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Lactic Acidosis Review

Lactic Acidosis: An Update

Lactic Acidosis: An Update

Clinical Chemistry and Laboratory Medicine (CCLM) Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R. Source Normalized Impact per Paper (SNIP) 2016: 1.112 [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 1975.00 / US$ 2960.00 / GBP 1619.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * [D] 2370.00 / US$ 3551.00 / GBP 1943.00 * *Prices in US$ apply to orders placed in the Americas only. Prices in GBP apply to orders placed in Great Britain only. Prices in represent the retail prices valid in Germany (unless otherwise indicated). Prices are subject to change without notice. Prices do not include postage and handling if applicable. RRP: Recommended Retail Price. Department of Anaesthesia and Critical Care, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Department of Clinical Chemistry, Adelaide and Meath Hospital, Tallaght, Dublin, Ireland Published Online: 2016-08-15 | DOI: Lactate is one of the most crucial intermediates in carbohydrate and nonessential amino acid metabolism. The complexity of cellular interactions and metabolism means that lactate can be considered a waste product for one cell but a useful substrate for another. The presence of elevated lactate levels in critically ill patients has important implications for morbidity and mortality. In this review, we provide a brief outline of the metabolism of lactate, the pathophysiology of lactic acidosis, the clinical significance of D-lactate, the role of lactate measurement in acutely ill patients, the methods used to measure lactate in blood or plasma and some of the methodological issues related to interferences Continue reading >>

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

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

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

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Systematic Review Of Current Guidelines, And Their Evidence Base, On Risk Of Lactic Acidosis After Administration Of Contrast Medium For Patients Receiving Metformin

Systematic Review Of Current Guidelines, And Their Evidence Base, On Risk Of Lactic Acidosis After Administration Of Contrast Medium For Patients Receiving Metformin

Systematic Review of Current Guidelines, and Their Evidence Base, on Risk of Lactic Acidosis after Administration of Contrast Medium for Patients Receiving Metformin 1From the Department of Diagnostic Imaging, Southern Health, 246 Clayton Rd, Clayton, VIC 3168, Australia (S.K.G., G.C.); and Centre for Clinical Effectiveness, Monash Institute of Health Services Research, Monash University, Clayton, Victoria, Australia (G.R., C.H.). From the 2008 RSNA Annual Meeting. Address correspondence to S.K.G. (e-mail: [emailprotected] ). To systematically review evidence about the relationship between metformin administration and the use of iodinated contrast medium and risk of lactic acidosis (LA) and to assess the quality of five current guidelines for use of contrast medium in patients who are taking metformin. A search strategy was developed by using search termsrelated to metformin, contrast media, and LA. Searches were conducted in MEDLINE (Ovid), all Evidence-based Medicine Reviews (Ovid), EMBASE, and Cochrane library databases and were augmented with searches for evidence-based guidelines on radiology and evidence-based medicine Web sites by using the Google Internet search engine. Guidelines were appraised by two independent reviewers by using the Appraisal of Guidelines Research and Evaluation Collaboration Instrument. Other studies were appraised by using structured appraisal checklists. Five guidelines were identified and five empirical studies met inclusion criteria. All guidelines had poor scores on some Appraisal of Guidelines for Research and Evaluation (AGREE) Collaboration criteria; poorer scores tended to occur in relation to objective assessment of rigor of guideline development, editorial independence, and applicability of the guideline to clinical practice. L Continue reading >>

Treatment Of Congenital Lactic Acidosis: A Review

Treatment Of Congenital Lactic Acidosis: A Review

@article{5f3665c8ab4249bc875974c9409bcc96, title = "Treatment of congenital lactic acidosis: A review", abstract = "Genetic defects causing congenital lactic acidosis involve fundamental processes of transformation of energy derived from food into useable ATP. The consequences are usually devastating, especially for high energy utilizing tissues such as the brain, heart, and skeletal muscles. While considerable progress has been made over the past 15 years in defining the specific biochemical, molecular, and genetic mechanisms of these defects, the development of effective approaches to treatment or prevention has been very limited. Potential strategies for treatment are specific to the particular cause and include changes in the fuel supply (diet), supplementation with enzyme co-factors (vitamins), use of enzyme activators (such as dichloroacetate), and, ultimately, organ or enzyme replacement. The success of these different kinds of interventions has been variable, but not very dramatic or definitive in most cases. Prenatal diagnosis has been successful in only a few cases, and will not prevent the majority of unexpected new cases. Future evaluation of therapeutic approaches will depend on clearer understanding of how various biochemical and genetic defects result in variable clinical outcomes, development of controlled clinical trials related to specific disorders, and advances in potential genetic interventions for correction of these complex, integrated energy-producing systems.", T1 - Treatment of congenital lactic acidosis N2 - Genetic defects causing congenital lactic acidosis involve fundamental processes of transformation of energy derived from food into useable ATP. The consequences are usually devastating, especially for high energy utilizing tissues such a Continue reading >>

Examining Clinical Similarities Between Myalgic Encephalomyelitis/chronic Fatigue Syndrome And D-lactic Acidosis: A Systematic Review

Examining Clinical Similarities Between Myalgic Encephalomyelitis/chronic Fatigue Syndrome And D-lactic Acidosis: A Systematic Review

The pursuit for clarity in diagnostic and treatment pathways for the complex, chronic condition of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) continues. This systematic review raises a novel question to explore possible overlapping aetiology in two distinct conditions. Similar neurocognitive symptoms and evidence of d-lactate producing bacteria in ME/CFS raise questions about shared mechanisms with the acute condition of d-lactic acidosis (d-la). d-la case reports published between 1965 and March 2016 were reviewed for episodes describing both neurological symptoms and high d-lactate levels. Fifty-nine d-la episodes were included in the qualitative synthesis comparing d-la symptoms with ME/CFS diagnostic criteria. A narrative review of d-la mechanisms and relevance for ME/CFS was provided. The majority of neurological disturbances reported in d-la episodes overlapped with ME/CFS symptoms. Of these, the most frequently reported d-la symptoms were motor disturbances that appear more prominent during severe presentations of ME/CFS. Both patient groups shared a history of gastrointestinal abnormalities and evidence of bacterial dysbiosis, although only preliminary evidence supported the role of lactate-producing bacteria in ME/CFS. Interpretation of results are constrained by both the breadth of symptoms included in ME/CFS diagnostic criteria and the conservative methodology used for d-la symptom classification. Several pathophysiological mechanisms in ME/CFS were not examined. Shared symptomatology and underlying microbiotagutbrain interactions raise the possibility of a continuum of acute (d-la) versus chronic (ME/CFS) presentations related to d-lactate absorption. Measurement of d-lactate in ME/CFS is needed to effectively evaluate whether subclinical d Continue reading >>

Lactic Acidosis: Clinical Implications And Management Strategies

Lactic Acidosis: Clinical Implications And Management Strategies

Lactic acidosis: Clinical implications and management strategies Cleveland Clinic Journal of Medicine. 2015 September;82(9):615-624 Quality Officer, Medical Intensive Care Unit, Departments of Pulmonary Medicine and Critical Care Medicine, Respiratory Institute, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Department of Pharmacy, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Medical ICU Clinical Specialist, Department of Pharmacy, Cleveland Clinic Director, Medical Intensive Care Unit, Department of Critical Care Medicine, Respiratory Institute, Cleveland Clinic Address: Anita J. Reddy, MD, Department of Critical Care Medicine, Respiratory Institute, A90, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: [email protected] ABSTRACTIn hospitalized patients, elevated serum lactate levels are both a marker of risk and a target of therapy. The authors describe the mechanisms underlying lactate elevations, note the risks associated with lactic acidosis, and outline a strategy for its treatment. Serum lactate levels can become elevated by a variety of underlying processes, categorized as increased production in conditions of hypoperfusion and hypoxia (type A lactic acidosis), or as increased production or decreased clearance not due to hypoperfusion and hypoxia (type B). The higher the lactate level and the slower the rate of normalization (lactate clearance), the higher the risk of death. Treatments differ depending on the underlying mechanism of the lactate elevation. Thus, identifying the reason for hyperlactatemia and differentiating between type A and B lactic acidosis are of the utmo Continue reading >>

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further Clarifying The Relationship Between Metformin, Acute Kidney Injury And Lactic Acidosis

Further clarifying the relationship between metformin, acute kidney injury and lactic acidosis Subscribe to Nature Reviews Nephrology for full access: Diabetes mellitus: complex interplay between metformin, AKI and lactic acidosis Bell, S., Soto-Pedre, E., Connelly, P., Livingstone, S. & Pearson, E. Clarifying the relationship between metformin, acute kidney injury and lactic acidosis . Nat. Rev. Nephrol. , (2017). Rhee, C. M., Kovesdy, C. P. & Kalantar-Zadeh, K. Risks of metformin in type 2 diabetes and chronic kidney disease: lessons learned from Taiwanese data Risk of acute kidney injury and survival in patients treated with metformin: an observational cohort study Acute kidney injury, plasma lactate concentrations and lactic acidosis in metformin users: a GoDarts study . Diabetes Obes. Metab. 19, 1579–1586 (2017). Inzucchi, S. E., Lipska, K. J., Mayo, H., Bailey, C. J. & McGuire, D. K. Metformin in patients with type 2 diabetes and kidney disease: a systematic review Restricting metformin in CKD: continued caution warranted . Am. J. Kidney Dis. 66, 1101–1102 (2015). Should restrictions be relaxed for metformin use in chronic kidney disease? Yes, they should be relaxed! What's the fuss? Should restrictions be relaxed for metformin use in chronic kidney disease? No, we should never again compromise safety! Metformin in chronic kidney disease: more harm than help? Lancet Diabetes Endocrinol. 3, 579–581 (2015). Metformin use in type 2 diabetes mellitus With CKD: is it time to liberalize dosing recommendations? Kalantar-Zadeh, K., Uppot, R. N. & Lewandrowski, K. B. Case records of the Massachusetts General Hospital. Case 23–2013. A 54-year-old woman with abdominal pain, vomiting, and confusion United States Renal Data System. USRDS 2017 Annual Data Report: Atlas Continue reading >>

Mortality Rate In So-called

Mortality Rate In So-called "metformin-associated Lactic Acidosis": A Review Of The Data Since The 1960s.

Mortality rate in so-called "metformin-associated lactic acidosis": a review of the data since the 1960s. This study shows that, in general, mortality from metformin-associated lactic acidosis (MALA) decreased from 50% to 25% from 1960s to the present.This Recommendation is of an article referenced in an F1000 Faculty Review also written by Orson W. Moe, Amy Quynh Trang Pham and Li Hao Richie Xu. To read the rest of this recommendation and access over 145,000 article recommendations from 3,700+ journals across biomedicine, register Send a recommendation to your institution's librarian or information manager to request an extended free trial for articles in biology and medicine, contributed inclusion in F1000Prime to help you filter recommendations, plus relevant articles as engine clusters of related articles and be alerted as soon as similar articles appear in If you think you should be able to access this content, please contact us . If you've forgotten your password, please enter your email address below and we'll send you instructions on how to reset your password. The email address should be the one you originally registered with F1000. Email address not recognised, please try again We are unable to reset your password, please contact [email protected] to reactivate your account, quoting error code UACC/DEL You registered with F1000 via Google, so we cannot reset your password. If you still need help with your Google account password, please click here . You registered with F1000 via Facebook, so we cannot reset your password. If you still need help with your Facebook account password, please click here . You registered with F1000 via ORCID, so we cannot reset your password. If you still need help with your ORCID account password, please click here . Email [email protected] Continue reading >>

Unusual Case Of Severe Lactic Acidosis In A Liver Transplant Patient

Unusual Case Of Severe Lactic Acidosis In A Liver Transplant Patient

Unusual Case of Severe Lactic Acidosis in a Liver Transplant Patient 1Department of Anesthesiology, Drexel University College of Medicine/Hahnemann University Hospital, Philadelphia, PA, USA 2Department of Surgery, Drexel University College of Medicine/Hahnemann University Hospital, Philadelphia, PA, USA Correspondence should be addressed to Michael S. Green Received 1 September 2017; Revised 30 October 2017; Accepted 3 December 2017; Published 17 December 2017 Copyright 2017 Shweta Yemul Golhar et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Lactic acidosis is a standard indicator for oxygen debt and some other very significant causes. We describe a case of liver transplant patient presenting with vague abdominal pain and lactic acidosis without any liver dysfunction/failure/ischemia/rejection or sepsis. The imaging studies showed vague bowel edema and normal hepatic perfusion. The patient continued to deteriorate with rising lactic acidosis when a repeat CT abdomen eventually showed signs of lymphomatosis peritonei. Biopsy revealed the unusual diagnosis of posttransplant lymphoproliferative disorder. Immediate discontinuation of immunosuppression and initiation of chemotherapy led to clinical improvement. Our intention of presenting this case is to increase awareness of posttransplant lymphoma and propose lactic acidosis as not only an indicator of liver dysfunction or rejection but also an aid for diagnosis of this unusual but fatal and potentially curable condition. Lactic acidosis is a universally accepted marker for adequacy of perfusion. It is the end product of anaerobic metabolism and thu Continue reading >>

Review: Lactate & Sepsis

Review: Lactate & Sepsis

On this snowy, Stockholm Sunday, I look out from my quarters on the Mlardrottningen across the still, icy waters and I think about a cirrhotic patient for whom I recently cared. She presented with significant dyspnea as she had stopped taking her diuretics. Instead, she was using excessivedoses of her friends albuterol inhaler to treat her shortness of breath. Additionally, she had been drinking alcohol heavily for seven days prior to admission. Her venous pH was 7.38, and her lactate concentration was over 7.0 mmol/L a sepsis alert was called. In a very recent and fantastic review by Suetrong and Walley , the mechanisms of lactate formation are revisited. Notably, a distinction is made between hyperlactatemia an elevated concentration of lactate in the blood and lactic acidosis, which is comprised of both hyperlactatemia and systemic acidosis. The authors discuss the mechanisms by which lactate is formed and aptly detail that many of these processes do not result in acid formation. Notably, while the generation of pyruvate from glucose does generate [H+], the conversion of pyruvate to lactate consumes an equimolar amount of [H+] such that the production of lactate does not result in a net gain of protons [i.e. acidosis]. So where does the acidosis with which we are so familiar come from? The excess protons are the result of an impaired Krebs Cycle. In states of true tissue oxygen debt, intracellular protons can no longer be consumed during the Krebs Cycle; consequently, intracellular acidosis and acidemia ensue. It is this latter means of hyperlactatemia to which we attach the label type A or lactic acidosis with clinical evidence of tissue hypoxia. However, as described 40 years ago , excessive lactate may come from clinical states where there is no evidence of tissu Continue reading >>

D-lactic Acidosis A Very Rare Form Of Metabolic Acidosis Explained

D-lactic Acidosis A Very Rare Form Of Metabolic Acidosis Explained

D-lactic acidosis a very rare form of metabolic acidosis explained Summarized from Kowgli N, Chhabra L. D-lactic acidosis: an underrecognized complication of short bowel syndrome. Gastroenterology Research and Practice 2015. Available on line at: Health demands that the pH of blood is maintained within a narrow range (7.35-7.45). Monitoring this physiological imperative and detection of so-called acid-base disturbance, in which blood pH is either increased or decreased, is one of the principal clinical utilities of blood gas analysis. Metabolic acidosis one of the four classes of acid-base disturbance identified by blood gas analysis is most commonly the result of abnormal accumulation of lactic acid, either due to increased metabolic production, reduced elimination or a combination of the two.This most common form of metabolic acidosis should, strictly speaking, be called L-lactic acidosis rather than simply lactic acidosis, as is usually the case. The nomenclature, L-lactic acidosis recognizes that in nature lactic acid can exist in two stereoisomeric forms: L-lactic acid and D-lactic acid. In humans (and indeed all mammals) lactic acid exists almost exclusively as the L-isoform, and it is accumulation of this isoform that accounts for almost all cases of lactic acidosis. A recently published article focuses on the very rare instance in which lactic acidosis is caused not by accumulation of L-lactic acid, but rather accumulation of D-lactic acid. The authors provide the detail of D-lactic acidosis under five headings: pathophysiology, clinical features, diagnosis and treatment. Central to an understanding of the pathophysiology of D-lactic acidosis is the recognition that many bacterial species normally present in the colon produce D-lactic acid. An overgrowth of the Continue reading >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe Continue reading >>

Does Metformin Increase The Risk Of Fatal Or Nonfatal Lactic Acidosis?

Does Metformin Increase The Risk Of Fatal Or Nonfatal Lactic Acidosis?

WILLIAM E. CAYLEY, JR., MD, MDiv, University of Wisconsin Department of Family Medicine, Eau Claire, Wisconsin Am Fam Physician. 2010 Nov 1;82(9):1068-1070. Clinical Scenario A 70-year-old woman with type 2 diabetes mellitus who is in otherwise good health is experiencing gradually increasing glucose levels. Her physician considers starting her on an oral diabetes agent, but is concerned that her age may put her at risk for adverse effects if she is treated with metformin (Glucophage). Clinical Question Does metformin increase the risk of fatal or nonfatal lactic acidosis? Evidence-Based Answer In patients without standard contraindications to metformin therapy, metformin does not increase the risk of lactic acidosis.1 (Strength of Recommendation = B, based on inconsistent or limited-quality patient-oriented evidence) Practice Pointers The first-line treatments recommended for type 2 diabetes are lifestyle changes and metformin, which is a biguanide antihyperglycemic agent.2 Demonstrated benefits of metformin include lower cardiovascular mortality than other oral diabetes medications3 and a reduced risk of death or myocardial infarction in overweight patients with type 2 diabetes.4 However, because an earlier biguanide, phenformin, was removed from the market after being linked to several cases of lactic acidosis, there have been concerns that metformin may predispose patients to lactic acidosis as well. In light of this, metformin is considered contraindicated in patients with chronic renal insufficiency, pulmonary disease, or hypoxic conditions; abnormal hepatic function; peripheral vascular disease; and in those older than 65 years. The use of metformin in patients with heart failure continues to be controversial.1 The authors of this Cochrane review found no cases o Continue reading >>

Lactic Acidosis | Nejm

Lactic Acidosis | Nejm

This article is available to subscribers. Subscribe now . Already have an account? Sign in Review Article Disorders of Fluids and ElectrolytesFree Preview When lactic acidosis accompanies low-flow states or sepsis, mortality rates increase sharply. This review summarizes our current understanding of the pathophysiological aspects of lactic acidosis, as well as the approaches to its diagnosis and management. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. Dr. Kraut reports holding pending patents related to the use of selective NHE1 inhibitors in the treatment of metabolic acidosis (lapsed without the filing of a nonprovisional application) and systems, methods, and compositions for improved treatment of acidosis. No other potential conflict of interest relevant to this article was reported. From Medical and Research Services, Membrane Biology Laboratory, and the Division of Nephrology, David Geffen School of Medicine, University of California, Los Angeles, and the Veterans Affairs Greater Los Angeles Healthcare System both in Los Angeles (J.A.K.); and the Department of Medicine, Division of Nephrology, St. Elizabeths Medical Center, and the Department of Medicine, Tufts University School of Medicine both in Boston (N.E.M.). Address reprint requests to Dr. Kraut at the Division of Nephrology, VHAGLA Healthcare System, 11301 Wilshire Blvd., Los Angeles, CA 90073; or at [emailprotected] ; or to Dr. Madias at the Department of Medicine, St. Elizabeths Medical Center, 736 Cambridge St., Boston, MA 02135, or at [emailprotected] . Continue reading >>

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