Page 209 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Phosphorus: Hypophosphatemia and Hyperphosphatemia 199

which could explain why severe hypophosphatemia may by metabolic or membrane defects affecting sodium
occur in people with severe respiratory failure who are transport, and the observed phosphaturia may be second-
mechanically ventilated. 99 ary to natriuresis. 109 Loop diuretics (e.g., furosemide)
Diabetic patients are especially at risk for hypophos- and distally acting diuretics (e.g., thiazides) have little
phatemia. They often have total body phosphate deficits effect on renal phosphate excretion, but proximally acting
because of a loss of muscle mass, urinary phosphate losses, diuretics (e.g., carbonic anhydrase inhibitors) may
and impaired tissue use of phosphate related to insulin defi- increase renal excretion of phosphate secondary to their
ciency. Most diabetic cats in one study had mild effects on proximal tubular sodium reabsorption. In
hypophosphatemia at presentation, whereas 20 of 48 one study, acetazolamide (10 mg/kg intravenously three
ketoticcatsinanotherstudywere hypophosphatemic. 23,146 times daily) did not cause hypophosphatemia when
Another study found only 7 of 104 diabetic cats to be administered to dogs over a 7-day period. 137 Eclampsia
hypophosphatemic. However, stratification of the cats into in the bitch may be associated with hypophosphatemia
ketoacidotic and nonketoacidotic groups revealed that 5 of and hypocalcemia. 8,10 Presumably, increased PTH secre-
38 ketoacidotic cats were hypophosphatemic and only 2 of tion in response to hypocalcemia leads to decreased renal
66 nonketotic cats were hypophosphatemic. 39 Interest- reabsorption of phosphate.
ingly, serum phosphorus concentrations are often normal Not reported in veterinary medicine, cranial trauma is
to increased at presentation in diabetic people, perhaps associated with renal losses of phosphorus and
because of metabolic acidosis by organic acids (e.g., hypophosphatemia. 132 Acquired diabetes insipidus has
b-hydroxybutyrate), insulin deficiency, osmotic effects of been suggested as a possible reason.
hyperglycemia, or renal insufficiency. 86,119 Hypophosphatemia caused by dietary deficiency is
Administration of large doses of insulin makes hypo- unlikely in animals eating commercial diets with adequate
phosphatemia even more likely in diabetic ketoacidotic protein content. A low-protein, low-phosphorus diet
patients. Severe hypophosphatemia has been reported in designed to dissolve struvite calculi (Prescription Diet
dogs and cats treated for diabetic ketoacidosis. 2,23,173 S/D, Hill’s Pet Nutrition, Inc., Topeka, Kansas.) did
Hypophosphatemia developed or worsened after insulin not cause significant hypophosphatemia when fed to dogs
1
administration, and clinical signs (e.g., hemolysis, over a 6-month period. Urinary phosphorus excretion
seizures)thoughtrelatedtohypophosphatemiadeveloped decreased and calcium excretion increased in this study.
in 11 animals. Interestingly, four of these cats developed Although vomiting and malabsorptive diseases poten-
hemolytic anemia despite intravenous supplementation tially can cause phosphate loss, these disorders rarely
of potassium phosphate, and it is not clear whether cause hypophosphatemia in dogs or cats. 31 Canine
the anemia was caused by inadequate phosphate malabsorptive intestinal disorders often are characterized
supplementation or Heinz body formation. 23 by hypocalcemia related to hypoalbuminemia, but serum
Although it is not documented in dogs and cats, phosphorus concentrations typically are normal. 20,55
hypophosphatemia may occur in people with certain rap- People have become hypophosphatemic after adminis-
idly growing tumors. Ostensibly, the rapidly dividing cells tration of magnesium- and aluminum-containing
use phosphorus, removing it from the blood. 99 antacids. 101 Whether phosphate depletion occurs
Increased urinary loss of phosphorus often produces depends on the patient’s phosphorus intake, dosage of
moderate hypophosphatemia in primary hyperparathy- the phosphate binding agent, duration of administration,
roidism, but clinical signs are caused by hypercalcemia. * and the preexisting phosphate balance of the patient.
If 2.5 mg/dL is considered the lower limit of normal, Vitamin D deficiency may cause hypophosphatemia
serum phosphorus concentration was decreased in approx- because hypocalcemia increases PTH secretion, which
imately one third of reported cases associated with parathy- increases renal phosphate excretion. Decreased intestinal
roid adenoma, but in six of six cases associated with phosphate absorption presumably also plays a role in this
44
parathyroid hyperplasia. Hypophosphatemia is seen setting.
inconsistently in cats with primary hyperparathyroid- It has been stated that 38% of hyperadrenocortical
ism. 43,82 The fractional excretion of phosphorus (FE Pi ) dogs have hypophosphatemia, but actual serum phos-
was increased in a few affected dogs. 172 The normal FE Pi phorus concentrations were not reported. 125 In one
was found to be 7.5% 4.6% in 10 normal dogs but study, an identifiable cause of hypophosphatemia could
10% to 23% in a dog with primary hyperparathyroidism. 29 not be found in the majority of dogs with this serum bio-
Fanconi syndrome in basenjis is associated with chemical abnormality. 31 Hypophosphatemia, hypercalce-
decreased renal fractional reabsorption of phosphate, mia, hyperglycemia, azotemia, hypokalemia, and acidosis
but serum phosphorus concentrations are normal. 18 have been reported in a dog and cat with hypothermia
The renal tubular transport abnormality may be caused caused by exposure to low environmental tempera-
ture. 138 The mechanisms responsible for these electrolyte
and acid-base disturbances are uncertain, but transloca-
*References 13, 29, 87, 98, 172, 174 tion seems likely.