Page 256 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Introduction to Acid-Base Disorders 247

(T M ) of approximately 3 mEq/min and a renal threshold being increased during volume depletion and decreased

of 25 mEq/L. However, renal reabsorption of HCO 3 is during volume expansion.
closely tied to reabsorption of sodium and defense of The anionic composition of glomerular ultrafiltrate
ECFV. A primary expansion of ECFV leads to natriuresis determines, to a large extent, the effect that sodium avid-

and a transient decrease in renal HCO 3 reabsorption. ity has on the electrolyte composition of the reabsorbed
Contraction of the ECFV increases renal tubular reab- tubular fluid. If an adequate amount of chloride is present

sorption of sodium and HCO 3 . When hypovolemia is in the filtrate, the kidneys reabsorb chloride with sodium,

induced experimentally, renal HCO 3 reabsorption and alkalosis does not develop. If there is insufficient
continues to increase even at extremely high plasma chloride in the filtrate, however, sodium is reabsorbed
HCO 3 concentrations. 43,61 Thus, the apparent T M for with HCO 3 , and alkalosis develops. The prevailing

HCO 3 changes depending on renal sodium avidity, acid-base status of the ECF can be viewed as a conse-
quence of factors governing sodium and chloride reab-
sorption in the kidneys. 54 At a given rate of renal
100
sodium reabsorption, a change in the reabsorption of

95 either Cl or HCO 3 must be accompanied by a recipro-
Percent total renal bicarbonate reabsorption 85 in arterial PCO 2 and decreased by a decrease in arterial
cal change in reabsorption of the other anion.
90

Renal HCO 3 reabsorption is increased by an increase
80
PCO 2 . This effect may be mediated by a decrease (or
increase) in pH within renal tubular cells and increased
15
þ
(or decreased) availability of H for secretion. There is
10

tration and the rate of renal HCO 3 reabsorption that
5 an inverse relationship between serum chloride concen-
results from the requirement for electroneutrality during
Prox. Loop CCT MCD sodium reabsorption (see preceding paragraph). When
tubule of serum chloride concentration is reduced, the filtered load
Henle
Figure 9-7 Segmental reabsorption of bicarbonate along the of chloride decreases, and the kidneys reabsorb more

nephron. The major portion of filtered bicarbonate is reabsorbed sodium with HCO 3 . When serum chloride concentra-
proximally. Fine-tuning of bicarbonate reabsorption occurs in distal tion is increased, the filtered load of chloride increases,
nephron segments, including the medullary and cortical collecting and the kidneys reabsorb more sodium with chloride
ducts, as well as the thick ascending limb of Henle's loop. (From and less with HCO 3 . The fact that chloride and HCO 3

Kokko JP, Tannen RL. Fluids and electrolytes, 3rd ed. Philadelphia: are the only important resorbable anions in tubular fluid
WB Saunders, 1996: 208.) is important in understanding the pathophysiology of
Tubular fluid Proximal tubule cell Interstitial fluid
Interstitial
Tubular fluid Collecting duct cell fluid
Na HPO 4
2
Na + Na + Na +
H + H + HCO 3 – 3HCO 3 – Regenerated
HCO 3 – Na 2 HPO 4 Cl –
NaH PO + ATP + –
2 4 H H HCO 3
H CO 3 NaH PO Regenerated
–
2
HCO
4
2
3
H CO
2 3
CA 3Na + +
ATP CA 3Na
CO + H O 2K + ATP +
2
2
CO + H O 2K
2
2
A B
Figure 9-8 A and B, Regeneration of new HCO 3 by titration of phosphate by secreted H ion in renal
þ

tubule. CA, Carbonic anhydrase. (Drawing by Tim Vojt.)