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Journal articles on the topic 'Metabolic alkalosis'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Marston, Nicholas, Devin Kehl, Jonathan Copp, Noureddin Nourbakhsh, and Dena E. Rifkin. "Alkalotics Anonymous: Severe Metabolic Alkalosis." American Journal of Medicine 127, no. 1 (2014): 25–27. http://dx.doi.org/10.1016/j.amjmed.2013.09.006.

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2

GALLA, JOHN H. "Metabolic Alkalosis." Journal of the American Society of Nephrology 11, no. 2 (2000): 369–75. http://dx.doi.org/10.1681/asn.v112369.

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3

Emmett, Michael. "Metabolic Alkalosis." Clinical Journal of the American Society of Nephrology 15, no. 12 (2020): 1848–56. http://dx.doi.org/10.2215/cjn.16041219.

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Metabolic alkalosis is a very commonly encountered acid-base disorder that may be generated by a variety of exogenous and/or endogenous, pathophysiologic mechanisms. Multiple mechanisms are also responsible for the persistence, or maintenance, of metabolic alkalosis. Understanding these generation and maintenance mechanisms helps direct appropriate intervention and correction of this disorder. The framework utilized in this review is based on the ECF volume-centered approach popularized by Donald Seldin and Floyd Rector in the 1970s. Although many subsequent scientific discoveries have advance

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4

Palmer, B. F., and R. J. Alpern. "Metabolic alkalosis." Journal of the American Society of Nephrology 8, no. 9 (1997): 1462–69. http://dx.doi.org/10.1681/asn.v891462.

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In summary, the kidney possesses numerous mechanisms that help to prevent metabolic alkalosis. Maintenance of metabolic alkalosis for any length of time means that renal homeostatic mechanisms for HCO3- excretion have been disrupted. Understanding the mechanisms that may perturb the kidney's ability to correct alkalosis will lead to improved clinical approaches to differential diagnosis and treatment of the patient. Although metabolic alkalosis is frequently not dangerous, in certain settings metabolic alkalosis may contribute to mortality and should be treated aggressively.

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5

Krishnan, Namrata, and Robert Jay Alpern. "Metabolic Alkalosis." Nephrology Self-Assessment Program 20, no. 2 (2022): 145–59. http://dx.doi.org/10.1681/nsap.2022.20.2.6.

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6

Lecker, Stewart H., and Keiko I. Greenberg. "Metabolic Alkalosis." Advances in Kidney Disease and Health 31, no. 6 (2024): 523–28. http://dx.doi.org/10.1053/j.akdh.2024.08.002.

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7

Achanti, Anand, and Waleed A. Elsheikh. "Metabolic Alkalosis." Nephrology Self-Assessment Program 23, no. 2 (2024): 137–47. http://dx.doi.org/10.58483/nsap.00162024.

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8

D'Eufemia, P., S. Lucarelli, O. Giardini, and E. Cardi. "Metabolic alkalosis." Acta Paediatrica 85, no. 12 (1996): 1518. http://dx.doi.org/10.1111/j.1651-2227.1996.tb13971.x.

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9

Rimmer, Jeffrey M., and F. John Gennari. "Metabolic Alkalosis." Journal of Intensive Care Medicine 2, no. 3 (1987): 137–50. http://dx.doi.org/10.1177/088506668700200304.

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10

AMUNDSON, DENNIS E., and JOEL DIAMANT. "Severe Metabolic Alkalosis." Southern Medical Journal 87, no. 2 (1994): 275–77. http://dx.doi.org/10.1097/00007611-199402000-00028.

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11

Schimert, Patrik, Vera Bernet-Buettiker, Christoph Rutishauser, Mohammed Schams, and Bernhard Frey. "Transplacental metabolic alkalosis." Journal of Paediatrics and Child Health 43, no. 12 (2007): 851–53. http://dx.doi.org/10.1111/j.1440-1754.2007.01239.x.

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12

Wesson, D. E. "Combined K+ and Cl- repletion corrects augmented H+ secretion by distal tubules in chronic alkalosis." American Journal of Physiology-Renal Physiology 266, no. 4 (1994): F592—F603. http://dx.doi.org/10.1152/ajprenal.1994.266.4.f592.

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NaCl administration enhances HCO3 secretion in the distal tubule of animals with chronic metabolic alkalosis but does not correct the augmented H+ secretion characteristic of this disorder. The present studies used in vivo microperfusion micropuncture to investigate whether combined repletion of K+ and Cl- corrected the augmented H+ secretion in the distal tubule of rats with chronic furosemide-induced metabolic alkalosis. Correction of alkalosis was induced in one group of animals with NaCl and in another group with a similar amount of Cl- as NaCl + KCl for 24 h; each group was compared with

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13

Sinha, Aditi, Aakanksha Sharma, Priyanka Khandelwal, Sanjeev Kumar, Pankaj Hari, and Arvind Bagga. "Hypertension with metabolic alkalosis." Asian Journal of Pediatric Nephrology 1, no. 2 (2018): 90. http://dx.doi.org/10.4103/ajpn.ajpn_20_18.

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14

Kang, Kyung Pyo, Sik Lee, Kyung Hoon Lee, and Sung Kyew Kang. "Mannitol-induced Metabolic Alkalosis." Electrolyte & Blood Pressure 4, no. 2 (2006): 61. http://dx.doi.org/10.5049/ebp.2006.4.2.61.

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15

Colombo, Jacopo, and Daniela Codazzi. "Acetazolamide in Metabolic Alkalosis." Pediatric Critical Care Medicine 18, no. 2 (2017): 201. http://dx.doi.org/10.1097/pcc.0000000000001039.

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16

Neary, R. H., and J. D. Edwards. "Metabolic alkalosis and hyperlactataemia." BMJ 294, no. 6585 (1987): 1462. http://dx.doi.org/10.1136/bmj.294.6585.1462.

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17

Galla, John H., and Robert G. Luke. "Pathophysiology of Metabolic Alkalosis." Hospital Practice 22, no. 10 (1987): 123–46. http://dx.doi.org/10.1080/21548331.1987.11703338.

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18

Escanero, JF, LM Elosegui, A. Cordova, et al. "Calcitonin and metabolic alkalosis." Biomedicine & Pharmacotherapy 45, no. 7 (1991): 307–9. http://dx.doi.org/10.1016/0753-3322(91)90085-8.

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19

Soifer, Jennifer T., and Hyung T. Kim. "Approach to Metabolic Alkalosis." Emergency Medicine Clinics of North America 32, no. 2 (2014): 453–63. http://dx.doi.org/10.1016/j.emc.2014.01.005.

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20

Ring, Troels. "Potassium and Metabolic Alkalosis." American Journal of Kidney Diseases 59, no. 2 (2012): 315. http://dx.doi.org/10.1053/j.ajkd.2011.10.052.

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21

Simons, P. "Metabolic alkalosis and myoclonus." Postgraduate Medical Journal 79, no. 933 (2003): 414–15. http://dx.doi.org/10.1136/pmj.79.933.414.

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22

Javaheri, S. "Effects of acetazolamide on cerebrospinal fluid ions in metabolic alkalosis in dogs." Journal of Applied Physiology 62, no. 4 (1987): 1582–88. http://dx.doi.org/10.1152/jappl.1987.62.4.1582.

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We hypothesized that inhibition of carbonic anhydrase in the central nervous system by acetazolamide should limit the rise in cisternal cerebrospinal fluid (CSF) [HCO3-] observed in metabolic alkalosis. To test this hypothesis, isosmotic isonatremic metabolic alkalosis was produced in two groups of anesthetized, paralyzed, and mechanically ventilated dogs (8 in each group). Group II animals received 50 mg/kg of acetazolamide intravenously 1 h before induction of metabolic alkalosis of 5-h duration. Renal effects of acetazolamide were eliminated by ligation of renal pedicles. In both groups cis

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23

Sierra, Caroline M., Elvin A. Hernandez, and Kristine A. Parbuoni. "Use of Arginine Hydrochloride in the Treatment of Metabolic Alkalosis or Hypochloremia in Pediatric Patients." Journal of Pediatric Pharmacology and Therapeutics 23, no. 2 (2018): 111–18. http://dx.doi.org/10.5863/1551-6776-23.2.111.

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OBJECTIVES Dosing of arginine for treatment of hypochloremia or metabolic alkalosis is laborious and has inherent variability in dose selection. The primary objective of this study was to determine the efficacy of arginine in the treatment of metabolic alkalosis and hypochloremia. Secondary objectives were to determine an optimal dose, route, and frequency for arginine administration in the treatment of these conditions. METHODS This single center, retrospective, descriptive study was conducted in children who received arginine for treatment of hypochloremia or metabolic alkalosis. Treatment s

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24

Gennari, F. John. "In Reply to ‘Potassium and Metabolic Alkalosis’ and ‘Metabolic Alkalosis due to Hypercalcemia’." American Journal of Kidney Diseases 59, no. 2 (2012): 315–16. http://dx.doi.org/10.1053/j.ajkd.2011.11.029.

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25

Jones, Mike Ward, and Matthew Williams. "Acid-Base Correction: A Case Report and Review of the Literature." Journal of the Intensive Care Society 11, no. 2 (2010): 126–29. http://dx.doi.org/10.1177/175114371001100211.

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Metabolic alkalosis is a common acid-base abnormality in hospitalised patients, though not frequently life-threatening. We present a case of severe metabolic alkalosis complicating colorectal surgery, which necessitated treatment with intravenous hydrochloric acid. The pathophysiology and treatment of severe metabolic alkalosis are reviewed, with an emphasis on the risks and benefits of hydrochloric acid use.

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26

Robinson, Elaine P., and Robert M. Hardy. "Clinical signs, diagnosis, and treatment of alkalemia in dogs: 20 cases (1982-1984)." Journal of the American Veterinary Medical Association 192, no. 7 (1988): 943–49. https://doi.org/10.2460/javma.1988.192.07.943.

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Summary Alkalemia (pH >7.50) was measured in 20 dogs admitted over a 3-year period for various clinical disorders. Alkalemia was detected in only 2.08% of all dogs in which blood pH and blood-gas estimations were made. Thirteen dogs had metabolic alkalosis (HCO3¯ >24 mEq/L Pco2 >30 mm of Hg), of which 8 had uncompensated metabolic alkalosis, and of which 5 had partially compensated metabolic alkalosis. Seven dogs had respiratory alkalosis Pco (Pco2 >30 mm of Hg, HCO3 ); 4 of these had uncompensated respiratory alkalosis and 3 had partially compensated respiratory alkalosis. Ten dog

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27

Schrock, H., and W. Kuschinsky. "Cerebrospinal fluid ionic regulation, cerebral blood flow, and glucose use during chronic metabolic alkalosis." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 4 (1989): H1220—H1227. http://dx.doi.org/10.1152/ajpheart.1989.257.4.h1220.

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Chronic metabolic alkalosis was induced in rats by combining a low K+ diet with a 0.2 M NaHCO3 solution as drinking fluid for either 15 or 27 days. Local cerebral blood flow and local cerebral glucose utilization were measured in 31 different structures of the brain in conscious animals by means of the iodo-[14C]antipyrine and 2-[14C]deoxy-D-glucose method. The treatment induced moderate [15 days, base excess (BE) 16 mM] to severe (27 days, BE 25 mM) hypochloremic metabolic alkalosis and K+ depletion. During moderate metabolic alkalosis no change in cerebral glucose utilization and blood flow

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28

Brimioulle, S., P. Lejeune, J. L. Vachiery, M. Leeman, C. Melot, and R. Naeije. "Effects of acidosis and alkalosis on hypoxic pulmonary vasoconstriction in dogs." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 2 (1990): H347—H353. http://dx.doi.org/10.1152/ajpheart.1990.258.2.h347.

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We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min–1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alk

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29

Mathew, Jennie T., and Laura L. Bio. "Injectable Ammonium Chloride Used Enterally for the Treatment of Persistent Metabolic Alkalosis in Three Pediatric Patients." Journal of Pediatric Pharmacology and Therapeutics 17, no. 1 (2012): 98–103. http://dx.doi.org/10.5863/1551-6776-17.1.98.

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Enteral administration of injectable ammonium chloride may offer an effective method for the treatment of persistent metabolic alkalosis, without the adverse effects associated with the intravenous route. This case series describes 3 pediatric patients who received ammonium chloride enterally for the treatment of persistent metabolic alkalosis. The patients were a 2-month-old female infant, a 6-week-old male infant, and a 3-year-old male toddler. Four to 18 doses of ammonium chloride were administered enterally (range, 3-144 mEq/dose). Two of the 3 patients achieved resolution of metabolic alk

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30

Curtin, William M., Emily A. O'Brien, Rachel M. Mauro, Elizabeth A. Lucarelli-Baldwin, Serdar H. Ural, and Christina T. DeAngelis. "Fetal Metabolic Alkalosis Resulting from Maternal Vomiting." American Journal of Perinatology Reports 14, no. 01 (2024): e48-e50. http://dx.doi.org/10.1055/s-0043-1778113.

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AbstractWe describe a pregnant patient with severe compulsive water ingestion and vomiting that lead to metabolic alkalosis and preterm delivery. A 21-year-old patient was hospitalized multiple times throughout pregnancy for symptoms initially thought to be related to hyperemesis gravidarum. Overtime, it became apparent that the patient induced vomiting by rapidly drinking large volumes of water. At 32 weeks' gestation, rapid ingestion of water caused 3 days of vomiting with findings of hyponatremia, hypokalemia, hypochloremia, metabolic alkalosis, and compensatory respiratory acidosis. Fetal

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31

Rodríguez Yánez, Tomas, Jorge Rico Fontalvo, Rodrigo Andres Daza Arnedo, et al. "Alcalosis metabólica en cuidados intensivos." Revista de la Sociedad Ecuatoriana de Nefrología, Diálisis y Trasplante 13, no. 2 (2025): 82–90. https://doi.org/10.56867/115.

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Introduction: In the ICU, metabolic alkalosis is the most common acid-base disorder. A link has been observed between this disorder and an increased risk of death. However, this increased mortality is likely primarily due to the severity of the underlying disease rather than to metabolic alkalosis itself. Objective of the review: This article is a narrative review aimed at updating the diagnosis, treatment, and prognosis of metabolic alkalosis in the context of intensive care management. Key points of the review: Metabolic alkalosis often develops during a hospital stay and is often a conseque

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32

Tarantino, Mario, Elena Vitale, and Ivo Casagranda. "Metabolic alkalosis: pathogenesis and physiopathology." Emergency Care Journal 4, no. 6 (2008): 9. http://dx.doi.org/10.4081/ecj.2008.6.9.

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33

Tzamaloukas, Antonios H. "Anion Gap in Metabolic Alkalosis." Southern Medical Journal 87, no. 11 (1994): 1192. http://dx.doi.org/10.1097/00007611-199411000-00032.

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34

Omron, LCDR Edward M. "Metabolic Alkalosis and Cystic Fibrosis." Chest 125, no. 3 (2004): 1169. http://dx.doi.org/10.1378/chest.125.3.1169.

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35

Gillion, Valentine, Michel Jadoul, Olivier Devuyst, and Jean-Michel Pochet. "The patient with metabolic alkalosis." Acta Clinica Belgica 74, no. 1 (2018): 34–40. http://dx.doi.org/10.1080/17843286.2018.1539373.

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36

Sethi, D., J. R. Curtis, D. L. Topham, and P. E. Gower. "Acute Metabolic Alkalosis during Haemodialysis." Nephron 51, no. 1 (1989): 119–20. http://dx.doi.org/10.1159/000185265.

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37

Baird, J. Scott, Patricia Walker, Agnes Urban, and Maria Berdella. "Metabolic Alkalosis and Cystic Fibrosis." Chest 122, no. 2 (2002): 755–56. http://dx.doi.org/10.1378/chest.122.2.755-a.

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38

Laski, Melvin E., and Sandra Sabatini. "Metabolic Alkalosis, Bedside and Bench." Seminars in Nephrology 26, no. 6 (2006): 404–21. http://dx.doi.org/10.1016/j.semnephrol.2006.09.001.

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39

Kildeberg, Poul. "Respiratory Compensation, in Metabolic Alkalosis." Acta Medica Scandinavica 174, no. 4 (2009): 515–22. http://dx.doi.org/10.1111/j.0954-6820.1963.tb07951.x.

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40

Tattersall, James. "Metabolic Alkalosis in CAPD Patients." Seminars in Dialysis 9, no. 1 (2007): 71. http://dx.doi.org/10.1111/j.1525-139x.1996.tb00904.x.

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41

Frise, Charlotte, Muna Noori, and Catherine Williamson. "Severe metabolic alkalosis in pregnancy." Obstetric Medicine 6, no. 3 (2013): 138–40. http://dx.doi.org/10.1258/om.2012.120030.

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Metabolic alkalosis is uncommon in pregnancy and is most often the result of severe vomiting. If this is present at the time of delivery, transient metabolic derangement in the fetus can occur, potentially requiring additional organ support. A 22-year-old woman is described, who presented at 37 weeks gestation with a severe metabolic alkalosis, vomiting and acute renal and hepatic impairment. The investigations, management options and maternal and fetal outcome are described.

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42

Pearl, Ronald G., and Meyer H. Rosenthal. "Metabolic alkalosis due to plasmapheresis." American Journal of Medicine 79, no. 3 (1985): 391–93. http://dx.doi.org/10.1016/0002-9343(85)90320-1.

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43

Holland, Anne, John Wilson, Tom Kotsimbos, and Matthew Naughton. "Metabolic Alkalosis and Cystic Fibrosis." Chest 125, no. 3 (2004): 1169–70. http://dx.doi.org/10.1016/s0012-3692(15)31970-x.

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44

Foy, Daniel, and Helio Autran de Morais. "Metabolic Alkalosis: A Quick Reference." Veterinary Clinics of North America: Small Animal Practice 38, no. 3 (2008): 435–38. http://dx.doi.org/10.1016/j.cvsm.2008.01.023.

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45

Howard, James S., and Stewart Wolf. "The psychosis of metabolic alkalosis." Integrative Physiological and Behavioral Science 28, no. 4 (1993): 353–58. http://dx.doi.org/10.1007/bf02690932.

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46

Agterhuis, Dinette E., and Kenrick Berend. "Metabolic Alkalosis Due to Hypercalcemia." American Journal of Kidney Diseases 59, no. 2 (2012): 315. http://dx.doi.org/10.1053/j.ajkd.2011.11.028.

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47

Devendra, D. "Unexplained hypokalaemia and metabolic alkalosis." Postgraduate Medical Journal 77, no. 912 (2001): 4e—4. http://dx.doi.org/10.1136/pmj.77.912.e4.

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48

OHTSUKA, Hiromichi, Kazunori MORI, Atsushi HATSUGAYA, et al. "Metabolic Alkalosis in Coliform Mastitis." Journal of Veterinary Medical Science 59, no. 6 (1997): 471–72. http://dx.doi.org/10.1292/jvms.59.471.

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49

Mudunuru, Sitarama Arvind, Jose E. Navarrete, and W. Charles O'Neill. "Metabolic Alkalosis in Hemodialysis Patients." Journal of the American Society of Nephrology 32, no. 10S (2021): 305. http://dx.doi.org/10.1681/asn.20213210s1305c.

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50

Vandorpe, David H., Steven P. Nadler, and David Z. Levine. "Distal tubule bicarbonate reabsorption during rebound metabolic alkalosis." Canadian Journal of Physiology and Pharmacology 69, no. 11 (1991): 1784–88. http://dx.doi.org/10.1139/y91-263.

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Rebound metabolic alkalosis is a transient alkalemia that is seen during recovery from NH4Cl-induced metabolic acidosis. The persistent elevation of plasma bicarbonate concentration is the result of continuing excretion of net acid by the kidney. Bicarbonate transport by inner medullary collecting ducts has been reported by others to proceed normally (i.e., bicarbonate reabsorption continues in this segment) during rebound metabolic alkalosis. No other segmental responses have been evaluated. Since the surface distal tubule of the rat is known to both reabsorb and secrete bicarbonate in vivo,

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