Page 210 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

200 ELECTROLYTE DISORDERS

Renal transplantation has been associated with regenerating liver, excessive renal losses are now consid-
hypophosphatemia in people and cats. 123 Ostensibly, ered to be responsible. 116 “Phosphate diabetes” is the
the cause is decreased renal tubular reabsorption of phos- term used for increased urinary phosphate excretion
phorus, which is currently believed to be due to due to decreased phosphate reabsorption, especially in
phosphatonins. There was no obvious consequence of hypophosphatemic patients. 96 The occurrence of
the hypophosphatemia in a report of 32 affected cats. hypophosphatemia after hepatic surgery in particular is
Hemolysis occurred, but the incidence was not statisti- not surprising because acute hepatic damage due to any
cally different from normophosphatemic renal transplant number of causes also is associated with hypophos-
cats. Changing the diet from a phosphorus-restricted diet phatemia. In fact, hypophosphatemia in people with
to a maintenance diet plus supplementing sodium phos- hepatic damage has been suggested to reflect healing
phate orally corrected the problem. and regeneration of the liver. 144 Hypophosphatemia
Disorders of renal tubular phosphate transport has been seen in dogs experimentally intoxicated with
associated with hypophosphatemia in humans include xylitol, 176 but it is uncertain whether hypophosphatemia
X-linked hypophosphatemia, autosomal dominant is due to hepatic damage or to other metabolic effects of
hypophosphatemic rickets, oncogenic hypophosphatemic xylitol.
osteomalacia, and hereditary hypophosphatemic rickets Hypophosphatemia previously has been associated
with hypercalciuria. 168 Naturally occurring mutations in with sepsis and gram-negative infections in people to
the npt2 gene encoding the type IIa sodium-phosphate the extent that some have suggested that it should be a
cotransporter have not been identified in these disorders, diagnostic tool. 171 Hypophosphatemia is believed to
but rather mutations have been found in other phos- occur in these people due to redistribution of phosphorus
phate-regulating genes. X-linked hypophosphatemia is into body cells. Recently, severe hypophosphatemia (<1
caused by a mutation in the PHEX gene (i.e., phos- mg/dL) has been reported to be a major risk factor for
phate-regulating gene with homology to endopeptidases mortality in these patients. 154 Decreased ventricular
on the X chromosome), which is expressed in bone, stroke work with subsequent decreased arterial pressure
whereas autosomal dominant hypophosphatemic rickets is believed to be caused in part by the hypophosphatemia.
is caused by a mutation in the FGF-23 gene, a member Intravenous administration of saccharated ferric oxide
of the fibroblast growth factor family. Oncogenic to treat iron deficiency has caused hypophosphatemia in
hypophosphatemic osteomalacia occurs as a result of people. 155 Similar changes have not been reported in
secretion of a humoral phosphaturic factor secreted by dogs or cats.
neoplastic cells. Hereditary hypophosphatemic rickets
with hypercalciuria is similar to X-linked hypophos- TREATMENT OF
phatemia and autosomal dominant hypophosphatemic HYPOPHOSPHATEMIA
rickets except that it is associated with appropriately Prevention, when possible, is preferred to therapy. The
increased serum concentrations of calcitriol, whereas clinician should anticipate potential hypophosphatemia
the other hereditary disorders are not. Renal tubular and either administer supplemental phosphorus (e.g.,
disorders of phosphate transport have not been conclu- patients receiving total parenteral nutrition or insulin
sively identified in dogs and cats, but hypophosphatemia, treatment for diabetic ketoacidosis) or carefully monitor
increased urinary FE Pi , low serum 25-hydroxychole- the patient for hypophosphatemia (e.g., patients receiv-
calciferol concentration, osteopenia, and pathologic ing phosphate binders).
fractures were reported in a young cat believed to have If hypophosphatemia occurs, one should seek to cor-
abnormal renal tubular phosphate transport and defective rect the underlying condition responsible for it. Whether
hepatic 25-hydroxylation of vitamin D. 74 phosphorus is administered depends on the magnitude of
Cats with decreased serum concentrations of cobala- the hypophosphatemia and whether clinical signs are
min and folate have been found to be at increased risk present. Asymptomatic animals with low serum phospho-
for hypophosphatemia. 135 Most of the hypophos- rus concentrations but without phosphorus depletion
phatemic cats had gastrointestinal tract disease or and those with serum phosphorus concentrations greater
pancreatitis. Therefore, it is not clear whether the changes than 1.8 mg/dL and unlikely to decrease any lower (e.g.,
in cobalamin and folate were epiphenomenon or cause- primary hyperparathyroidism) often do not require phos-
and-effect. However, as these patients frequently require phate administration.
nutritional supplementation (either enteral or parenteral), Phosphate supplementation seems appropriate for
the need to avoid the refeeding syndrome was noted. asymptomatic patients deemed at risk for developing symp-
Postsurgical hypophosphatemia is a well-established tomatic hypophosphatemia (e.g., diabetic ketoacidotic cat
problem in people. It is more common and can be partic- with serum phosphorus concentration of 1.6 mg/dL)
ularly severe after hepatic surgery, especially major resec- and patients with clinical signs believed to result from
tion and transplantation. 41 Although the mechanism was hypophosphatemia. The clinician should keep in mind that
once suggested to be uptake of phosphorus by the oversupplementation (especially but not exclusively