Hyperchloremic normal gap metabolic acidosis.

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  • Author(s): Palmer BF;Palmer BF; Clegg DJ; Clegg DJ; Clegg DJ
  • Source:
    Minerva endocrinologica [Minerva Endocrinol] 2019 Dec; Vol. 44 (4), pp. 363-377. Date of Electronic Publication: 2019 Jul 24.
  • Publication Type:
    Journal Article; Review
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Edizioni Minerva medica Country of Publication: Italy NLM ID: 8406505 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1827-1634 (Electronic) Linking ISSN: 03911977 NLM ISO Abbreviation: Minerva Endocrinol Subsets: MEDLINE
    • Publication Information:
      Original Publication: Torino : Edizioni Minerva medica,
    • Subject Terms:
      Acid-Base Equilibrium* ; Acidosis*/diagnosis ; Acidosis*/etiology ; Acidosis*/metabolism; Chlorides/*blood ; Kidney/*metabolism; Acidosis, Renal Tubular/diagnosis ; Aldosterone/physiology ; Ammonia/urine ; Bicarbonates/blood ; Buffers ; Diarrhea/complications ; Glomerular Filtration Rate ; Humans ; Hypokalemia/metabolism ; Kidney Tubules/metabolism ; Models, Biological ; Postoperative Complications/etiology ; Postoperative Complications/metabolism ; Protons ; Renal Insufficiency, Chronic/metabolism ; Urinary Diversion/adverse effects
    • Abstract:
      Metabolic acidosis is defined as a pathologic process that, when unopposed, increases the concentration of hydrogen ions (H+) in the body and reduces the bicarbonate (HCO3-) concentration. Metabolic acidosis can be of a kidney origin or an extrarenal cause. Assessment of urinary ammonium excretion by calculating the urine anion gap or osmolal gap is a useful method to distinguish between these two causes. Extrarenal processes include increased endogenous acid production and accelerated loss of bicarbonate from the body. Metabolic acidosis of renal origin is due to a primary defect in renal acidification with no increase in extrarenal hydrogen ion production. This situation can occur because either the renal input of new bicarbonate is insufficient to regenerate the bicarbonate lost in buffering endogenous acid as with distal renal tubular acidosis (RTA) or the RTA of renal insufficiency, or the filtered bicarbonate is lost by kidney wasting as in proximal RTA. In either condition, because of loss of either NaHCO3 (proximal RTA) or NaA (distal RTA), effective extracellular volume is reduced and as a result the avidity for chloride reabsorption derived from the diet is increased and results in a hyperchloremic normal gap metabolic acidosis. The RTA of renal insufficiency is also characterized by a normal gap acidosis, however, with severe reductions in the glomerular filtration rate an anion gap metabolic acidosis eventually develops.
    • Accession Number:
      0 (Bicarbonates)
      0 (Buffers)
      0 (Chlorides)
      0 (Protons)
      4964P6T9RB (Aldosterone)
      7664-41-7 (Ammonia)
    • Publication Date:
      Date Created: 20190727 Date Completed: 20200819 Latest Revision: 20200819
    • Publication Date:
      20231215
    • Accession Number:
      10.23736/S0391-1977.19.03059-1
    • Accession Number:
      31347344