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 >>
Kidney Stones 2012: Pathogenesis, Diagnosis, And Management
Kidney Stones 2012: Pathogenesis, Diagnosis, and Management Department of Internal Medicine, Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390 Address all correspondence and requests for reprints to: Khashayar Sakhaee, M.D., 5323 Harry Hines Boulevard, Dallas, Texas 75390. Search for other works by this author on: Department of Internal Medicine, Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390 Search for other works by this author on: Department of Internal Medicine, Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 97, Issue 6, 1 June 2012, Pages 18471860, Khashayar Sakhaee, Naim M. Maalouf, Bridget Sinnott; Kidney Stones 2012: Pathogenesis, Diagnosis, and Management, The Journal of Clinical Endocrinology & Metabolism, Volume 97, Issue 6, 1 June 2012, Pages 18471860, The pathogenetic mechanisms of kidney stone formation are complex and involve both metabolic and environmental risk factors. Over the past decade, major advances have been made in the understanding of the pathogenesis, diagnosis, and treatment of kidney stone disease. Both original and review articles were found via PubMed search reporting on pathophysiology, diagnosis, and management of kidney stones. These resources were integrated with the authors' knowledge of the field. Nephrolithiasis remains a major economic and health burden worldwide. Nephrolithiasis is considered a systemic disorder associated with chronic kidney disease Continue reading >>
Pathophysiology, Diagnosis, And Management Of Aortic Dissection - Oxford Medicine
Have a high index of suspicion for aortic dissection in patients presenting with chest pain and remember it is the great masquerader that can mimic disease of any organ. Aortic dissection kills via: rupture, cardiac tamponade, acute aortic insufficiency, and organ ischaemia. Use liberal imaging (usually by CT and echocardiography). Remember the utility of the triple rule-out CT (to rule out dissection, myocardial infarction, pulmonary embolism). Upon diagnosis, start anti-impulse treatment (Rx). Do not use unopposed afterload reduction (glyceryl trinitrate, nitroprusside) without concomitant -blockade to decrease dp/dt. Ascending aortic dissection requires urgent surgery; Descending aortic dissection is treated medically. Diagnosis of aortic dissection is both difficult and of paramount importance for the reasons mentioned in the introductory paragraph. The quintessential symptom is pain with characteristics that vividly reflect the nature of the disorder. The pain is described as the most severe possible (more than a kidney stone and more than childbirth), with a tearing or knife-like quality. With ascending dissection, the pain originates and is maximal under the breastbone. With descending dissection, the pain typically originates between the shoulder blades in the upper thoracic back. The pain may migrate distally as the dissection splits the layers further, travelling toward the abdomen and legs. The pain usually has an abrupt onset and is often preceded by acute physical exertion or an acute emotional event. A family history of aortic aneurysm, aortic valve disease (bicuspid valve is strongly associated with aortic dissection), or premature sudden cardiac death should be sought. This may be negative, but occasionally, the murmur of aortic insufficiency is heard, Continue reading >>
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Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus
University of Gondar, Ethopia *Corresponding Author: Habtamu Wondifraw Baynes Lecturer Clinical Chemistry University of Gondar, Gondar Amhara 196, Ethiopia Tel: +251910818289 E-mail: [email protected] Citation: Baynes HW (2015) Classification, Pathophysiology, Diagnosis and Management of Diabetes Mellitus. J Diabetes Metab 6:541. doi:10.4172/2155-6156.1000541 Copyright: © 2015 Baynes HW. 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 author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Diabetes Mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglycemia either immune-mediated (Type 1 diabetes), insulin resistance (Type 2), gestational or others (environment, genetic defects, infections, and certain drugs). According to International Diabetes Federation Report of 2011 an estimated 366 million people had DM, by 2030 this number is estimated to almost around 552 million. There are different approaches to diagnose diabetes among individuals, The 1997 ADA recommendations for diagnosis of DM focus on fasting Plasma Glucose (FPG), while WHO focuses on Oral Glucose Tolerance Test (OGTT). This is importance for regular follow-up of diabetic patients with the health care provider is of great significance in averting any long term complications. Keywords Diabetes mellitus; Epidemiology; Diagnosis; Glycemic management Abbreviations DM: Diabetes Mellitus; FPG: Fasting Plasma Glucose; GAD: Glutamic Acid Decarboxylase; GDM: Gestational Diabetes Mellitus; HDL-cholesterol: High Density Lipoprotein cholesterol; HLA: Human Leucoid Antigen; IDD Continue reading >>
Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Pathophysiology 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 >>
Bicarbonate Therapy In Severe Metabolic Acidosis
Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>
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 >>
Lactic Acidosis: Pathophysiology, Diagnosis And Treatment - Sassit
Lactic acidosis: pathophysiology, diagnosis and treatment - SASSiT The Netherlands Journal of Medicine 2001;58:128136 Review Lactic acidosis: pathophysiology, diagnosis and treatment * A. van der Beek , P.H.E.M. de Meijer, A.E. Meinders Department of General Internal Medicine, Leiden University Medical Center, Albinusdreef 2, 2300 RC Leiden, The Netherlands Received 5 December 2000; accepted 12 December 2000 Abstract Lactic acidosis is common in severely ill patients. We describe four patients with a lactic acidosis combined with other acidbase disturbances. In daily practice it is important to consider these combined disturbances since there is no specific treatment in lactic acidosis. Treating the underlying causes of the acidbase disturbances is the only warranted intervention. However, lactic acidosis is still associated with high mortality. 2001 Elsevier Science B.V. All rights reserved. Keywords: Lactic acidosis; Combined acidbase disturbances; Anion gap; Predicted pCO ; Metabolic acidosis 2 Introduction subcutaneous hematomas. He had a myocardial infarction 24 years previously. Although he had a We describe four patients who presented in the long history of alcohol abuse there were no hospital emergency room with lactic acidosis. The lactic admissions due to alcohol-related problems. His acidoses originated from different causes. Partially medication consisted of fenprocoumon and metodue to these causes the patients had other acidbase prolol. His general practitioner had stopped the disturbances as well. In the discussion we deal with fenprocoumon 7 days before because of the hematothe diagnostic work-up for combined acidbase mas. Nevertheless his condition deteriorated: he was disturbances. We rely on the calculation of the anion no longer able to walk, did not Continue reading >>
Pediatric Traumatic Brain Injury: Epidemiology, Pathophysiology, Diagnosis, And Treatment
Home Pediatric Traumatic Brain Injury: Epidemiology, Pathophysiology, Diagnosis, and Treatment Pediatric Traumatic Brain Injury: Epidemiology, Pathophysiology, Diagnosis, and Treatment Pediatric Traumatic Brain Injury: Epidemiology, Pathophysiology, Diagnosis, and Treatment Laleh Gharahbaghian, MD, Clinical Instructor of Surgery / Emergency Medicine; Associate Director, Emergency Ultrasound, Stanford University School of Medicine, Stanford, CA Bill Schroeder, DO, FAAP, Clinical Instructor of Surgery / Emergency Medicine, Stanford University School of Medicine, Stanford, CA Robert Mittendorff, MD, Emergency Physician, Kaiser Permanente, Diablo Services Area, Walnut Creek, CA N. Ewen Wang, MD, Assistant Professor of Surgery / Emergency Medicine; Associate Director, Pediatric Emergency Medicine, Stanford University School of Medicine, Stanford, CA Ron Perkin, MD, MA, Professor and Chairman, Department of Pediatrics, The Brody School of Medicine at East Carolina University, Greenville, NC Pediatric head trauma is a common presenting complaint to the emergency department (ED) and is a major cause of pediatric death and disability. This article will address the epidemiology, pathophysiology, diagnosis, and management of moderate to severe pediatric traumatic brain injury (TBI), with a focus on strategies to improve outcome. Pediatric mild head injuries will be addressed in a future issue of Pediatric Emergency Medicine Reports. TBI accounts for a significant number of pediatric deaths, disability, and permanent injury. Pediatric head trauma results in approximately 400,000 ED patient presentations and 30,000 hospitalizations annually.1 Severe pediatric TBI, which ranges between 10% and 30% of annual pediatric head injury presentations, is estimated to have a mortality rate o Continue reading >>
Details And Download Full Text Pdf: Metabolic Acidosis: Pathophysiology, Diagnosis And Management.
Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol 2010 May 23;6(5):274-85. Epub 2010 Mar 23. 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 administration of base for th Continue reading >>
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 >>
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 >>
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 >>
"alkali Therapy In Lactic Acidosis" By Zeid J. Khitan, Md, Deepak Malhotra, Md Et Al.
This report attempts to frame the debate about clinical administration of sodium bicarbonate in the setting of lactic acidosis in terms of simple questions. Specifically, we address why we develop lactic acidosis in some circumstances, how acute lactic acidosis impairs cardiovascular function and why sodium bicarbonate may have deleterious effects which limit its utility. We also attempt to explore treatment alternatives to sodium bicarbonate. All authors have no conflict of interest to disclose. 1. Jung B, Rimmele T, Le Goff C, Chanques G, Corne P, Jonquet O, Muller L, Lefrant JY, Guervilly C, Papazian L, Allaouchiche B and Jaber S. Severe metabolic or mixed acidemia on intensive care unit admission: incidence, prognosis and administration of buffer therapy. A prospective, multiple-center study. Crit Care. 2011;15:R238. 2. Kraut JA and Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010;6:274-85. 3. Lee SW, Hong YS, Park DW, Choi SH, Moon SW, Park JS, Kim JY and Baek KJ. Lactic acidosis not hyperlactatemia as a predictor of in hospital mortality in septic emergency patients. Emerg Med J. 2008;25:659-65. 4. Gabow PA, Kaehny WD, Fennessey PV, Goodman SI, Gross PA and Schrier RW. Diagnostic importance of an increased serum anion gap. N Engl J Med. 1980;303:854-8. 5. Kraut JA and Madias NE. Lactic acidosis. N Engl J Med. 2014;371:2309-19. 6. Luft FC. Lactic acidosis update for critical care clinicians. J Am Soc Nephrol. 2001;12 Suppl 17:S15-9. 7. Adeva-Andany M, Lopez-Ojen M, Funcasta-Calderon R, Ameneiros-Rodriguez E, Donapetry-Garcia C, Vila-Altesor M and Rodriguez-Seijas J. Comprehensive review on lactate metabolism in human health. Mitochondrion. 2014;17:76-100. 8. Madias NE. Lactic acidosis. Kidney Int. 1986;29:752-74. 9. C Continue reading >>
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 >>
