Urease and the acidosis of urinary intestinal diversion

Michael Koch, W. S. McDougal, M. D. Flora

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Previous investigators have suggested that urinary tract infections with urea-splitting organisms may be a primary etiologic factor in the acidosis which is seen after urinary diversion. This study employs a model in which small intestinal segments are perfused with an artificial urine solution over a three hour period. Urease is then added in order to determine its effect on acid-base balance and net intestinal electrolyte transport. Urease created no significant increase in acid load (delta HCO3- = -7.5 ± 2.2 for controls vs. -8.7 ± 2.9 for urease group), but did increase the osmolality of the intestinal contents and resulted in a 24% increase in free water loss (p = .037). Analysis of sodium and chloride movement following the addition of urease to the perfusate suggests that both ammonium and bicarbonate are absorbed by the intestinal segment. Thus any acidosis resulting from increased ammonium absorption following the addition of urease appears to be offset by concomitant bicarbonate absorption. The azotemia of urinary diversion appears to be primarily the result of urea absorption, partially the result of ammonium absorption, and is not significantly increased by urease.

Original languageEnglish (US)
Pages (from-to)458-462
Number of pages5
JournalJournal of Urology
Volume146
Issue number2
StatePublished - 1991
Externally publishedYes

Fingerprint

Urinary Diversion
Urease
Acidosis
Ammonium Compounds
Urea
Azotemia
Gastrointestinal Contents
Acid-Base Equilibrium
Bicarbonates
Sodium Chloride
Urinary Tract Infections
Osmolar Concentration
Electrolytes
Research Personnel
Urine
Acids
Water

Keywords

  • Acidosis
  • Urinary diversion
  • Urinary tract infection

ASJC Scopus subject areas

  • Urology

Cite this

Koch, M., McDougal, W. S., & Flora, M. D. (1991). Urease and the acidosis of urinary intestinal diversion. Journal of Urology, 146(2), 458-462.

Urease and the acidosis of urinary intestinal diversion. / Koch, Michael; McDougal, W. S.; Flora, M. D.

In: Journal of Urology, Vol. 146, No. 2, 1991, p. 458-462.

Research output: Contribution to journalArticle

Koch, M, McDougal, WS & Flora, MD 1991, 'Urease and the acidosis of urinary intestinal diversion', Journal of Urology, vol. 146, no. 2, pp. 458-462.
Koch, Michael ; McDougal, W. S. ; Flora, M. D. / Urease and the acidosis of urinary intestinal diversion. In: Journal of Urology. 1991 ; Vol. 146, No. 2. pp. 458-462.
@article{2105daeb92b44bf78306777edc973e95,
title = "Urease and the acidosis of urinary intestinal diversion",
abstract = "Previous investigators have suggested that urinary tract infections with urea-splitting organisms may be a primary etiologic factor in the acidosis which is seen after urinary diversion. This study employs a model in which small intestinal segments are perfused with an artificial urine solution over a three hour period. Urease is then added in order to determine its effect on acid-base balance and net intestinal electrolyte transport. Urease created no significant increase in acid load (delta HCO3- = -7.5 ± 2.2 for controls vs. -8.7 ± 2.9 for urease group), but did increase the osmolality of the intestinal contents and resulted in a 24{\%} increase in free water loss (p = .037). Analysis of sodium and chloride movement following the addition of urease to the perfusate suggests that both ammonium and bicarbonate are absorbed by the intestinal segment. Thus any acidosis resulting from increased ammonium absorption following the addition of urease appears to be offset by concomitant bicarbonate absorption. The azotemia of urinary diversion appears to be primarily the result of urea absorption, partially the result of ammonium absorption, and is not significantly increased by urease.",
keywords = "Acidosis, Urinary diversion, Urinary tract infection",
author = "Michael Koch and McDougal, {W. S.} and Flora, {M. D.}",
year = "1991",
language = "English (US)",
volume = "146",
pages = "458--462",
journal = "Journal of Urology",
issn = "0022-5347",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - Urease and the acidosis of urinary intestinal diversion

AU - Koch, Michael

AU - McDougal, W. S.

AU - Flora, M. D.

PY - 1991

Y1 - 1991

N2 - Previous investigators have suggested that urinary tract infections with urea-splitting organisms may be a primary etiologic factor in the acidosis which is seen after urinary diversion. This study employs a model in which small intestinal segments are perfused with an artificial urine solution over a three hour period. Urease is then added in order to determine its effect on acid-base balance and net intestinal electrolyte transport. Urease created no significant increase in acid load (delta HCO3- = -7.5 ± 2.2 for controls vs. -8.7 ± 2.9 for urease group), but did increase the osmolality of the intestinal contents and resulted in a 24% increase in free water loss (p = .037). Analysis of sodium and chloride movement following the addition of urease to the perfusate suggests that both ammonium and bicarbonate are absorbed by the intestinal segment. Thus any acidosis resulting from increased ammonium absorption following the addition of urease appears to be offset by concomitant bicarbonate absorption. The azotemia of urinary diversion appears to be primarily the result of urea absorption, partially the result of ammonium absorption, and is not significantly increased by urease.

AB - Previous investigators have suggested that urinary tract infections with urea-splitting organisms may be a primary etiologic factor in the acidosis which is seen after urinary diversion. This study employs a model in which small intestinal segments are perfused with an artificial urine solution over a three hour period. Urease is then added in order to determine its effect on acid-base balance and net intestinal electrolyte transport. Urease created no significant increase in acid load (delta HCO3- = -7.5 ± 2.2 for controls vs. -8.7 ± 2.9 for urease group), but did increase the osmolality of the intestinal contents and resulted in a 24% increase in free water loss (p = .037). Analysis of sodium and chloride movement following the addition of urease to the perfusate suggests that both ammonium and bicarbonate are absorbed by the intestinal segment. Thus any acidosis resulting from increased ammonium absorption following the addition of urease appears to be offset by concomitant bicarbonate absorption. The azotemia of urinary diversion appears to be primarily the result of urea absorption, partially the result of ammonium absorption, and is not significantly increased by urease.

KW - Acidosis

KW - Urinary diversion

KW - Urinary tract infection

UR - http://www.scopus.com/inward/record.url?scp=0026315728&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026315728&partnerID=8YFLogxK

M3 - Article

VL - 146

SP - 458

EP - 462

JO - Journal of Urology

JF - Journal of Urology

SN - 0022-5347

IS - 2

ER -