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 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. 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 >>
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 >>
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 >>
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 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 >>
Acidosis
Acidosis, abnormally high level of acidity, or low level of alkalinity, in the body fluids, including the blood. There are two primary types of acidosis: respiratory acidosis and metabolic acidosis. Respiratory acidosis results from inadequate excretion of carbon dioxide from the lungs. This may be caused by severe acute or chronic lung disease, such as pneumonia or emphysema, or by certain medications that suppress respiration in excessive doses, such as general anesthetic agents. Metabolic acidosis occurs when acids are produced in the body faster than they are excreted by the kidneys or when the kidneys or intestines excrete excessive amounts of alkali from the body. Causes of metabolic acidosis include uncontrolled diabetes mellitus, shock, certain drugs or poisons, and renal failure, among others. Both respiratory and metabolic acidosis can be life-threatening and often require immediate medical attention. Compare alkalosis. Continue reading >>
Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Management Of Metabolic Acidosis
Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>
Treatment Of Acidosis In Ckd
Barts Health National Health Service Trust and William Harvey Research Institute, London, United Kingdom Dr. Muhammad M. Yaqoob, Barts Health National Health Service Trust and William Harvey Research Institute, Renal Unit, Royal London Hospital, Whitechapel, London E1 1BB, UK. Email: m.m.yaqoob{at}qmul.ac.uk Metabolic acidosis (MA) in advanced CKD results from a progressive reduction in the capacity of the kidneys to generate sufficient ammonia to excrete the daily production of hydrogen ions (equivalent to approximately 1 mmol/kg body weight) leading to the formation of a new steady state at the cost of a reduction in blood pH. MA is a relatively common complication in patients with advanced CKD, particularly when GFR falls below 30 ml/min ( 1 ). MA adversely affects protein and muscle metabolism and bone turnover, compounding the mineral-bone disorder of uremia. In addition, MA is also associated with increased inflammatory mediators, insulin resistance, and corticosteroid and parathyroid hormone production. This may result in growth restriction in children, loss of bone and muscle mass, negative nitrogen balance, and possibly an accelerated decline in renal function ( 2 ). Currently, there is good experimental but limited clinical evidence that MA contributes to protein energy wasting (PEW) in CKD patients ( 3 ). Several clinical trials in patients with ESRD, albeit of small size and limited follow-up, have demonstrated a benefit from the correction of acidosis on serum albumin and prealbumin levels, a reduction in the normalized protein catabolic rate ( 4 6 ), as well as an increase in the concentrations of branched chain and total essential amino acids ( 7 , 8 ). The evidence supporting a role for MA in the progression of CKD is less convincing. Some preclinical s Continue reading >>
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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 >>
Electrolyte And Acid-base Disorders In Chronic Kidney Disease And End-stage Kidney Failure
Electrolyte and Acid-Base Disorders in Chronic Kidney Disease and End-Stage Kidney Failure Department of Medicine, Division of Nephrology and Hypertension 200 First Street SW, Rochester, MN 55905 (USA) The kidneys play a pivotal role in the regulation of electrolyte and acid-base balance. With progressive loss of kidney function, derangements in electrolytes and acid-base inevitably occur and contribute to poor patient outcomes. As chronic kidney disease (CKD) has become a worldwide epidemic, medical providers are increasingly confronted with such problems. Adequate diagnosis and treatment will minimize complications and can potentially be lifesaving. In this review, we discuss the current understanding of the disease process, clinical presentation, diagnosis and treatment strategies, integrating up-to-date knowledge in the field. Although electrolyte and acid-base derangements are significant causes of morbidity and mortality in CKD and end-stage renal disease patients, they can be effectively managed through a timely institution of combined preventive measures and pharmacological therapy. Exciting advances and several upcoming outcome trials will provide further information to guide treatment and improve patient outcomes. Chronic kidney disease (CKD) has become a global epidemic with an estimated prevalence of 14% in the United States and 5-15% throughout the world [ 1 , 2 ]. It is associated with an increased risk of adverse cardiovascular outcomes, progression to end-stage renal disease (ESRD), and decreased survival. As the kidneys play a central role in the regulation of body fluids, electrolytes and acid-base balance, CKD and ESRD predictably result in multiple derangements including hyperkalemia, metabolic acidosis and hyperphosphatemia which, in turn, lead to Continue reading >>
Metabolic Acidosis And Progression Of Chronic Kidney Disease: Incidence, Pathogenesis, And Therapeutic Options
Nefrologia (English Version) 2012;32:724-30 | doi: 10.3265/Nefrologia.pre2012.Jul.11515 Metabolic acidosis and progression of chronic kidney disease: incidence, pathogenesis, and therapeutic options Acidosis metablica y avance de la enfermedad renal crnica: incidencia, patognesis y opciones teraputicas a Allegheny General Hospital, Pittsburgh, Pennsylvania, USA, b nephrology and hypertension, allegheny general hospital, pittsburgh, pennsylvania, USA, c Nephrology and Hypertension, Allegheny General Hospital. WPAHS, Temple University School of Medicine, Pittsburgh, Pennsylvania, USA, d nephrology and hypertension, Allegheny general hosptial.WPAHS,Temple University School of Medicine, Pittsburgh, Pennsylvania, USA, Tab. 1. Correlation of serum bicarbonate to changes in serum creatinine Hay una prevalencia importante de la acidosis metablica en los pacientes que padecen enfermedad renal crnica, presentndose en niveles tempranos de prdida de filtrado glomerular. La patognesis se basa en la falta de sntesis de bicarbonato srico con la acumulacin de cidos de naturaleza orgnica e inorgnica, ocasionando dao tubulointersticial a travs de la retencin de amoniaco y el depsito de complemento, aunque esta ltima hiptesis se ha cuestionado en el pasado. El uso emprico de bicarbonato oral representa una opcin teraputica interesanteque ha sido utilizada en estudios clnicos recientes. La disponibilidad de bicarbonato de sodio oral en sus diversas formas representa una opcin barata y simple de utilizar para decelerar la progresin de la enfermedad renal, sin mencionar las mejoras en el catabolismo proteico, la osteodistrofia renal y la mortalidad. In the chronic kidney disease population metabolic acidosis is prevalent presenting already in the early stages of renal dysfunction. The patho Continue reading >>
Renal Tubular Acidosis: Pathophysiology, Diagnosis And Treatment
Volume 23, Issue 6 , March 1977, Pages 1-66 Renal tubular acidosis: Pathophysiology, diagnosis and treatment Author links open overlay panel Robert G.Narins MartinGoldberg Choose an option to locate/access this article: Check if you have access through your login credentials or your institution. Robert G. Narins is Associate Professor of Medicine and Associate Director of Nephrology at the University of California, Los Angeles. Doctor Narins received his M.D. degree from State University of New York, Upstate Medical Center at Syracuse. Actively involved in UCLA's expanding clinical and research training program in nephrology, he has maintained an interest in acid-base physiology and in the pathophysiology of the metabolic acidoses and alkaloses. The control of renal ammonia synthesis and the acid-base changes associated with phosphate depletion have been areas of recent research activity. Martin Goldberg is Professor of Medicine, University of Pennsylvania School of Medicine and Chief, Renal Electrolyte Section, Hospital of the University of Pennsylvania. Doctor Goldberg received his M.D. degree from Temple University. A member of numerous professional societies, he serves on the Board of Governors of the American Board of Internal Medicine and on the Executive Committee of the American Society of Nephrology. Renal diseases, renal physiology, and fluid and electrolyte metabolism are among his scientific interests. Copyright 1977 Published by Mosby, Inc. Continue reading >>
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 >>
