The pathophysiology of hyperchloremic metabolic acidosis after urinary diversion through intestinal segments.
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.
D000138:Acidosis / Q000097:blood / Q000503:physiopathology* / Q000652:urine; D000641:Ammonia / Q000652:urine; D000818:Animals; D002712:Chlorides / Q000097:blood*; D004195:Disease Models, Animal; D004285:Dogs; D004573:Electrolytes / Q000097:blood / Q000652:urine; D005260:Female; D007082:Ileum / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D011188:Potassium / Q000097:blood / Q000652:urine; D014513:Ureter / Q000378:metabolism; D014547:Urinary Diversion / Q000009:adverse effects* / Q000379:methods
D002712:Chlorides; D004573:Electrolytes; D000641:Ammonia; D011188:Potassium