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Hypochloremic Metabolic Acidosis

Acidosis-induced Hypochloremic Alkalosis In Diabetic Ketoacidosis Confirmed By The Modified Base Excess Method

Acidosis-induced Hypochloremic Alkalosis In Diabetic Ketoacidosis Confirmed By The Modified Base Excess Method

The Journal of Clinical Endocrinology & Metabolism Acidosis-Induced Hypochloremic Alkalosis in Diabetic Ketoacidosis Confirmed by The Modified Base Excess Method Department of Endocrinology and Internal Medicine, Matsunami General Hospital, Gifu 501-6062, Japan Address all correspondence and requests for reprints to: Keigo Yasuda, MD, PhD, Department of Endocrinology and Internal Medicine, Matsunami General Hospital, 185-1 Dendai, Kasamatsu, Gifu 501-6062, Japan. Search for other works by this author on: Department of Endocrinology and Internal Medicine, Matsunami General Hospital, Gifu 501-6062, Japan Search for other works by this author on: Department of Endocrinology and Internal Medicine, Matsunami General Hospital, Gifu 501-6062, Japan Search for other works by this author on: Department of Endocrinology and Internal Medicine, Matsunami General Hospital, Gifu 501-6062, Japan Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 101, Issue 6, 1 June 2016, Pages 23902395, Keigo Yasuda, Makoto Hayashi, Masanori Murayama, Noriyoshi Yamakita; Acidosis-Induced Hypochloremic Alkalosis in Diabetic Ketoacidosis Confirmed by The Modified Base Excess Method, The Journal of Clinical Endocrinology & Metabolism, Volume 101, Issue 6, 1 June 2016, Pages 23902395, Diabetic ketoacidosis (DKA) is associated with a metabolic alkalosis, which is thought to be due to vomiting. However, alkalosis can occur in DKA without vomiting. We retrospectively reviewed the acid-base disturbances in DKA admissions without vomiting. We included admissions of the patients with blood glucose and beta-hydroxybutyrate (OHB) levels > 250 mg/dL and > 1.0 mmol/L, respectively. Admissions without vomiting were classified into a group with a OHB > 3.0 mmol/L (D Continue reading >>

Hypochloremia - Symptoms, Causes And Treatment

Hypochloremia - Symptoms, Causes And Treatment

Hypochloremia is an imbalance in electrolyte, where there is abnormal chlorine ion depletion in the blood. Normal value ranges from 97-107 mEq/L. However, in hypochloremia, the chloride levels become less than 98mEq/L. It is often associated with hypokalemia, hyponatremia and metabolic acidosis. Chloride is the major anion seen in both, the blood and the extracellular fluid. According to The Vitamins and Nutrition Center, chloride, potassium and calcium are among the most important serum electrolytes. Anion is nothing, but the negatively charged portion of some substances like sodium chloride (NaCl) or table salt, on getting dissolved in liquid. Maximum of chloride ions we get by the food we eat. The normal values increase as we consume more of canned foods rich in salt. Helps in keeping the acid-base balance in the body. Sea water and human fluids has the same concentration of chloride ions. Chloride ion balance is regulated and maintained by the body. Any significant decrease or increase may have harmful or fatal consequences. During digestion, the intestines absorb the chloride. Excess chloride after the digestion process, gets excreted in the urine. Kidneys control the chloride levels in the blood. Abnormal elevation of chloride may be found in diarrhea, hyperparathyroidism and kidney diseases. Chloride joins with hydrogen for forming HCl (hydrochloric acid). Due to volume depletions, the chloride level decreases. Hence, the kidneys retain the bi-carbonate and sodium ions for balancing the incurred loss. As a result, bicarbonate accumulates in the ECF, thereby raising the pH level leading to hypochloremic metabolic alkalosis. Serum chloride levels < 98 mEq/L confirm the diagnosis. Serum osmolarity < 280mOsm/L (normal = 280295 mOsm/L ) This reflects the decrease in Continue reading >>

The Incidence And Prognostic Value Of Hypochloremia In Critically Ill Patients

The Incidence And Prognostic Value Of Hypochloremia In Critically Ill Patients

The Incidence and Prognostic Value of Hypochloremia in Critically Ill Patients 1Department of Anesthesiology and Resuscitology, Okayama University Hospital, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan 2Perioperative Management Center, Okayama University Hospital, 2-5-1 Shikata-cho, Kita-ku, Okayama, Japan 3Medical School, Okayama University, 2-5-1 Shikata-cho, Kita-ku, Okayama, Japan Received 23 January 2012; Accepted 25 March 2012 Academic Editors: W. W.Butt, F.Hammarqvist, B.Laviolle, and R.Wu Copyright 2012 Makiko Tani 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. Little is known on the clinical effects of chloride on critically ill patients. We conducted this retrospective, observational study in 488 critically ill patients to investigate the incidence of chloride abnormalities, effects of hypochloremia in acid-base disorders, and association between chloride and clinical outcome. The study involved retrieval of arterial blood gas analyses, biochemical and demographical data from electrical records as well as quantitative acid-base analyses. For statistical analysis, the patients were stratified into three groups according to their chloride level (normal range: 98106 mEq/L). The distribution of chloride levels was hyperchloremia 16.6%, normochloremia 74.6%, and hypochloremia 8.8%. The hypochloremic group was significantly alkalemic ( ) and has significantly higher apparent strong ion difference (SIDa) ( ) compared to the two other groups. The hypochloremic group had significantly longer stays in the ICU and hospital ( ). However, multiple regression analysis showed that chloride was Continue reading >>

Hypochloremic Metabolic Acidosis - Usmle Forum

Hypochloremic Metabolic Acidosis - Usmle Forum

I have no idea. It's an impossible phenomenon. are you sure it is not typo intestinal blind loop syndrome has hypochloremic metab acidosis Serum chloride is elevated in normal Anion Gap metabolic acidosis, however if a patient is exposed to alkalyting agent, it result in hychloremia, so watch for metabolic alkalosis Acid-base has always been challenging to me, my post get cut . this means that in the normal anion gap metabolic acidosis as seen in RTA or diarrhea, we will have hyperchloremia i am having tuf time differentiating surreptious vomiting and diuretic use since both have low urine chloride and both are chlotide sensitive. i assume in vomiting, serum sodium will be raised and not in diuretic. is there any other difference i am missing. hypochloremic met. acidosis is extremely rare phenomenon and usually means there is also a coexisting met. alkalosis. yazdoc, I am not sure about differentiating surreptious vomiting and diuretic use, I think if you want to make the difference based on urinay chloride, since diuretic interfere with reabsorption of NACL, the effect of diuretic use on urinary chloride levels is high while the diuretic is acting, but drops to low levels later, so if you check more often the urinary chloride you can see the diff. value. Continue reading >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Normal albumin-corrected anion gap acidosis Hyperchloremic acidosis is a common acid-base disturbance in critical illness, often mild (standard base excess >-10 mEq/L). Definitions of hyperchloremic acidosis vary. The best are not based on chloride concentrations, but on the presence of metabolic acidosis plus the absence of significant concentrations of lactate or other unmeasured anions. 2. standard base excess less than -3 mEq/L or bicarbonate less than 22 mmol/L, 3. Albumin corrected anion gap normal (5-15 mEq/L). A normal strong ion gap is an alternative indicator of the absence of unmeasured anions, although rarely used clinically and offering little advantage over the albumin corrected anion gap. The degree of respiratory compensation is relevant. It is appropriate if PaCO2 approximates the two numbers after arterial pH decimal point (e.g. pH=7.25, PaCO2=25 mm Hg; this rule applies to any primary metabolic acidosis down to a pH of 7.1). Acidosis is severe if standard base excess is less than -10 mEq/L, or pH is less than 7.3, or bicarbonate is less than 15 mmol/L. Common causes in critical illness are large volume saline administration, large volume colloid infusions (e.g. unbalanced gelatine or starch preparations) following resolution of diabetic keto-acidosis or of other raised anion gap acidosis, and post hypocarbia. Hyperchloremic acidosis often occurs on a background of renal impairment/tubular dysfunction. It is usually well tolerated, especially with appropriate respiratory compensation. The prognosis is largely that of the underlying condition. If associated with hyperkalemia, think of hypo-aldosteronism (Type 4 RTA), especially if diabetic. With persistent hypokalemia, think of RTA Types 1 and 2. Hyperchloremic acidosis is usually well tolerated in the Continue reading >>

Mechanism Of Normochloremic And Hyperchloremic Acidosis In Diabetic Ketoacidosis

Mechanism Of Normochloremic And Hyperchloremic Acidosis In Diabetic Ketoacidosis

Oh M.S. · Carroll H.J. · Uribarri J. Man S. Oh, MD, Department of Medicine, State University of New York, Health Science Center at Brooklyn, Brooklyn, NY 11203 (USA) Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses , in particular the renal tubular acidoses (RTAs). [ 1 , 2 ] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG Continue reading >>

Types Of Disturbances

Types Of Disturbances

The different types of acid-base disturbances are differentiated based on: Origin: Respiratory or metabolic Primary or secondary (compensatory) Uncomplicated or mixed: A simple or uncomplicated disturbance is a single or primary acid-base disturbance with or without compensation. A mixed disturbance is more than one primary disturbance (not a primary with an expected compensatory response). Acid-base disturbances have profound effects on the body. Acidemia results in arrythmias, decreased cardiac output, depression, and bone demineralization. Alkalemia results in tetany and convulsions, weakness, polydipsia and polyuria. Thus, the body will immediately respond to changes in pH or H+, which must be kept within strict defined limits. As soon as there is a metabolic or respiratory acid-base disturbance, body buffers immediately soak up the proton (in acidosis) or release protons (alkalosis) to offset the changes in H+ (i.e. the body compensates for the changes in H+). This is very effective so minimal changes in pH occur if the body is keeping up or the acid-base abnormality is mild. However, once buffers are overwhelmed, the pH will change and kick in stronger responses. Remember that the goal of the body is to keep hydrogen (which dictates pH) within strict defined limits. The kidney and lungs are the main organs responsible for maintaining normal acid-base balance. The lungs compensate for a primary metabolic condition and will correct for a primary respiratory disturbance if the disease or condition causing the disturbance is resolved. The kidney is responsible for compensating for a primary respiratory disturbance or correcting for a primary metabolic disturbance. Thus, normal renal function is essential for the body to be able to adequately neutralize acid-base abnor Continue reading >>

Is Correcting Hyperchloremic Acidosis Beneficial?

Is Correcting Hyperchloremic Acidosis Beneficial?

You are here: Home / PULMCrit / Is correcting hyperchloremic acidosis beneficial? Is correcting hyperchloremic acidosis beneficial? An elderly woman presents with renal failure due to severe dehydration from diarrhea. She has a hyperchloremic acidosis from diarrhea with a chloride of 115 mEq/L, bicarbonate of 15 mEq/L, and a normal anion gap. During her volume resuscitation, should isotonic bicarbonate be used to correct her hyperchloremic acidosis? Does correcting her hyperchloremic acidosis actually help her, or does this just make her numbers better? The use of bicarbonate for treatment of metabolic acidosis is controversial. However, this controversy centers primarily around use of bicarbonate for management of lactic acidosis or ketoacidosis.Treatment of these disorders requires reversing the underlying disease process, with bicarbonate offering little if any benefit.Hyperchloremic metabolic acidosis is different.Whether due to bicarbonate loss or volume repletion with normal saline, the primary problems is a bicarbonate deficiency.Treating this with bicarbonate is a logical and accepted approach: Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial. Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base, which, given time, can be converted back to bicarbonate However, clinicians are often reluctant to treat hyperchloremic metabolic acidosis with bicarbonate, since the benefits of treatment are unclear.This post will attempt to clarify the rationale for treatment. Resuscitation with balanced crystalloids improves renal function There is growing evidence that resuscitation with normal saline impairs renal blood flow and function ( Young 2014 ).For example, Chowdhury 2012 inve Continue reading >>

Hypochloremia - An Overview | Sciencedirect Topics

Hypochloremia - An Overview | Sciencedirect Topics

In Veterinary Medicine (Eleventh Edition) , 2017 Hypochloremia occurs as a result of an increase in the net loss of the electrolyte in the intestinal tract in acute intestinal obstruction, dilatation and impaction, and volvulus of the abomasum and in enteritis (Fig. 5-7). Normally a large amount of chloride is secreted in the abomasum by the mucosal cells in exchange for bicarbonate, which moves into the plasma. The hydrogen, chloride, and potassium ions secreted in gastric juice are normally absorbed by the small intestine. Failure of abomasal emptying and obstruction of the proximal part of the small intestine will result in the sequestration of large quantities of chloride, hydrogen, and potassium ions, which leads to a hypochloremic hypokalemic metabolic alkalosis. A severe hypochloremia can be experimentally produced in calves by feeding them a low-chloride diet and daily removal of abomasal contents. Clinical findings include anorexia, weight loss, lethargy, mild polydipsia, and polyuria. A marked metabolic alkalosis occurs resulting in hypokalemia, hyponatremia, azotemia, and death. Stephen P. DiBartola, in Small Animal Clinical Diagnosis by Laboratory Methods (Fifth Edition) , 2012 Many causes of hyponatremia also produce hypochloremia. If changes in sodium are proportional to changes in chloride (hypochloremia with normal corrected chloride or artifactual hypochloremia), it is usually easier to search for the cause of the hyponatremia. Corrected hypochloremia results from excessive loss of chloride relative to sodium or administration of fluids containing high sodium concentration relative to chloride (see Box 6-5). The most common causes of corrected hypochloremia are chronic vomiting of gastric contents and aggressive furosemide or thiazide therapy. Administ Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis Paraldehyde, Phenformin (neither used in U.S. now) Propofol Infusion Syndrome has been proposed as a replacement in mnemonic Salicylate s (do not miss Chronic Salicylate Poisoning ) IV. Causes: Metabolic Acidosis and Normal Anion Gap (Hyperchloremia) Renal Tubular Acidosis (proximal or distal) V. Causes: Metabolic Acidosis and Elevated Osmolal Gap PaCO2 drops 1.2 mmHg per 1 meq/L bicarbonate fall Calculated PaCO2 = 1.5 x HCO3 + 8 (+/- 2) Useful in High Anion Gap Metabolic Acidosis Measured PaCO2 discrepancy: respiratory disorder Investigate normal Anion Gap Metabolic Acidosis Elevated in normal Anion Gap Metabolic Acidosis VII. Labs: Consider in Metabolic Acidosis with Increased Anion Gap Basic chemistry panel as above ( Serum Glucose , Blood Urea Nitrogen ) Rutecki (Dec 1997) Consultant, p. 3067-74 Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Metabolic Acidosis." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). Increased acidity in the blood secondary to acid base imbalance. Causes include diabetes, kidney failure and shock. ACIDOSIS METABOLIC, metabolic acidosis, metabolic acidosis (diagnosis), Acidosis metabolic, Metabolic acidosis NOS, Metabolic Acidoses, Acidosis, Metabolic, Acidoses, Metabolic, Metabolic Acidosis, acidosis metabolic, metabolic acidosis disorder, Acidosis, Metabolic acidosis (disorder), acidosis; metabolic, metabolic; acidosis, Metabolic acidosis, NOS, M Continue reading >>

Hypochloremic Hypokalemic Metabolic Alkalosis

Hypochloremic Hypokalemic Metabolic Alkalosis

SDN members see fewer ads and full resolution images. Join our non-profit community! Hypochloremic Hypokalemic Metabolic Alkalosis Example: gastric outlet obstruction or pyloric stenosis Can somebody explain this electrolyte abnormality in terms that make sense and are also correct? I understand it, at least I think I do. However, I keep hearing slightly conflicting explanations about the renal compensations going on. P.S. -- this is a super highly pimped topic in my experience Example: gastric outlet obstruction or pyloric stenosis Can somebody explain this electrolyte abnormality in terms that make sense and are also correct? I understand it, at least I think I do. However, I keep hearing slightly conflicting explanations about the renal compensations going on. P.S. -- this is a super highly pimped topic in my experience Example: gastric outlet obstruction or pyloric stenosis Can somebody explain this electrolyte abnormality in terms that make sense and are also correct? I understand it, at least I think I do. However, I keep hearing slightly conflicting explanations about the renal compensations going on. P.S. -- this is a super highly pimped topic in my experience Pyloric stenosis is results from hypertrophy of the circular muscle of the pylorus. This in turn results in gastric outlet obstruction from the constricted circular muscle. The gastric outlet obstruction then causes non-bilious, projectile vomiting (hallmark of the diagnosis of pyloric stenosis) which depletes hydrochloric acid from the stomach. This depletion of hydrochloric acid causes a hypocholemic metabolic alkalosis and dehydration because of the loss of H+ and Cl- ions in addition to fluid. Renal compensation for this loss of H+ ions is by preserving protons at the expense of potassium and thus hyp Continue reading >>

Final Diagnosis -- Hypochloremic Metabolic Alkalosis

Final Diagnosis -- Hypochloremic Metabolic Alkalosis

FINAL DIAGNOSIS HYPOCHLOREMIC METABOLIC ALKALOSIS. I. INTRODUCTION Metabolic alkalosis is an acid-base disorder in which the pH of the blood is elevated beyond the normal range of 7.35-7.45. This metabolic condition occurs mainly due to decreased hydrogen ion concentration in the blood, leading to compensatory increased levels of serum bicarbonate, or alternatively, as a direct result of increased bicarbonate concentrations. An elevated PaCO2 is often present as a result of compensatory alveolar hypoventilation. II. CAUSES OF METABOLIC ALKALOSIS The five main major causes of metabolic alkalosis are. Loss of hydrogen ions - Vomiting or nasogastric suction Primary mineralocorticoid excess Renal Hydrogen Loss - Primary mineralocorticoid excess Loop or thiazide diuretics Posthypercapnic alkalosis Hypercalcemia and the milk-alkali syndrome Shift of hydrogen ions into intracellular space - Hypokalemia. Alkalotic agents - Alkalotic agents in excess, such as bicarbonate or antacids. Contraction alkalosis - Due to loss of water in the extracellular space from diuretic use. Sweat losses in cystic fibrosis Villous adenoma or factitious diarrhea III. PHYSIOLOGY OF BICARBONATE HOMEOSTASIS IN THE BODY Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular buffering via respiratory and renal mechanisms [1]. The control of arterial CO2 tension by central nervous system and respiratory system and control of plasma bicarbonate by kidneys stabilize the arterial pH by excretion or retention of acid and alkali. This balance is represented by the Henderson-Hassalbalch equation given by Figure 1. Henderson-Hassalbalch equation. Where HCO3- represents in the plasma bicarbonate concentration and pCO2 is the plasma carbon dioxide tension in the blood. At norm Continue reading >>

Hypochloremia - An Overview | Sciencedirect Topics

Hypochloremia - An Overview | Sciencedirect Topics

Steven W. Salyer PAC, ... Chris R. McNeil, in Essential Emergency Medicine , 2007 Hypochloremia is defined as a chloride level less than 95mEq/L. Hypochloremia is usually caused by excess use of loop diuretics, nasogastric suction, or vomiting. Metabolic alkalosis is usually present with hypochloremia. Vomiting causes loss of hydrochloric acid. In the presence of ECF volume contraction, there is an increase in Na and resorption in the kidney, which helps to maintain the alkalosis. Aldosterone accelerates the retention of sodium and at the expense of hydrogen, K, and chloride. There are no specific signs or symptoms of hypochloremia. A Chem 7 test should be performed, then urine chloride should be analyzed to determine whether chlorideresponsive alkalosis is present. The diagnosis of hypochloremia is made based on the patient's history of diuretic therapy, vomiting, or nasogastric suctioning along with the assessment of chloride values in the presence of metabolic alkalosis. If urine chloride is less than 10mEq/L, then hypochloremia is due to chloride responsive alkalosis. If greater than 40mEq/L, hypochloremia is due to volume overload or dilution. These patients usually have a metabolic alkalosis due to excess mineralocorticoid or glucocorticoid. Treatment is aimed at therapy for the underlying disorder. Chlorideresponsive alkalosis is treated with normal saline. Chlorideresistant metabolic alkalosis requires IV normal saline plus K. Give one fourth as KCl and three fourths as NaCl. Kelly Ann Traeger, ... Arjang Djamali, in Pathophysiology of Kidney Disease and Hypertension , 2009 Hypochloremia can contribute to the maintenance of metabolic alkalosis by increasing the reabsorption of and reducing the secretion of bicarbonate in the distal tubule. Increased distal reab Continue reading >>

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