH means that your blood is more acidic, while a higher pH means that your blood is more basic. The pH of your blood should be around 7.4. According to the American Association for Clinical Chemistry (AACC), acidosis is characterized by a pH of 7.35 or lower. Alkalosis is characterized by a pH level of 7.45 or higher. While seemingly slight, these numerical differences can be serious. Acidosis can lead to numerous health issues, and it can even be life-threatening. There are two types of acidosis, each with various causes. The type of acidosis is categorized as either respiratory acidosis or metabolic acidosis, depending on the primary cause of your acidosis. Respiratory acidosis Respiratory acidosis occurs when too much CO2 builds up in the body. Normally, the lungs remove CO2 while you breathe. However, sometimes your body can’t get rid of enough CO2. This may happen due to: chronic airway conditions, like asthma injury to the chest obesity, which can make breathing difficult sedative misuse deformed chest structure Metabolic acidosis Metabolic acidosis starts in the kidneys instead of the lungs. It occurs when they can’t eliminate enough acid or when they get rid of too much base. There are three major forms of metabolic acidosis: Diabetic acidosis occurs in people with diabetes that’s poorly controlled. If your body lacks enough insulin, keton Continue reading >>

5.4 Metabolic Acidosis - Metabolic Effects

5.4 Metabolic Acidosis - Metabolic Effects

5.4 Metabolic Acidosis - Metabolic Effects A metabolic acidosis can cause significant physiological effects, particularly affecting the respiratory and cardiovascular systems. Hyperventilation ( Kussmaul respirations ) - this is the compensatory response Shift of oxyhaemoglobin dissociation curve (ODC) to the right Decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) Sympathetic overactivity (incl tachycardia, vasoconstriction,decreased arrhythmia threshold) Resistance to the effects of catecholamines Increased bone resorption (chronic acidosis only) Shift of K+ out of cells causing hyperkalaemia 5.4.2 Some Effects have Opposing Actions. The cardiac stimulatory effects of sympathetic activity and release of catecholamines usually counteract the direct myocardial depression while plasma pH remains above 7.2. At systemic pH values less than this, the direct depression of contractility usually predominates. The direct vasodilatation is offset by the indirect sympathetically mediated vasoconstriction and cardiac stimulation during a mild acidosis. The venoconstriction shifts blood centrally and this causes pulmonary congestion. Pulmonary artery pressure usually rises during acidosis. The shift of the oxygen dissociation curve to the right due to the acidosis occurs rapidly. After 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Acidosis is commonly said to cause hyperkalaemia by a shift of potassium out of cells. The effect on potassium levels is extremely variable and indirect effects due to the type of acidosis present are much more important. For example hyperkalaemia is due to renal failure in uraemic acidosis rather than the acidosis. Significant potassium loss du Continue reading >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

Risks Of Chronic Metabolic Acidosis In Patients With Chronic Kidney Disease - Sciencedirect

Risks Of Chronic Metabolic Acidosis In Patients With Chronic Kidney Disease - Sciencedirect

Volume 67, Supplement 95 , June 2005, Pages S21-S27 Risks of chronic metabolic acidosis in patients with chronic kidney disease Author links open overlay panel Joel D.Kopple Risks of chronic metabolic acidosis in patients with chronic kidney disease Metabolic acidosis is associated with chronic renal failure (CRF). Often, maintenance dialysis therapies are not able to reverse this condition. The major systemic consequences of chronic metabolic acidosis are increased protein catabolism, decreased protein synthesis, and a negative protein balance that improves after bicarbonate supplementation. Metabolic acidosis also induces insulin resistance and a decrease in the elevated serum leptin levels associated with CRF. These three factors may promote protein catabolism in maintenance dialysis patients. Available data suggest that metabolic acidosis is both catabolic and anti-anabolic. Several clinical studies have shown that correction of metabolic acidosis in maintenance dialysis patients is associated with modest improvements in nutritional status. Preliminary evidence indicates that metabolic acidosis may play a role in 2-microglobulin accumulation, as well as the hypertriglyceridemia seen in renal failure. Interventional studies for metabolic acidosis have yielded inconsistent results in CRF and maintenance hemodialysis patients. In chronic peritoneal dialysis patients, the mitigation of acidemia appears more consistently to improve nutritional status and reduce hospitalizations. Large-scale, prospective, randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in maintenance hemodialysis patients. To avoid adverse events, an aggressive management approach is necessary to correct metabolic acidosis. Clinicians should attempt Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Metabolic Acidosis In Maintenance Dialysis Patients: Clinical Considerations - Sciencedirect

Metabolic Acidosis In Maintenance Dialysis Patients: Clinical Considerations - Sciencedirect

Volume 64, Supplement 88 , December 2003, Pages S13-S25 Author links open overlay panel RajnishMehrotra Joel D.Kopple MarshaWolfson Metabolic acidosis in maintenance dialysis patients: Clinical considerations. Metabolic acidosis is a common consequence of advanced chronic renal failure (CRF) and maintenance dialysis (MD) therapies are not infrequently unable to completely correct the base deficit. In MD patients, severe metabolic acidosis is associated with an increased relative risk for death. The chronic metabolic acidosis of the severity commonly encountered in patients with advanced CRF has two well-recognized major systemic consequences. First, metabolic acidosis induces net negative nitrogen and total body protein balance, which improves upon bicarbonate supplementation. The data suggest that metabolic acidosis is both catabolic and antianabolic. Emerging data also indicate that metabolic acidosis may be one of the triggers for chronic inflammation, which may in turn promote protein catabolism among MD patients. In contrast to these findings, metabolic acidosis may be associated with a decrease in hyperleptinemia associated with CRF. Several studies have shown that correction of metabolic acidosis among MD patients is associated with modest improvements in the nutritional status. Second, metabolic acidosis has several effects on bone, causing physicochemical dissolution of bone and cell-mediated bone resorption (inhibition of osteoblast and stimulation of osteoclast function). Metabolic acidosis is probably also associated with worsening of secondary hyperparathyroidism. Data on the effect of correction of metabolic acidosis on renal osteodystrophy, however, are limited. Preliminary evidence suggest that metabolic acidosis may play a role in 2-microglobulin accum Continue reading >>

Effect Of Metabolic Acidosis On Renal Brushborder Membrane Adaptation To Low Phosphorus Diet - Sciencedirect

Effect Of Metabolic Acidosis On Renal Brushborder Membrane Adaptation To Low Phosphorus Diet - Sciencedirect

Volume 22, Issue 3 , September 1982, Pages 225-233 Effect of metabolic acidosis on renal brushborder membrane adaptation to low phosphorus diet Author links open overlay panel Stephen A.Kempson1 Effect of metabolic acidosis on renal brushborder membrane adaptation to low phosphorus diet. In previous in vitro studies the level of oxidized nicotinamide adenine dinucleotide (NAD+) in renal cortex changed parallel to changes in gluconeogenesis and NAD+ inhibited phosphate transport by renal cortical brushborder membrane (BBM) vesicles. To determine whether or not changes in renal gluconeogenesis in vivo were accompanied by altered renal handling of phosphate, possibly related to NAD+ action on BBM phosphate transport in vivo, renal gluconeogenesis was stimulated in rats by metabolic acidosis. Chronic acidosis in rats previously adapted to low phosphorus diet was associated with increased UPiV (controls, 68 19; acidotic, 1055 428 nmoles/mg creatinine; P < 0.05) without changes in plasma phosphate and creatinine (Cr) and in UCrV compared to controls. The initial rate of sodium gradient-dependent transport of phosphate by renal cortical BBM vesicles was lower in acidotic TPTX rats compared to TPTX controls (controls, 3.10 0.16; acidotic, 1.50 0.06 nmole/mg protein/0.5 min; P < 0.001), attributed to a decrease in the apparent Vmax. In renal cortex, gluconeogenesis and the NAD+/NADH ratio were increased in acidosis. Decreased BBM transport of phosphate in proximal tubules of acidotic rats may explain the increased UPiV. This change indicates reversal of the adaptation of the BBM phosphate transport system to dietary phosphorus deprivation and may be related to increases in gluconeogenesis and the NAD+/NADH ratio in renal cortex. Effets de l'acidose mtabolique sur l'adaptation d Continue reading >>

Causes And Consequences Of Fetal Acidosis

Causes And Consequences Of Fetal Acidosis

The causes and consequences ofacute (minutes or hours) andchronic (days or weeks) fetal acidosis are different In the past much attention has been paid to acute acidosis during labour, but in previously normal fetuses this israrely associated with subsequent damage In contrast, chronic acidosis, which is often not detected antenatally, is associated with a significant increase in neurodevelopmental delay The identification of small for gestational age fetuses by ultrasound scans and the use of Doppler waveforms to detect which of these have placental dysfunction mean that these fetuses can be monitored antenatally Delivery before hypoxia has produced chronic acidosis, may prevent subsequent damage and good timing of delivery remains the only management option at present. What is acidosis? Acidosis means a high hydrogen ion concentration in the tissues. Acidaemia refers to a high hydrogen ion concentration in the blood and is the most easily measured indication of tissue acidosis. The unit most commonly used is pH, which is log to base 10 of the reciprocal of the hydrogen ion concentration. Whereas blood pH can change quickly, tissue pH is more stable. The cut off taken to define acidaemia in adults is a pH of less than 7.36, but after labour and normal delivery much lower values commonly occur in the fetus (pH 7.00), often with no subsequent ill effects. Studies looking at the pH of fetuses from cord blood samples taken antenatally and at delivery have established reference ranges. Other indices sometimes used to assess acidosis are the base excess or bicarbonate. Neither of these is measured by conventional blood gas machines but is calculated from the measured pH and pCO2. The major sources of hydrogen ions in the fetus are carbonic and lactic acids from aerobic and a Continue reading >>

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

Pathogenesis, Consequences, And Treatment Of Metabolic Acidosis In Chronic Kidney Disease

The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2018 UpToDate, Inc. All topics are updated as new evidence becomes available and our peer review process is complete. INTRODUCTION — Most individuals produce approximately 15,000 mmol (considerably more with exercise) of carbon dioxide and 50 to 100 meq of nonvolatile acid each day. Acid-base balance is maintained by normal elimination of carbon dioxide by the lungs (which affects the partial pressure of carbon dioxide [PCO2]) and normal excretion of nonvolatile acid by the kidneys (which affects the plasma bicarbonate concentration). The hydrogen ion concentration of the blood is determined by the ratio of the PCO2 and plasma bicarbonate concentration. (See "Simple and mixed acid-base disorders", section on 'Introduction'.) Acidosis associated with chronic kidney disease (CKD) will be discussed in this topic. An overview of simple acid-base disorders and renal tubular acidosis, as well as the approach to patients with metabolic acidosis, are presented elsewhere. (See "Simple and mixed acid-base disorders" and "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance" and "Approach to the adult with metabolic acidosis" and "Approach to the child with metabolic acidosis".) ACID-BASE BALANCE IN CHRONIC KIDNEY DISEASE — Acid-base balance is normally maintained by the renal excretion of the daily acid load (about 1 meq/kg per day, derived mostly from the generation of sulfuric acid during the metabolism of sulf Continue reading >>

Metabolic And Clinical Consequences Of Metabolic Acidosis.

Metabolic And Clinical Consequences Of Metabolic Acidosis.

1. J Nephrol. 2006 Mar-Apr;19 Suppl 9:S70-5. Metabolic and clinical consequences of metabolic acidosis. (1)Division of Nephrology, Baylor College of Medicine, Houston, Texas, USA. [email protected] Acid-base balance is precisely regulated by pulmonary and renal responses whilebody buffers help to control pH. When its regulation becomes abnormal,accumulation of hydrogen ions cause metabolic acidosis and several responses are activated. These responses interfere with the metabolism of bones and muscle.Metabolic acidosis induces abnormalities in the release and function of severalhormones including defects in growth hormone, IGF-1, insulin, glucocorticoids,thyroid hormone, parathyroid hormone and vitamin D. Clinical consequences ofthese abnormal metabolic responses include impaired growth of infants andchildren and loss of bone and muscle mass in adults. Notably, abnormalities inbone and muscle metabolism can be present even when there is little or nodecrease in the plasma bicarbonate concentration. The abnormalities can becorrected by treatment with NaHCO 3 . In patients with chronic kidney disease,many abnormalities in bone and muscle metabolism can be directly linked to thepresence of metabolic acidosis and these abnormalities can be largely correctedby treating acidosis with NaHCO3. Recent insights indicate that severalconsequences of metabolic acidosis including the development of insulinresistance can stimulate muscle protein degradation by activating proteolyticmechanisms. To avoid abnormalities in metabolism and the loss of bone and muscle,metabolic acidosis must be corrected in normal adults and in patients with kidneydisease. Continue reading >>

Endocrine Consequences Of Metabolic Acidosis

Endocrine Consequences Of Metabolic Acidosis

Endocrine Consequences of Metabolic Acidosis Metabolic acidosis, particularly its chronic form, is a systemic process with systemic consequences that includes disturbances in the function of some endocrine systems. Such disturbances likely have short-term adverse consequences such as less sensitivity to the actions of hormones that might require higher hormone levels, e.g., insulin, to obtain needed hormonal effects. These disturbances might also have long-term consequences, however, like the association of decreased insulin sensitivity with increased cardiovascular mortality. For example, because some studies support that metabolic acidosis decreases insulin sensitivity, correction of chronic metabolic acidosis might improve insulin sensitivity and thereby possibly reduce cardiovascular mortality. These consequences point out the increasing need for clinicians to identify chronic metabolic acidosis and to treat it to confer the resulting benefits on patients supported by published studies. Regarding the latter, there are few published studies examining the benefit of correction of metabolic acidosis on endocrine systems, a deficit that must be corrected. Insulin sensitivityGrowth hormone sensitivityThyroid hormoneAngiotensinAldosteroneEndothelinCatecholamines This is a preview of subscription content, log in to check access Kovesdy CP, Anderson JE, Kalantar-Zadeh K. Association of serum bicarbonate levels with mortality in patients with non-dialysis-dependent CKD. Nephrol Dial Transplant. 2009;24:12327. CrossRef PubMed PubMedCentral Google Scholar Dobre M, Yang W, Chen J, Drawz P, Hamm LL, Horwitz E, et al. Association of serum bicarbonate with risk of renal and cardiovascular outcomes in CKD: a report from the Chronic Renal Insufficiency Cohort (CRIC) Study. Am J Kid Continue reading >>

Physiological Effects Of Hyperchloraemia And Acidosis

Physiological Effects Of Hyperchloraemia And Acidosis

Physiological effects of hyperchloraemia and acidosis Chelsea and Westminster NHS Foundation Trust Chelsea and Westminster NHS Foundation Trust BJA: British Journal of Anaesthesia, Volume 101, Issue 2, 1 August 2008, Pages 141150, J. M. Handy, N. Soni; Physiological effects of hyperchloraemia and acidosis, BJA: British Journal of Anaesthesia, Volume 101, Issue 2, 1 August 2008, Pages 141150, The advent of balanced solutions for i.v. fluid resuscitation and replacement is imminent and will affect any specialty involved in fluid management. Part of the background to their introduction has focused on the non-physiological nature of normal saline solution and the developing science about the potential problems of hyperchloraemic acidosis. This review assesses the physiological significance of hyperchloraemic acidosis and of acidosis in general. It aims to differentiate the effects of the causes of acidosis from the physiological consequences of acidosis. It is intended to provide an assessment of the importance of hyperchloraemic acidosis and thereby the likely benefits of balanced solutions. Hyperchloraemic acidosis is increasingly recognized as a clinical entity, a new enemy within, that had gone otherwise unnoticed for decades. Although any associated morbidity may be subtle at present, there is a trend in current evidence to suggest that hyperchloraemic acidosis may have adverse consequences which may be circumvented by the use of balanced solutions. These consequences, both theoretical and clinical, may result from hyperchloraemia, acidosis, or both. There is some evidence of hyperchloraemia causing problems, but at present the clinical relevance is uncertain. The literature does appear to be unified in stating that acidosis results in adverse physiological effects bu Continue reading >>

Metabolic Acidosis: Practice Essentials, Background, Etiology

Metabolic Acidosis: Practice Essentials, Background, Etiology

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. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. An acid is a substance that can donate hydrogen ions (H+). A base is a substance that can accept H+ ions. The ion exchange occurs regardless of the substance's charge. Strong acids are those that are completely ionized in body fluids, and weak acids are those that are incompletely ionized in body fluids. Hydrochloric acid (HCl) is considered a strong acid because it is present only in a completely ionized form in the body, whereas carbonic acid (H2 CO3) is a weak acid because it is ionized incompletely, and, at equilibrium, all three reactants are present in body fluids. See the reactions below. The law of mass action states that the velocity of a reaction is proportional to the product of the reactant concentrations. On the basis of this law, the addition of H+ or bicarbonate (HCO3-) drives the reaction shown below to the left. In body fluids, the concentration of hydrogen ions ([H+]) is maintained within very narrow limits, with the normal physiologic concentration being 40 nEq/L. The concentration of HCO3- (24 mEq/L) is 600,000 times that of [H+]. The tight regulation of [H+] at this low concentration is crucial for normal cellular activities because H+ at higher concentrations can b Continue reading >>

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