Page 478 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

466 FLUID THERAPY

Arginine Glycine Guanidinoacetic acid
NH 2 H
C
NH H–C–NH 2 NH 2
NH COOH Glycine C
NH
CH 2 NH Liver
CH 2 Aminotransferase CH 2
CH 2 COOH
H–C–NH 2
COOH S-Adenosylmethionine
ATP
Guanidinoacetate
methyltransferase
S-Adenosylhomosysteine
ADP

NH 2
C
NH
Creatine
N–CH 3
CH 2
COOH
H Blood Urine
N C
O
NH
C Creatinine

N CH 2
CH 3
Muscle
Figure 19-8 Diagrammatic representation of hepatic contribution to creatine synthesis. (Adapted from
Heymsfield SB, Arteaga C, McManus C, et al. Measurement of muscle mass in humans: validity of the 24-hour
urinary creatinine method. Am J Clin Nutr 1983;37:478–494.)

increased urine NH 4 /NH 3 ratio. Mechanistically, potas- ATPase that facilitates reabsorption of K in exchange
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þ 119,154
sium infused into the hypokalemic patient replaces intra- for H . Potassium deficiency also may increase
cellular hydrogen ions. The displaced cellular hydrogen luminal electronegativity in the proximal tubule,
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ions decrease blood pH, promoting conversion of NH 3 stimulating HCO 3 secretion. Hypokalemia arising
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to the less-diffusible NH 4 form. This small shift in pH from diuretics used to treat ascites can cause
is not great enough to stimulate renal ammoniagenesis, hyperammonemia secondary to metabolic alkalosis
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but reduced urine pH leads to increased excretion of resulting from renal H loss.
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NH 4 . This effect may be augmented by increased plasma
aldosteronegivenitsabilitytoincreasehydrogeniondeliv- Hypophosphatemia in Liver Disease
ery into distal renal tubular fluid. 188 Hypophosphatemia also may complicate hepatic insuffi-
ciency. In human patients, hypophosphatemia and early
Serum Potassium Concentration and phosphorus administration are associated with a good
Ammoniagenesis prognosis in acute liver failure, whereas hyperpho-
Experimental and clinical observations of potassium sphatemia is predictive of poor recovery. 18 Cats with
depletion and loading suggest that renal NH 3 production HL are at increased risk for development of
is intimately linked with potassium homeostasis. Low hypophosphatemia, especially when associated with dia-
serum potassium concentrations stimulate and high betes mellitus or pancreatitis. Although symptomatic
serum potassium concentrations suppress renal hypophosphatemia may develop after rehydration and
ammoniagenesis. 154,214 A closed-loop regulatory system insulin therapy, it is most common as a result of refeeding
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modulates NH 3 production, hydrogen ion homeostasis, in cats with HL. Serum potassium, magnesium, and
and urinary potassium excretion in response to acute phosphorus concentrations in 157 cats with severe HL
and chronic changes in serum potassium concentration. are shown in Figure 19-9. In this population, only 22
Potassium deficiency stimulates H secretion in the distal of 157 (14%) HL cats had hypophosphatemia at presen-
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nephron and may stimulate HCO 3 production by tation, but more than 35% of those undergoing
increasing collecting duct expression of an H -K - nutritional support became hypophosphatemic with
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