Page 565 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Managing Fluid and Electrolyte Disorders in Renal Failure 553

The b-agonist albuterol has been to treat hyperkalemia Symptomatic hypocalcemia (tetany) occurs infre-
in people because it causes an intracellular shift of potas- quently in renal disease. Hypocalcemia may be more
sium. 10 The cation exchange resin sodium polystyrene severe with antifreeze induced acute renal failure because
sulfonate (Kayexalate, Kionex) can be administered orally antifreeze contains phosphate that can cause severe
or by enema at a dose of 2 g/kg in 3 to 4 divided doses as hyperphosphatemia, and the ethylene glycol is converted
a suspension in 20% sorbitol. 13 This substance binds to oxalate, which complexes calcium. Treatment with cal-
potassium in the GI tract and releases sodium. It takes cium increases the risk of soft-tissue mineralization in
several hours to work, and side effects include hyperphosphatemic patients. The minimal dose of cal-
hypernatremia and constipation. cium gluconate that controls clinical signs should be used
The potassium lowering effects of these drugs, with the when therapy is needed. Calcium gluconate 10% can be
exception of polystyrene sulfonate, are temporary. Serum used at a dose of 0.5 to 1.5 mL/kg IV over 20 to 30
potassium concentrations gradually rise again within sev- minutes. As when treating hyperkalemia, monitor the
eral hours after administration unless urine production is EKG during infusion.
induced. Once even minimal urine production resumes, Hypercalcemia based on total calcium is usually mild
serum potassium concentrations usually decrease. Perito- and associated with normal ionized calcium; no specific
neal or hemodialysis may be necessary to ultimately treatment is necessary. If the ionized calcium is elevated,
control potassium if oliguria or anuria persist. treatment is warranted. Hypercalcemia may respond to
Certain drugs that contribute to hyperkalemia should fluid therapy, although calcium containing fluids (such
be avoided, and these drugs include nonspecific as LRS) should be avoided. Saline (0.9% NaCl) is an ideal
b-blockers, digoxin, angiotensin converting enzyme fluid choice, as the sodium content increases calciuresis.
inhibitors, angiotensin receptor antagonists, nonsteroidal Furosemide also promotes urinary calcium loss. Sodium
antiinflammatory drugs, potassium-sparing diuretics bicarbonate therapy decreases ionized calcium as more
(spironolactone, amiloride, triamterene), high doses of calcium binds to serum proteins. Hypercalcemia from
trimethoprim, cyclosporine, and total parenteral renal failure is not likely to be glucocorticoid-respon-
nutrition. 48 sive. 51 Calcitonin or bisphosphonates could be consid-
ered if the hypercalcemia is severe, although
CALCIUM bisphosphonates can induce renal failure. 51
Most of the body calcium is found in the skeleton as
hydroxyapatite. The extracellular calcium occurs in three MAGNESIUM
fractions: ionized calcium (55%), which is the active form; Magnesium concentrations may be elevated in severe
protein bound (35%), a storage form generally bound to renal failure because the kidneys are the major route of
albumin; and complexed calcium (10%), which is bound excretion of magnesium, but specific therapy is generally
to substances such as citrate, lactate, bicarbonate, or not necessary. Supplemental magnesium, such as that
phosphate. Total calcium (including all three fractions) found in some phosphate binders, should be avoided in
is the most common measure of calcium, although ion- those situations. Hypomagnesemia may occur with
ized calcium measurement is becoming more readily polyuric renal failure. Hypokalemia may be refractory
available in practice settings. to therapy if concurrent hypomagnesemia is present. In
There are multiple reasons for calcium disorders in those cases, correction of the magnesium deficit may be
patients with renal failure. An acute decrease in glomeru- necessary to correct the hypokalemia. Magnesium sulfate
lar filtration may lead to an abrupt increase in phospho- or magnesium chloride can be used for intravenous sup-
rus, causing a decrease in calcium by the law of mass plementation, and various forms are available for oral
action. The decrease in calcium stimulates parathyroid supplementation. 3
hormone synthesis and release, which works toward
increasing the calcium back to normal. On the other PHOSPHORUS
hand, chronic kidney failure may cause parathyroid hyper- Dietary phosphorus is readily absorbed from the gastro-
plasia, which rarely leads to hypercalcemia. Metabolic aci- intestinal tract and excreted by the kidneys. Decreased
dosis increases the ionized calcium fraction, although excretion commonly leads to hyperphosphatemia in both
over half of dogs with CKD and metabolic acidosis were acute and chronic renal failure. Intravenous fluid therapy
hypocalcemic. 29 may partially control phosphorus concentration by
Based on ionized calcium, 36% to 56% of dogs with addressing the hemodynamic component and improving
CKD are hypocalcemic, 20% to 55 % are normocalcemic, renal blood flow. There are no other specific treatments to
and 9% to 24% are hypercalcemic. 29,52 Based on total cal- decrease serum phosphorus in the acute stage. A phos-
cium, 8% to 19% are hypocalcemic, 60% to 76% are phate-restricted diet is recommended for long-term
normocalcemic, and 16% to 22% are hypercalcemic. control of hyperphosphatemia. Because protein is
The concordance between ionized calcium and total cal- phosphate-rich, this necessitates a protein-restricted diet.
cium is poor, especially in dogs with CKD. 29,52 While diet may be sufficient to control phosphorus