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      Mechanisms of the Effects of Acidosis and Hypokalemia on Renal Ammonia Metabolism

      review-article
      Author(s): , M.D.
      Publication date (Electronic):
      Journal: Electrolytes & Blood Pressure : E & BP
      Publisher: The Korean Society of Electrolyte Metabolism
      Keywords: kidney, ammonia, acids, hypokalemia

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          Abstract

          Renal ammonia metabolism is the predominant component of net acid excretion and new bicarbonate generation. Renal ammonia metabolism is regulated by acid-base balance. Both acute and chronic acid loads enhance ammonia production in the proximal tubule and secretion into the urine. In contrast, alkalosis reduces ammoniagenesis. Hypokalemia is a common electrolyte disorder that significantly increases renal ammonia production and excretion, despite causing metabolic alkalosis. Although the net effects of hypokalemia are similar to metabolic acidosis, molecular mechanisms of renal ammonia production and transport have not been well understood. This mini review summarizes recent findings regarding renal ammonia metabolism in response to chronic hypokalemia.

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          A role for Rhesus factor Rhcg in renal ammonium excretion and male fertility.

          Sophie Biver, Hendrica Belge, Soline Bourgeois … (2008)
          The kidney has an important role in the regulation of acid-base homeostasis. Renal ammonium production and excretion are essential for net acid excretion under basal conditions and during metabolic acidosis. Ammonium is secreted into the urine by the collecting duct, a distal nephron segment where ammonium transport is believed to occur by non-ionic NH(3) diffusion coupled to H(+) secretion. Here we show that this process is largely dependent on the Rhesus factor Rhcg. Mice lacking Rhcg have abnormal urinary acidification due to impaired ammonium excretion on acid loading-a feature of distal renal tubular acidosis. In vitro microperfused collecting ducts of Rhcg(-/-) acid-loaded mice show reduced apical permeability to NH(3) and impaired transepithelial NH(3) transport. Furthermore, Rhcg is localized in epididymal epithelial cells and is required for normal fertility and epididymal fluid pH. We anticipate a critical role for Rhcg in ammonium handling and pH homeostasis both in the kidney and the male reproductive tract.
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            Mechanisms in hyperkalemic renal tubular acidosis.

            Fiona Karet (2009)
            The form of renal tubular acidosis associated with hyperkalemia is usually attributable to real or apparent hypoaldosteronism. It is therefore a common feature in diabetes and a number of other conditions associated with underproduction of renin or aldosterone. In addition, the close relationship between potassium levels and ammonia production dictates that hyperkalemia per se can lead to acidosis. Here I describe the modern relationship between molecular function of the distal portion of the nephron, pathways of ammoniagenesis, and hyperkalemia.
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              Role of NH3 and NH4+ transporters in renal acid-base transport.

              I. David Weiner, Jill W. Verlander (2010)
              Renal ammonia excretion is the predominant component of renal net acid excretion. The majority of ammonia excretion is produced in the kidney and then undergoes regulated transport in a number of renal epithelial segments. Recent findings have substantially altered our understanding of renal ammonia transport. In particular, the classic model of passive, diffusive NH3 movement coupled with NH4+ "trapping" is being replaced by a model in which specific proteins mediate regulated transport of NH3 and NH4+ across plasma membranes. In the proximal tubule, the apical Na+/H+ exchanger, NHE-3, is a major mechanism of preferential NH4+ secretion. In the thick ascending limb of Henle's loop, the apical Na+-K+-2Cl- cotransporter, NKCC2, is a major contributor to ammonia reabsorption and the basolateral Na+/H+ exchanger, NHE-4, appears to be important for basolateral NH4+ exit. The collecting duct is a major site for renal ammonia secretion, involving parallel H+ secretion and NH3 secretion. The Rhesus glycoproteins, Rh B Glycoprotein (Rhbg) and Rh C Glycoprotein (Rhcg), are recently recognized ammonia transporters in the distal tubule and collecting duct. Rhcg is present in both the apical and basolateral plasma membrane, is expressed in parallel with renal ammonia excretion, and mediates a critical role in renal ammonia excretion and collecting duct ammonia transport. Rhbg is expressed specifically in the basolateral plasma membrane, and its role in renal acid-base homeostasis is controversial. In the inner medullary collecting duct (IMCD), basolateral Na+-K+-ATPase enables active basolateral NH4+ uptake. In addition to these proteins, several other proteins also contribute to renal NH3/NH4+ transport. The role and mechanisms of these proteins are discussed in depth in this review.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Electrolyte Blood Press
                Journal ID (publisher-id): EBP
                Title: Electrolytes & Blood Pressure : E & BP
                Publisher: The Korean Society of Electrolyte Metabolism
                ISSN (Print): 1738-5997
                ISSN (Electronic): 2092-9935
                Publication date (Print): December 2011
                Publication date (Electronic): 31 December 2011
                Volume: 9
                Issue: 2
                Pages: 45-49
                Affiliations
                Department of Anatomy, Ewha Womans University School of Medicine, Seoul, Korea.
                Author notes
                Corresponding author: Ki-Hwan Han, M.D., Ph.D. Department of Anatomy, Ewha Womans University School of Medicine, 911-1, Mok-6-dong, Yangcheon-gu, Seoul, 158-710, Korea. Tel: +82-2-2650-5710, khhan@ 123456ewha.ac.kr
                Article
                DOI: 10.5049/EBP.2011.9.2.45
                PMC ID: 3302905
                PubMed ID: 22438855
                SO-VID: 3f867456-73cf-4d05-9ace-09d1b94f4f68
                Copyright © Copyright © 2011 The Korean Society of Electrolyte Metabolism
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 05 December 2011
                Date accepted : 18 December 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: acids,hypokalemia,kidney,ammonia
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: acids, hypokalemia, kidney, ammonia

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