The pathophysiology of hyperchloremic metabolic acidosis after urinary diversion through intestinal segments

Michael Koch, W. S. McDougal

Research output: Contribution to journalArticle

120 Citations (Scopus)

Abstract

The pathophysiology of hyperchloremic metabolic acidosis after urinary diversion through intestinal segments has not been defined. This study employs a canine model in which an ileal segment is interposed between one kidney and the urinary bladder. Comparison of urinary solute excretion rates between the normal and interposed renal units allows quantitation of solute reabsorption and secretion by the ileal segment. Ileal segments reabsorb urinary chloride, potassium, and ammonium. Ammonium is reabsorbed in part as its conjugate free base, ammonia, with the liberated hydrogen ion reabsorbed with chloride or excreted as titratable acid. Inability to excrete acid as ammonium results in depletion of body buffers and a diminished capacity to compensate an additional acid challenge. Bicarbonate is secreted by the ileal segments but not in amounts that are physiologically significant. Impaired renal function predisposes to the development of this syndrome but is not a primary pathophysiologic mechanism.

Original languageEnglish (US)
Pages (from-to)561-570
Number of pages10
JournalSurgery
Volume98
Issue number3
StatePublished - 1985
Externally publishedYes

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Urinary Diversion
Acidosis
Kidney
Ammonium Compounds
Acids
Ammonium Chloride
Potassium Chloride
Bicarbonates
Ammonia
Protons
Canidae
Chlorides
Buffers
Urinary Bladder

ASJC Scopus subject areas

  • Surgery

Cite this

The pathophysiology of hyperchloremic metabolic acidosis after urinary diversion through intestinal segments. / Koch, Michael; McDougal, W. S.

In: Surgery, Vol. 98, No. 3, 1985, p. 561-570.

Research output: Contribution to journalArticle

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