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      Postoperative Compensatory Ammonium Excretion Subsequent to Systemic Acidosis in Cardiac Patients

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          Abstract

          Background

          Postoperative acid-base imbalances, usually acidosis, frequently occur after cardiac surgery. In most cases, the human body, not suffering from any severe preexisting illnesses regarding lung, liver, and kidney, is capable of transient compensation and final correction. The aim of this study was to correlate the appearance of postoperatively occurring acidosis with renal ammonium excretion.

          Materials and Methods

          Between 07/2014 and 10/2014, a total of 25 consecutive patients scheduled for elective isolated coronary artery bypass grafting with cardiopulmonary bypass were enrolled in this prospective observational study. During the operative procedure and the first two postoperative days, blood gas analyses were carried out and urine samples collected. Urine samples were analyzed for the absolute amount of ammonium.

          Results

          Of all patients, thirteen patients developed acidosis as an initial disturbance in the postoperative period: five of respiratory and eight of metabolic origin. Four patients with respiratory acidosis but none of those with metabolic acidosis subsequently developed a base excess > +2 mEq/L.

          Conclusion

          Ammonium excretion correlated with the increase in base excess. The acidosis origin seems to have a large influence on renal compensation in terms of ammonium excretion and the possibility of an overcorrection.

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          Most cited references34

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          Role of pump prime in the etiology and pathogenesis of cardiopulmonary bypass-associated acidosis.

          The development of metabolic acidosis during cardiopulmonary bypass (CPB) is well recognized but poorly understood. The authors hypothesized that the delivery of pump prime fluids is primarily responsible for its development. Accordingly, acid-base changes induced by the establishment of CPB were studied using two types of priming fluid (Haemaccel, a polygeline solution, and Ringer's Injection vs. Plasmalyte 148) using quantitative biophysical methods. A prospective, double-blind, randomized trial was conducted at a tertiary institution with 22 patients undergoing CPB for coronary artery bypass surgery. Sampling of arterial blood was performed at three time intervals: before CPB (t1), 2 min after initiation of CPB at full flows (t2), and at the end of the case (t3). Measurements of Na+, K+, Mg2+, Cl-, HCO3-, phosphate, Ca2+, albumin, lactate, and arterial blood gases at each collection point were performed. Results were analyzed in a quantitative manner. Immediately on delivery of pump prime fluids, all patients developed a metabolic acidosis (base excess: 0. 95 mEq/l (t1) to -3.65 mEq/l (t2) (P < 0.001) for Haemaccel-Ringer's and 1.17 mEq/l (t1) to -3.20 mEq/l (t2). The decrease in base excess was the same for both primes (-4.60 vs. -4.37; not significant). However, the mechanism of metabolic acidosis was different. With the Haemaccel-Ringer's prime, the metabolic acidosis was hyperchloremic (Delta Cl-, +9.50 mEq/l; confidence interval, 7.00-11.50). With Plasmalyte 148, the acidosis was induced by an increase in unmeasured anions, most probably acetate and gluconate. The resolution of these two processes was different because the excretion of chloride was slower than that of the unmeasured anions (Delta base excess from t1 to t3 = -1.60 for Haemaccel-Ringer's vs. +1.15 for Plasmalyte 148; P = 0.0062). Cardiopulmonary bypass-induced metabolic acidosis appears to be iatrogenic in nature and derived from the effect of pump prime fluid on acid-base balance. The extent of such acidosis and its duration varies according to the type of pump prime.
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            Collecting duct-specific Rh C glycoprotein deletion alters basal and acidosis-stimulated renal ammonia excretion.

            NH3 movement across plasma membranes has traditionally been ascribed to passive, lipid-phase diffusion. However, ammonia-specific transporters, Mep/Amt proteins, are present in primitive organisms and mammals express orthologs of Mep/Amt proteins, the Rh glycoproteins. These findings suggest that the mechanisms of NH3 movement in mammalian tissues should be reexamined. Rh C glycoprotein (Rhcg) is expressed in the collecting duct, where NH3 secretion is necessary for both basal and acidosis-stimulated ammonia transport. To determine whether the collecting duct secretes NH3 via Rhcg or via lipid-phase diffusion, we generated mice with collecting duct-specific Rhcg deletion (CD-KO). CD-KO mice had loxP sites flanking exons 5 and 9 of the Rhcg gene (Rhcg(fl/fl)) and expressed Cre-recombinase under control of the Ksp-cadherin promoter (Ksp-Cre). Control (C) mice were Rhcg(fl/fl) but Ksp-Cre negative. We confirmed kidney-specific genomic recombination using PCR analysis and collecting duct-specific Rhcg deletion using immunohistochemistry. Under basal conditions, urinary ammonia excretion was less in KO vs. C mice; urine pH was unchanged. After acid-loading for 7 days, CD-KO mice developed more severe metabolic acidosis than did C mice. Urinary ammonia excretion did not increase significantly on the first day of acidosis in CD-KO mice, despite an intact ability to increase urine acidification, whereas it increased significantly in C mice. On subsequent days, urinary ammonia excretion slowly increased in CD-KO mice, but was always significantly less than in C mice. We conclude that collecting duct Rhcg expression contributes to both basal and acidosis-stimulated renal ammonia excretion, indicating that collecting duct ammonia secretion is, at least in part, mediated by Rhcg and not solely by lipid diffusion.
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              Roles and mechanisms of urinary buffer excretion.

              Excretion of acid (or generation of bicarbonate) by the kidneys is necessary for acid-base homeostasis. Most of this acid is excreted in the form of ammonia and titratable acid, the latter representing the amount of acid required to titrate the urine buffers from the plasma pH to urine pH. The transport of ammonia in the kidney is now recognized to entail more than simple nonionic diffusion of NH3 and trapping of NH4+. NH4+ transport in the kidney probably occurs by passive diffusion and by transport on the Na+-H+ exchanger, the Na+-K+-2Cl- transporter and on Na+-K+-ATPase. NH3 diffusion is stimulated by an acid disequilibrium pH in various nephron segments. Also, diffusion equilibrium of NH3 in various regions of the kidney has now been disproved. These various mechanisms of ammonia transport are considered in terms of their possible changes with acid-base disturbances. Phosphate is the most predominant urine buffer; its urinary excretion increases with acidosis. The mechanisms probably involve a decrease in the preferentially transported species, HPO4(2-), and a direct effect of pH on proximal tubule apical phosphate transport. With chronic acidosis, changes in the activity of the apical Na+-phosphate transporter occur. These effects of systemic acid-base balance interact with parathyroid hormone and dietary phosphate status to alter phosphate reabsorption. Citrate transport in the kidney is analyzed because of its sensitivity to systemic pH and because of the possible influence on systemic acid-base status in certain circumstances. Alterations in citrate excretion with acid-base disturbances depend on changes in the concentration of the transported species, citrate2-, and on changes in renal metabolism.
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                Author and article information

                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi
                2314-6133
                2314-6141
                2017
                22 May 2017
                : 2017
                : 5383574
                Affiliations
                1Institute of Physiological Chemistry, University Hospital Essen, University of Duisburg-Essen, Hufelandstrasse 55, Essen, 45147 North Rhine-Westphalia, Germany
                2Department of Thoracic and Cardiovascular Surgery, West German Heart Center, University Hospital Essen, Hufelandstrasse 55, Essen, 45147 North Rhine-Westphalia, Germany
                Author notes

                Academic Editor: Francesco Onorati

                Author information
                http://orcid.org/0000-0001-8397-5943
                http://orcid.org/0000-0001-8105-7911
                Article
                10.1155/2017/5383574
                5458371
                2c29b888-b435-4817-9568-572f7971187e
                Copyright © 2017 Friederike Roehrborn 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.

                History
                : 19 January 2017
                : 1 March 2017
                : 26 April 2017
                Categories
                Research Article

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