Metabolic Acidosis
Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>
8.3 Acidosis And Renal Failure
Metabolic acidosis occurs with both acute and chronic renal failure and with other types of renal damage. The anion gap may be normal or may be elevated. If the renal damage affects both glomeruli and tubules, the acidosis is a high-anion gap acidosis. It is due to failure of adequate excretion of various acid anions due to the greatly reduced number of functioning nephrons. If the renal damage predominantly affects the tubules with minimal glomerular damage, a different type of acidosis may occur. This is called Renal Tubular Acidosis (RTA) and this is a normal anion gap or hyperchloraemic type of acidosis. The GFR may be normal or only minimally affected. The acidosis occurring in uraemic patients 1 is due to failure of excretion of acid anions (particularly phosphate and sulphate) because of the decreased number of nephrons. There is a major decrease in the number of tubule cells which can produce ammonia and this contributes to uraemic acidosis. Serious acidosis does not occur until the GFR has decreased to about 20 mls/min. This corresponds to a creatinine level of about 0.30-0.35 mmols/l. The plasma bicarbonate in renal failure with acidosis is typically between 12 & 20 mmols/l. Intracellular buffering and bone buffering are important in limiting the fall in bicarbonate. This bone buffering will cause loss of bone mineral (osteomalacia). Most other forms of metabolic acidosis are of relatively short duration as the patient is either treated with resolution of the disorder or the patient dies. Uraemic acidosis is a major exception as these patients survive with significant acidosis for many years. This long duration is the reason why loss of bone mineral (and bone buffering ) is significant in uraemic acidosis but is not a feature of other causes of metabolic acid Continue reading >>
Metabolic Acidosis And Kidney Disease: Does Bicarbonate Therapy Slow The Progression Of Ckd?
Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD? Correspondence and offprint requests to: Csaba P. Kovesdy; E-mail: [email protected] Search for other works by this author on: Nephrology Dialysis Transplantation, Volume 27, Issue 8, 1 August 2012, Pages 30563062, Csaba P. Kovesdy; Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD?, Nephrology Dialysis Transplantation, Volume 27, Issue 8, 1 August 2012, Pages 30563062, Metabolic acidosis is a common complication associated with progressive loss of kidney function. The diminishing ability of the kidneys to maintain acidbase homeostasis results in acid accumulation, leading to various complications such as impairment in nutritional status, worsened uremic bone disease and an association with increased mortality. In addition to these adverse effects which are related to acid retention, metabolic acidosis may also cause kidney damage, possibly through the stimulation of adaptive mechanisms aimed at maintaining acidbase homeostasis in the face of decreasing kidney function. Recent clinical trials have suggested that correction or prevention of metabolic acidosis by alkali administration is able to attenuate kidney damage and to slow progression of chronic kidney disease (CKD), and may hence offer an effective, safe and affordable renoprotective strategy. We review the physiology and pathophysiology of acidbase homeostasis in CKD, the mechanisms whereby metabolic acidosis may be deleterious to kidney function, and the results of clinical trials suggesting a benefit of alkali therapy, with special attention to details related to the practical implementation of the results of these trials. bicarbonate , chronic kidney disease , metabolic ac Continue reading >>
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 >>
Metabolic Acidosis And Kidney Disease: Does Bicarbonate Therapy Slow The Progression Of Ckd?
Nephrol Dial Transplant. 2012 Aug;27(8):3056-62. doi: 10.1093/ndt/gfs291. Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD? Division of Nephrology, Salem Veterans Affairs Medical Center, Salem, VA, USA. [email protected] Metabolic acidosis is a common complication associated with progressive loss of kidney function. The diminishing ability of the kidneys to maintain acid-base homeostasis results in acid accumulation, leading to various complications such as impairment in nutritional status, worsened uremic bone disease and an association with increased mortality. In addition to these adverse effects which are related to acid retention, metabolic acidosis may also cause kidney damage, possibly through the stimulation of adaptive mechanisms aimed at maintaining acid-base homeostasis in the face of decreasing kidney function. Recent clinical trials have suggested that correction or prevention of metabolic acidosis by alkali administration is able to attenuate kidney damage and to slow progression of chronic kidney disease (CKD), and may hence offer an effective, safe and affordable renoprotective strategy. We review the physiology and pathophysiology of acid-base homeostasis in CKD, the mechanisms whereby metabolic acidosis may be deleterious to kidney function, and the results of clinical trials suggesting a benefit of alkali therapy, with special attention to details related to the practical implementation of the results of these trials. Continue reading >>
Metabolic Acidosis And The Progression Of Chronic Kidney Disease
Metabolic acidosis and the progression of chronic kidney disease 1Division of Nephrology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA 2Department of Epidemiology & Population Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Ullmann 615, Bronx, NY 10461, USA 1Division of Nephrology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA 2Department of Epidemiology & Population Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Ullmann 615, Bronx, NY 10461, USA Received 2014 Jan 8; Accepted 2014 Mar 31. Copyright 2014 Chen and Abramowitz; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated. This article has been cited by other articles in PMC. Metabolic acidosis is a common complication of chronic kidney disease. Accumulating evidence identifies acidosis not only as a consequence of, but as a contributor to, kidney disease progression. Several mechanistic pathways have been identified in this regard. The dietary acid load, even in the absence of overt acidosis, may have deleterious effects. Several small trials now suggest that the treatment of acidosis with oral alkali can slow the progression of kidney disease. Keywords: Bicarbonate, Dietary acid, Net endogenous acid production, Sodium bicarbonate, Alkali, Ammonia, Complement, Endothelin, Aldosterone Metabolic acidosis is a common complication of chronic kidney disease (CKD). Based on a cr Continue reading >>
Acid/base Disorders: Metabolic Acidosis
Are there clinical practice guidelines to inform decision-making? Does this patient have metabolic acidosis? Metabolic acidosis is generally defined by the presence of a low serum bicarbonate concentration (normal range 22-28 mEq/L), although occasionally states can exist where the serum bicarbonate is normal with an elevated anion gap (e.g., patients with a lactic acidosis who have received a bicarbonate infusion or patients on hemodialysis). In general, a metabolic acidosis is associated with a low urine pH but depending on the presence or absence of a respiratory alkalosis, this may also be normal or elevated. Thus, a patient can have an acidosis but not be acidemic. Metabolic acidoses occur when there is excess acid in the plasma. In the basal state, the body generates about 12,000 to 13,000 mmol of carbon dioxide (CO2), and 1-1.5 mmol per kilogram body weight of nonvolatile acid. The body has a large buffering capacity, with CO2-HCO3 as the major buffer system. The two major routes of acid excretion are the lungs (for CO2) and the kidneys (for nonvolatile acids) A metabolic acidosis can be caused by three major mechanisms: 1) increased acid production; 2) bicarbonate loss; and 3) decreased renal acid excretion Increased acid production leads to anion-gap (AG) metabolic acidosis, and involves a variety of different clinical processes, see An anion gap acidosis may also result for ingestion of an acid load. Both bicarbonate loss and decreased renal acid excretion lead to normal-anion gap (NG) metabolic acidosis. When there is HCO3 loss, chloride is retained to maintain electrical neutrality. The different clinical processes are summarized in Toxic ingestions are common causes of AG metabolic acidosis. The commonest causes are methanol and ethylene glycol intoxicatio Continue reading >>
Metabolic Acidosis And Progression Of Chronic Kidney Disease
Metabolic Acidosis and Progression of Chronic Kidney Disease Department of Medicine, University of California San Francisco, San Francisco, California The concentration of hydrogen ion is normally managed by several buffering and elimination systems, including the kidney. Consequently, progressive renal failure is accompanied by an increasing inability to excrete metabolites of fuel consumption, lower blood pH, and reduced plasma bicarbonate levels, 1 , 2 but is the inverse true? Can correcting this chronic metabolic acidosis slow or prevent progressive kidney damage? An elegant series of experiments several years ago by Mitch and colleagues 3 6 found that metabolic acidosis in the rat activates the ubiquitin-proteasome pathway, leading to increased protein breakdown to amino acids, including glutamate, which is excreted by the proximal tubule as ammonium. Nath et al. 7 observed even earlier that nitrogen nucleophiles such as ammonia are injurious to the kidney and stimulate chronic tubulointerstitial inflammation through a complement-mediated pathway. Both findings together suggest a deleterious multisystem mechanism contributing to progression of chronic kidney disease (CKD). Data from studies of rats on the effects of alkali therapy in CKD have been contradictory: Some studies posit alkali therapy is protective 5 , 8 or neutral, 9 whereas others suggest the oppositethat metabolic acidosis is protective. 10 , 11 Investigation of this issue in humans also reveals divergent results. In an early report from 1931, Lyon and Stewart 12 treated 17 patients with moderate renal failure for periods of several weeks to months with both low-acid diets and sufficient oral supplementation with sodium bicarbonate and potassium citrate to maintain an alkaline urine pH. This work adv Continue reading >>
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 >>
Why Does Renal Failure Cause Metabolic Acidosis
Why Does Renal Failure Cause Metabolic Acidosis Renal failure patients will have many symptoms and discomforts among which metabolic acidosis, water and electrolytes disorders are the most common. Metabolic acidosis is due to excessive accumulation of acidic substances in the blood due to diminished renal filtering functions. Metabolic acidosis can cause the patients to have the following clinical symptoms such as loss of appetite, nausea, vomiting, fatigue, long and deep breath, etc. These symptoms will become more obvious and serious when the clearance rate of creatinine falls below 25ml/min and serum creatinine level is significantly elevated. If left untreated, metabolic acidosis, along with renal hypertension, high blood potassium, fluid and sodium retention, anemia can cause heart failure, arrhythmia and myocardial damages, therefore it is very important to seek proper treatments as soon as possible. Healthy kidneys have the functions of maintaining acid-base balances, in case of kidney failure this function is severely affected and the impaired kidneys can not remove metabolic acidic materials such as phosphoric acid and sulfuric acid from the blood. They will accumulate in the body and cause metabolic acidosis. In the early stage patients can have no obvious symptoms and when HCO3 in blood is lower than 15mmol/L, patients will have poor appetite, vomiting, fatigue, deep breath, etc. Knowing the root cause of metabolic acidosis in renal failure, we know that to treat renal failure and improve renal filtration functions can cure metabolic acidosis from the root. Micro-Chinese Medicine Osmotherapy and Immunotherapy can help repaired damaged renal tissues, restore renal structures and improve kidney functions so that acidic substances can be discharged through the Continue reading >>
The Acidosis Of Chronic Renal Failure.
1. Med Clin North Am. 1983 Jul;67(4):845-58. The acidosis of chronic renal failure is not due to bicarbonate wastage per se;rather, bicarbonate reabsorption per nephron is markedly enhanced. The ability tolower the urine pH is preserved. While overall ammonium production may bedecreased in chronic renal failure, both ammonium production and excretion aremarkedly increased when expressed per remaining nephron. Titratable acidexcretion in chronic renal failure is essentially maximal, owing to the effect ofparathyroid hormone on phosphate excretion by the kidney. Thus, it appears thatthe acidosis of chronic renal failure is solely the consequence of the reduction in functional renal mass. Extrarenal buffering may contribute substantially tothe maintenance of a near normal acid-base status in patients with markedreduction in glomerular filtration rate. That homeostasis is so well preserveduntil glomerular filtration rate falls to approximately 10 per cent of normal is remarkable; the price, however, may be considerable. Prolonged acidosis maymagnify the tendency of renal failure to cause osteodystrophy. An obvioustreatment for the acidosis of renal failure is exogenous alkali therapy. Mostclinicians withhold alkali therapy until the bicarbonate concentration fallsbelow 20 mEq per L. If the acidosis cannot be safely corrected with exogenoustherapy, dialysis should be initiated. Continue reading >>
Renal Tubular Acidosis And Uraemic Acidosis
Metabolic acidosis can occur in both acute and chronic renal disorders the anion gap may be elevated, due to uraemic acidosis the anion gap may be normal, due to renal tubular acidosis (RTA) Uraemic acidosis results from the loss of functional nephrons decreased glomerular filtration rate (GFR) (e.g. <20 mL/min) accumulation of acidic anions such as phosphate and sulfate occurs causes high anion gap metabolic acidosis (HAGMA) patients manifest as renal failure, often have prolonged survival and develop chronic complications such as bone demineralisation Renal tubular acidosis (RTA) involves defects isolated to the renal tubules only GFR may be normal or only minimally affected primary problem is defective renal acid-base regulation due to impaired ability to acidify the urine and excrete acid results in net acid retention and hyperchloremic normal anion gap metabolic acidosis (NAGMA) may be incomplete and only develop in the presence of an acid load occurs despite a normal or only mildly reduced glomerular filtration rate (GFR) RTA is often detected incidentally through an abnormal blood workup, but some patients present with clinical features such as poor growth, dehydration, or altered mental state COMPARISON OF TYPES OF RENAL TUBULAR ACIDOSIS (RTA) urine pH remains >5.5 despite severe acidaemia (HCO3 < 15mmol/L) HCO3loading test leads to increased urinary HCO3 may require an acid load test to see whether urinary pH remains > 5.5 hyperchloraemic acidosis, alkaline urine, and renal stone formation secondary hyperaldosteronism results in increased K+ loss in urine NaHCO3 (corrects Na+ deficit, ECF volume and corrects hypokalaemia) sodium and potassium citrate solutions can be useful if hypokalaemia persistent citrate also binds Ca2+ in the urine and can help to prevent Continue reading >>
Metabolic Acidosis
What is metabolic acidosis? The buildup of acid in the body due to kidney disease or kidney failure is called metabolic acidosis. When your body fluids contain too much acid, it means that your body is either not getting rid of enough acid, is making too much acid, or cannot balance the acid in your body. What causes metabolic acidosis? Healthy kidneys have many jobs. One of these jobs is to keep the right balance of acids in the body. The kidneys do this by removing acid from the body through urine. Metabolic acidosis is caused by a build-up of too many acids in the blood. This happens when your kidneys are unable to adequately remove the acid from your blood. What are the signs and symptoms? Not everyone will have signs or symptoms. However, you may experience: Long and deep breaths Fast heartbeat Headache and/or confusion Weakness Feeling very tired Vomiting and/or feeling sick to your stomach (nausea) Loss of appetite If you experience any of these, it is important to let your healthcare provider know immediately. What are the complications of metabolic acidosis if I have kidney disease or kidney failure? Increased bone loss (osteoporosis): Metabolic acidosis can lead to a loss of bone in your body. This can lead to a higher chance of fractures in important bones like your hips or backbone. Progression of kidney disease: Metabolic acidosis can make your kidney disease worse. Exactly how this happens is not clear. As acid builds up, kidney function lowers; and as kidney function lowers, acid builds up. This can lead to the progression of kidney disease. Muscle loss: Albumin is an important protein in your body that helps build and keep muscles healthy. Metabolic acidosis lowers the amount of albumin created in your body, and leads to muscle loss, or what is called � Continue reading >>
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 >>
Urine Ammonium, Metabolic Acidosis And Progression Of Chronic Kidney Disease
Urine Ammonium, Metabolic Acidosis and Progression of Chronic Kidney Disease Pourafshar N.a · Pourafshar S.a · Soleimani M.b,c aDepartment of Medicine at University of Virginia, Charlottesville, VA, USA bDepartment of Medicine, University of Cincinnati, Cincinnati, OH, USA cDepartment of Medicine Services, Veterans Medical Center, Cincinnati, OH, USA The metabolism of a typical Western diet generates 50–100 mEq of acid (H+) per day, which must be excreted in the urine for the systemic acid-base to remain in balance. The 2 major mechanisms that are responsible for the renal elimination of daily acid under normal conditions are ammonium (NH4+) excretion and titratable acidity. In the presence of systemic acidosis, ammonium excretion is intensified and becomes the crucial mechanism for the elimination of acid. The impairment in NH4+ excretion is therefore associated with reduced acid excretion, which causes excess accumulation of acid in the body and consequently results in metabolic acidosis. Chronic kidney disease (CKD) is associated with the impairment in acid excretion and precipitation of metabolic acidosis, which has an adverse effect on the progression of CKD. Recent studies suggest that the progressive decline in renal ammonium excretion in CKD is an important determinant of the ensuing systemic metabolic acidosis and is an independent factor for predicting the worsening of kidney function. While these studies have been primarily performed in hypertensive individuals with CKD, a closer look at renal NH4+ excretion in non-hypertensive individuals with CKD is warranted to ascertain its role in the progression of kidney disease. The elimination of acid (H+) by kidney is the most crucial step in the maintenance of systemic acid-base homeostasis [ 1 , 2 ]. The rena Continue reading >>
