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Keppra Lactic Acidosis

Four Important Epilepsy Trials

Four Important Epilepsy Trials

This feature requires the newest version of Flash. You can download it here . American Academy of Neurology Meeting: 4 Important Epilepsy Trials Welcome. This is Dr. Andrew Wilner reporting from Medscape with highlights from the 65th Annual Meeting of the American Academy of Neurology in San Diego, California. Today I will be summarizing 4 interesting posters on epilepsy. The first poster, by Liu and colleagues, is titled, "The New Antiepileptic Drugs (Levetiracetam and Oxcarbazepine) Compared with Traditional Antiepileptic Drugs (Carbamazepine and Valproate) in the Initial 52 Weeks of Monotherapy for Epilepsy Induced by MELAS -- An Open-Label, Prospective, Randomised Controlled Multicenter Study."[ 1 ] MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is caused by mutations in mitochondrial DNA. The major findings of this study are shown in the Table. Although one could take issue with the dosages used, all of the antiepileptic drugs were similar in terms of efficacy and adverse events with the exception of valproate. This study is important because it provides guidance for selecting antiepileptic drugs in the uncommon but important cases of MELAS. The next poster is titled, "Seizures and Epilepsy After Stroke: Resources and Costs Assessment," by Guekht and colleagues.[ 2 ] In this study, there were 298 patients with stroke, as follows: 3 patients (1%) had both early and late seizures; and 3 patients (1%) had late seizures only. These patients were compared with control patients who had similar National Institutes of Health stroke scale scores (10.5 in cases vs. 9.5 in controls). Cases with seizures had a mortality rate of 50%, whereas control patients had a mortality rate of only 5.7%. The group with seizures spent more days in the in Continue reading >>

Wookycongress Sin2015 56 Congresso Nazionale Societ Italiana Di Nefrologia

Wookycongress Sin2015 56 Congresso Nazionale Societ Italiana Di Nefrologia

Efficacia della SLED nellIRA da acidosi lattica associata allassunzione di metformina in quattro pazienti LAcidosi lattica, associata allimpiego di metformina nella nostra esperienza, non una rara complicanza. Essa potenzialmente fatale solo se non trattata. Il farmaco pu provocare Acidosi lattica per la presenza di concause che facilitano la tossicit del farmaco come la disidratazione, linsufficienza renale acuta, lipossia, lepatopatia, la cardiopatia, luso di mezzi di contrasto o per luso della stessa a dosi incongrue. I quattro casi da noi osservati nel corso di appena 4 mesi, in pazienti con presenza di lievi comorbilit, sono correlati alluso di metformina a dosaggi superiori ai 2 grammi die. Questo dosaggio sembra essere il fattore chiave dei numerosi casi osservati. La terapia di supporto, rappresentata dallespansione del volume, dal supporto aminico e dal rimpiazzo di bicarbonato non risulta essere efficace se contemporaneamente non sinizia subito un trattamento sostitutivo. La SLED (Sustained Low EfficiencyDialysis) una valida alternativa allemodiafiltrazione continua nel trattamento di questa complicanza. Descriviamo 4 casi osservati nel corso di 4 mesi Caso 1:paziente femmina di 66 anni, recente esecuzione di coronarografia con angioplastica e posizionamento di stent medicato, il giorno dopo il trattamento contrazione della diuresi, lieve algia addominale e diarrea, pressione arteriosa (PA) di 100/70, F.C. di 95/b/min., ipotermia (35.5C), oligo-anuria. Gli esami ematochimici evidenziavano creatinina di 6.9 mg/dl, K di 6.6 mmol/l, allemogasanalisi (ega) arteriosa lattati di 17 mmol/l (v.n. fino a 0.75 mmol/l), pH di 6.85, bicarbonati di 5.6 mmol/l, anion gap di 48.7 mmol/l e pCO2 di 18.6 mmHg. Lanamnesi patologica includeva diabete tipo 2, ipertensione arterio Continue reading >>

Lactic Acidosis Linked To Chronic Fatigue Syndrome / Fibromyalgia Symptoms

Lactic Acidosis Linked To Chronic Fatigue Syndrome / Fibromyalgia Symptoms

Lactic Acidosis linked to Chronic Fatigue Syndrome / Fibromyalgia Symptoms Chronic Fatigue Syndrome (CFS) or Fibromyalgia symptoms can be due to various reasons. It is identified that lactic acidosis can be a one of the factor and also there is a link between both. Many researches are going on to understand more about the causes and treatment for fibromyalgia and chronic conditions. Understanding the link between lactic acidosis and CFS or Fibromyalgia can be very helpful in finding out the association of this condition with that of other problems in the body. In simple terms it is said that, when lactate builds up in the body that condition is called as lactic acidosis. This can result to a situation where the body will have low pH. During this body will have excessive amount of acid affecting the normal metabolism of the body. It is identified that this can be responsible for Chronic Fatigue Syndrome or Fibromyalgia Symptoms. Or in other situations, lactic acidosis can also be due to the effect of chronic conditions, poisoning, fatigue, overdoses, medication etc. Though these are the causes for lactic acidosis to occur, there are also other symptoms seen such as vomiting, irritable bowel syndrome, systemic inflammatory response syndrome, infections etc. It is easy to identify Lactic Acidosis with the help of clinical analysis of blood. Blood samples can be used to find this out. After it is identified, the next step is to identify the cause of lactic acidosis in order to look for treatment. As a treatment measure in some patients, blood purification process is carried out but it can just be a temporary solution. The changes to diet is also suggested to patients who have rare form of lactic acidosis which can also be chronic condition. This is caused by mitochondrial Continue reading >>

Will You Have Lactic Acidosis With Levetiracetam - From Fda Reports - Ehealthme

Will You Have Lactic Acidosis With Levetiracetam - From Fda Reports - Ehealthme

Top other side effects for these people *: Hypotension (abnormally low blood pressure): 35 people, 61.40% Cardiopulmonary Failure (cessation of normal circulation of the blood due to failure of the heart to contract): 33 people, 57.89% Mental Status Changes (general changes in brain function, such as confusion, amnesia (memory loss), loss of alertness, loss of orientation): 22 people, 38.60% * Approximation only. Some reports may have incomplete information. How to use the study: print a copy of the study and bring it to your health teams to ensure drug risks and benefits are fully discussed and understood. A study for a 74 year old woman who takes Atrovent NOTE: The study is based on active ingredients and brand name. Other drugs that have the same active ingredients (e.g. generic drugs) are NOT considered. WARNING: Please DO NOT STOP MEDICATIONS without first consulting a physician since doing so could be hazardous to your health. DISCLAIMER: All material available on eHealthMe.com is for informational purposes only, and is not a substitute for medical advice, diagnosis, or treatment provided by a qualified healthcare provider. All information is observation-only, and has not been supported by scientific studies or clinical trials unless otherwise stated. Different individuals may respond to medication in different ways. Every effort has been made to ensure that all information is accurate, up-to-date, and complete, but no guarantee is made to that effect. The use of the eHealthMe site and its content is at your own risk. You may report adverse side effects to the FDA at or 1-800-FDA-1088 (1-800-332-1088). If you use this eHealthMe study on publication, please acknowledge it with a citation: study title, URL, accessed date. Continue reading >>

Lactic Acidosis With Keppra

Lactic Acidosis With Keppra

Since the mirena was put in due to heavy periods and fibroids, I have had really sore muscles and ligaments. Especially upon waking. I did a couple of push ups and now have tendonitis. When I get up in the morning, it feels like lactic acid and like Lactic Acidosis Clinical Trials and Studies Treatments might be new drugs or new combinations of drugs, new surgical procedures or devices, or new ways to use existing treatments. The goal of clinical trials is to determine if a new test or treatment works and is safe. Clinical trials can also look at other aspects of care, such as improving the quality of life for people with chronic illnesses. People participate in clinical trials for a variety of reasons. Healthy volunteers say they participate to help others and to contribute to moving science forward. Participants with an illness or disease also participate to help others, but also to possibly receive the newest treatment and to have the additional care and attention from the clinical trial staff. Continue reading >>

Causes And Evaluation Of Hyperkalemia In Adults

Causes And Evaluation Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem. Potassium enters the body via oral intake or intravenous infusion, is largely stored in the cells, and is then excreted in the urine. The major causes of hyperkalemia are increased potassium release from the cells and, most often, reduced urinary potassium excretion (table 1). This topic will review the causes and evaluation of hyperkalemia. The clinical manifestations, treatment, and prevention of hyperkalemia, as well as a detailed discussion of hypoaldosteronism (an important cause of hyperkalemia), are presented elsewhere. (See "Clinical manifestations of hyperkalemia in adults" and "Treatment and prevention of hyperkalemia in adults" and "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)".) BRIEF REVIEW OF POTASSIUM PHYSIOLOGY An understanding of potassium physiology is helpful when approaching patients with hyperkalemia. Total body potassium stores are approximately 3000 meq or more (50 to 75 meq/kg body weight) [1]. In contrast to sodium, which is the major cation in the extracellular fluid and has a much lower concentration in the cells, potassium is primarily an intracellular cation, with the cells containing approximately 98 percent of body potassium. The intracellular potassium concentration is approximately 140 meq/L compared with 4 to 5 meq/L in the extracellular fluid. The difference in distribution of the two cations is maintained by the Na-K-ATPase pump in the cell membrane, which pumps sodium out of and potassium into the cell in a 3:2 ratio. The ratio of the potassium concentrations in the cells and the extracellular fluid is the major determinant of the resting membrane potential across the cell membrane, which sets the stage for the generation of the action potential that is e Continue reading >>

Brenda - Information On Ec 3.6.3.44 - Xenobiotic-transporting Atpase

Brenda - Information On Ec 3.6.3.44 - Xenobiotic-transporting Atpase

Oral cyclosporin A inhibits CD4 T cell P-glycoprotein activity in HIV-infected adults initiating treatment with nucleoside reverse transcriptase inhibitors. The expression of P-glycoprotein and cellular kinases is modulated at the transcriptional level by infection and highly active antiretroviral therapy in a primate model of AIDS. The human multidrug resistance P-glycoprotein is inactive when its maturation is inhibited: potential for a role in cancer chemotherapy. Effect of CYP2C19 and ABCB1 single nucleotide polymorphisms on outcomes of treatment with ticagrelor versus clopidogrel for acute coronary syndromes: a genetic substudy of the PLATO trial. Genetic polymorphisms of CYP2C19*2 and ABCB1 C3435T affect the pharmacokinetic and pharmacodynamic responses to clopidogrel in 401 patients with acute coronary syndrome. Genetic variants in ABCB1 and CYP2C19 and cardiovascular outcomes after treatment with clopidogrel and prasugrel in the TRITON-TIMI 38 trial: a pharmacogenetic analysis. Near patient anti-platelet response testing over time and gene analysis in patients admitted with acute coronary syndromes. Effect of new oxicam derivatives on efflux pumps overexpressed in resistant a human colorectal adenocarcinoma cell line. Effects of cyclosporin A and a non-immunosuppressive analogue, O-acetyl cyclosporin A, upon the growth of parent and multidrug resistant human lung cancer cells in vitro. Effects of P-glycoprotein expression on cyclic AMP and volume-activated ion fluxes and conductances in HT-29 colon adenocarcinoma cells. Effects of the flavonoid biochanin A on gene expression in primary human hepatocytes and human intestinal cells. Electroporation adopting trains of biphasic pulses enhances in vitro and in vivo the cytotoxic effect of doxorubicin on multidrug re Continue reading >>

Lactic Acid Buildup After Seizures? : Epilepsy

Lactic Acid Buildup After Seizures? : Epilepsy

Feel free to edit your flair to reflect your treatment: [Drug 1, Dosage; Drug 2, Dosage...] Example: Keppra: 1000 mg; Lamictal 150 mg. If you are a parent, sibling or a child of someone with epilepsy feel free to note it as you wish. The mission of /r/epilepsy is to provide a community forum for people that are effected by epilepsy. To share ideas about the direction of research and available treatment regarding epilepsy, seizure disorders and SUDEP, and overcome the challenges created by epilepsy through discussion and support. NOTE: /r/epilepsy IS NOT A PLACE FOR MEDICAL ADVICE. DO NOT TAKE A STRANGER'S WORD OVER YOUR DOCTOR'S/NEUROLOGIST'S For urgent medical matters at any time, please call your doctor's office. For life-threatening medical emergencies, please call 911. Always follow reddit rules & reddiquette We enforce a standard of common decency and civility here. All users are expected to be respectful to other users at all times. Personal attacks, bigotry, fighting words, otherwise inappropriate behavior or content, comments that insult or demean a specific user or group of users will be removed. Regular or egregious violations will result in bans. Posts related politics or religion should be left to subreddits involving politics or religion. Posts related to Illegal recreational drug use will be removed and can result in a ban. Posts related to the selling of merchandise (self promotion) will be removed. Posts related to self harm will be removed immediately and the poster will be banned. Call 911 if you have an emergency. IMPORTANT Message the mods before posting any surveys, polls, questionnaires. Any unapproved post will be removed. In your message to our mods team please include information about yourself your study - the data being collected, and how the Continue reading >>

Antiepileptic Drug Poisoning: Three-year Experience

Antiepileptic Drug Poisoning: Three-year Experience

Antiepileptic drug poisoning: Three-year experience Author links open overlay panel Yahya KemalGnaydna Antiepileptic drugs, which are also called anticonvulsants, are used in the therapy and prophylaxis of epileptic seizures. The purpose of this paper was to investigate the relevant epidemiological data and to determine which of these drugs was the most frequent cause of intoxication. Another purpose of this study was to determine the neurological, cardiac, and biochemical problems caused by antiepileptics. This retrospective study included 95 consecutive patients under 18 years of age with antiepileptic intoxication, presenting to and being followed-up in, the Toxicology Unit between January 2010 and February 2013. The data were obtained by screening the patient files. Of the cases, 67 (70.5%) were self-poisoned by first generation antiepileptics (FGAEs) and 28 (29.5%) by second generation antiepileptics (SGAEs). The Glasgow Coma Scale (GCS) scores and the serum lactate levels of the patients poisoned by FGAEs and SGAEs on admission to emergency department were 15 (25th: 12; 75th: 15; 95th: 15; IQR: 3) and 1.9 (25th: 1.4; 75th: 3.1; 95th: 5.6; IQR: 1.7), and 15 (25th: 14.3; 75th: 15; 95th: 15; IQR: 0.75) and 1.07 (25th: 0.9; 75th: 1.6; 95th: 5.5; IQR: 0.71), respectively. The serum lactate levels of patients poisoned by FGAEs were significantly higher (p<0.001). Among the cases poisoned by carbamazepine, the most frequent cause of intoxication, the GCS score was significantly lower and serum lactate level was significantly higher in the group with high serum levels of carbamazepine (p=0.004 and p<0.001, respectively). In cases poisoned by valproic acid (VPA), the second frequent cause of intoxication, there was neither a significant association between the serum VPA l Continue reading >>

Status Epilepticus

Status Epilepticus

continuous seizure activity for 5 minutes or more without return of consciousness, or recurrent seizures (2 or more) without an intervening period of neurological recovery seizure activity which fails to respond to first-line antiepileptic therapies (see below) accounts for about a third of status epilepticus patients older definitions required seizure activity to continue for 30 minutes to be considered status epilepticus most seizures terminate within 5 minutes and those that dont are often prolonged significant neuronal injury occurs well before 30 minutes rapid seizure control is important because: limits seizure-induced neuronal injury (animal studies; also associated with better outcomes in humans) benzodiazepine effectiveness decreases over time (likely to changes in GABA subunits with ongoing seizure activity) prevent duration-dependent kindling and cytokine-mediated effects (experimental models) seizures account for about 1% of all ED presentations and about 30% of neurological presentations prolonged seizures have higher mortality and worse outcomes mortality of status epilepticus ranges from ~ 10-30% in different studies, depending on thedefinition used non-IV benzodiazepines (e.g. IM midazolam) are often preferred first-line therapy in prehospital settings respiratory decompensation is more commonly encountered in untreated status epilepticus than in status epilepticus treated with benzodiazepines Titrate AEDs to therapeutic levels. When checking post-load drug levels, on should wait at least 2 hours post infusion for fosphenytoin and phenytoin, or immediately post infusion of valproate Phenytoin is typically avoided in drug-induced seizures, barbiturates are widely recommended following first line benzodiazepine therapy Brophy, Gretchen M., et al. Guidelin Continue reading >>

Etiology And Therapeutic Approach To Elevated Lactate

Etiology And Therapeutic Approach To Elevated Lactate

Etiology and therapeutic approach to elevated lactate aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States Corresponding author: Michael W. Donnino Beth Israel Deaconess Medical Center One Deaconess Road, W/CC 2 Boston, Boston, MA 02215 Phone: 617-754-2450 Fax: 617-754-2350 [email protected] The publisher's final edited version of this article is available at Mayo Clin Proc See other articles in PMC that cite the published article. Lactate levels are commonly evaluated in acutely ill patients. Although most commonly used in the context of evaluating shock, lactate can be elevated for many reasons. While tissue hypoperfusion is probably the most common cause of elevation Continue reading >>

Is Lactic Acidosis A Side Effect Of Keppra ? ( Factmed.com )

Is Lactic Acidosis A Side Effect Of Keppra ? ( Factmed.com )

Introduction This page is designed to help you determine the relationship, if any, between KEPPRA and LACTIC ACIDOSIS. In doing so, we compare KEPPRA with other drugs that cause LACTIC ACIDOSIS, to help you evaluate whether or not KEPPRA causes LACTIC ACIDOSIS. Likewise, this page shows the most highly-reported side effects of KEPPRA, so you can see if LACTIC ACIDOSIS ranks among KEPPRA's most well-known side effects. Reports of KEPPRA causing LACTIC ACIDOSIS: 17 Reports of any side effect of KEPPRA : 19758 Percentage of KEPPRA patients where LACTIC ACIDOSIS is a reported side effect: 0.0860% FDA reports of any drug causing LACTIC ACIDOSIS : 6476 Average percentage for all medicated patients where LACTIC ACIDOSIS is reported as a complication: 0.0406% Physician opinion on KEPPRA as adverse event culprit: Overall opinion for all reports of this drug: Most frequent diagnoses/indications for prescribing KEPPRA: DRUG USE FOR UNKNOWN INDICATION ( 387 patients ) PRODUCT USED FOR UNKNOWN INDICATION ( 349 patients ) COMPLEX PARTIAL SEIZURES ( 192 patients ) Is it safe to take Coricidin HBP while taking Keppra? I have von Willebrand disease and a factorXl deficiency. I took 500 mg kepra twice a day. Keppra is increased to 3x 500 mg a day. Suddenly bleeding wounds does not stop bleeding. Instead of PTT test being the maxium which is 30 it is now 71. It is always been higher than normal. The neurologist says the increase [PTT] is not related to the keppra. Am I right to be worried and could it be related to the Keppra after many years of usage [2x 500 mg. a day]? frouke goldberg The skin of my hands and arms is easily bruised. As my dermatologist says "aging, thinning, sun-damaged skin." I've been advised to make sure I don't have a Vitamin K deficiency and am wondering if Keppra Continue reading >>

Will You Have Lactic Acidosis With Keppra - From Fda Reports - Ehealthme

Will You Have Lactic Acidosis With Keppra - From Fda Reports - Ehealthme

A study for a 76 year old man who takes Losartin Potassium NOTE: The study is based on active ingredients and brand name. Other drugs that have the same active ingredients (e.g. generic drugs) are NOT considered. WARNING: Please DO NOT STOP MEDICATIONS without first consulting a physician since doing so could be hazardous to your health. DISCLAIMER: All material available on eHealthMe.com is for informational purposes only, and is not a substitute for medical advice, diagnosis, or treatment provided by a qualified healthcare provider. All information is observation-only, and has not been supported by scientific studies or clinical trials unless otherwise stated. Different individuals may respond to medication in different ways. Every effort has been made to ensure that all information is accurate, up-to-date, and complete, but no guarantee is made to that effect. The use of the eHealthMe site and its content is at your own risk. You may report adverse side effects to the FDA at or 1-800-FDA-1088 (1-800-332-1088). If you use this eHealthMe study on publication, please acknowledge it with a citation: study title, URL, accessed date. Continue reading >>

Seizures & Syncope | Clinical Neurology, 9e | Accessmedicine | Mcgraw-hill Medical

Seizures & Syncope | Clinical Neurology, 9e | Accessmedicine | Mcgraw-hill Medical

Consciousness is lost when the function of both cerebral hemispheres or the brainstem reticular activating system is compromised. Episodic dysfunction of these anatomic regions produces transient, and often recurrent, loss of consciousness. There are two major causes of episodic loss of consciousness. Seizures are disorders characterized by temporary neurologic signs or symptoms resulting from abnormal, paroxysmal, and hypersynchronous electrical neuronal activity in the cerebral cortex. Syncope is loss of consciousness due to reduced blood flow to both cerebral hemispheres or the brainstem. It can result from pancerebral hypoperfusion caused by vasovagal reflexes, orthostatic hypotension, decreased cardiac output, or from selective hypoperfusion of the brainstem resulting from vertebrobasilar ischemia. Inquire about prodromal and initial symptoms. A witness may be critical. The often brief, stereotyped premonitory symptoms (aura) at the onset of some seizures may localize the central nervous system (CNS) abnormality responsible for seizures. Note that more than one type of aura may occur in an individual patient. A sensation of fear, olfactory or gustatory hallucinations, or visceral or dj vu sensations are commonly associated with seizures originating in the temporal lobe. Progressive light-headedness, dimming of vision, and faintness suggest decreased cerebral blood flow (eg, simple faints, cardiac arrhythmias, orthostatic hypotension). Posture When Loss of Consciousness Occurs Orthostatic hypotension and simple faints occur in the upright or sitting position. Episodes that also or only occur in the recumbent position suggest seizure or cardiac arrhythmia as a likely cause, although syncope induced by strong emotional stimuli (eg, phlebotomy) can also occur in recum Continue reading >>

Drug-induced Metabolic Acidosis

Drug-induced Metabolic Acidosis

Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis1. Humans possess homeostatic mechanisms that maintain acid-base balance (Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis (Figure 1). Figure 1. Excretion of acid and ways to jeopardize the system. 1. A strong non-volatile acid HA dissociates to release H+ and poses an immediate threat to plasma pH. 2. Bicarbonate buffers the H+ and generates CO2, which is expelled in the lungs and results in depletion of body HCO3-. Non-bicarbonate buffers (collectively referred to as B) carry the H+ until the kidneys excrete it. 3. The kidneys split CO2 into H+ and HCO3- and selectively secrete H+ into the lumen and HCO3- into the blood. In addition, any excess H+ from the body fluid is also excreted. 4. Most H+ excreted in the urine is carried by urinary buffers (UBs). 5. Some organic anions (A) (e.g. lactate, ketoanions) can be metabolized to regenerate the HCO3-. If A is not metabolizable (e.g. phosphate or sulfate), it is excreted in the uri Continue reading >>

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