Page 165 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Calcium: Hypercalcemia and Hypocalcemia 155

return to hypercalcemia despite maximal doses of predni- noted (Chew, unpublished observations). Overuse of cal-
sone. When dietary modification and treatment with cium-containing intestinal phosphate binders can occa-
prednisolone have been unsuccessful in resolving IHC, sionally cause hypercalcemia. 111 An unusual case of
intravenous pamidronate treatment can be considered. hypercalcemia was attributed to the chronic ingestion
Beneficial effects from the chronic administration of of calcium carbonate in the form of limestone rocks. 296
subcutaneous fluids or oral furosemide to cats with Malignant histiocytosis in dogs was reported in associa-
IHC have not been evaluated. Treatment with tion with hypercalcemia in one dog. 586
calcimimetics could be of benefit. Calcimimetics interact The ingestion of large amounts of grapes or raisins may
with the calcium receptor and are effective in decreasing result in hypercalcemia. Seven of 10 dogs with renal fail-
calcium, phosphorus, and PTH in human patients. 55 ure associated with grape or raisin ingestion had increased
serum tCa concentrations (12.3 to 26 mg/dL) and
Uncommon Causes of Hypercalcemia increased serum phosphorus (6.4 to 22 mg/dL) 24
AIRF in dogs is occasionally associated with mild hyper- hours to several days following ingestion. 230 In four dogs,
calcemia. Hypercalcemia may occur more commonly ingestion was estimated to be from 0.41 to 1.1 ounces of
after conversion of oliguria to polyuria, possibly as cal- grapes or raisins per kilogram of body weight. Oliguria or
cium salts that were deposited during oliguria are anuria was noted in 5 of 10 dogs, and 5 of 10 dogs sur-
mobilized from soft tissues. Sudden improvement in vived. These cases were clustered from 1999 to 2001, and
renal function also may result in a rapid decrease of serum raisin/grape toxicity had not been previously reported.
phosphorus concentration, changing mass law Vomiting following ingestion of what appears to be a
interactions between phosphorus and calcium and trivial quantity of raisins or grapes in some dogs leads to
resulting in transient hypercalcemia. Mild hypercalcemia the development of AIRF usually within 48 hours. Not all
(11.5 to 12.5 mg/dL) is observed uncommonly in some dogs that consume grapes or raisins develop clinical signs
dogs with severe oliguria and decreased GFR during or acute renal failure. Of 132 dogs reported with raisin or
intrinsic renal failure. Animals with severe hyperphos- grape ingestion, 33 developed no clinical signs or azote-
phatemia during AIRF usually have normal or low serum mia, and 14 of 133 dogs developed clinical signs but no
calcium concentrations. azotemia. 169 Of 132 cases, 43 dogs developed clinical
Nonmalignant skeletal lesions are occasionally signs and AIRF. The pathogenesis of nephrotoxicity
associated with hypercalcemia in dogs. Bacterial and fun- associated with raisins and grapes remains unknown,
gal osteomyelitis can potentially result in hypercalcemia if but it is speculated that ochratoxin may be a toxic compo-
the rate of osteolysis is sufficient. 111 Hypercalcemia nent. 449 Tubular degeneration and necrosis of varying
associated with hepatozoonosis and skeletal involvement severity are consistently described and most pronounced
has been reported. 351 In 30 dogs with systemic aspergil- in proximal tubules. 169,394
losis, 27% had hypercalcemia. 523 Neonatal septicemia has In some cases of grape or raisin ingestion with AIRF,
been associated with hypercalcemia on rare occasions in mild to severe hypercalcemia develops, and in some dogs,
puppies after septic embolization of bone and subsequent serum tCa concentration can change dramatically from
osteolysis. 111 Mild hypercalcemia occurs in some dogs day to day during various treatments. 363 With acute renal
with hypertrophic osteodystrophy, and the hypercalcemia failure following ingestion of raisins or grapes, hypercal-
may be aggravated by ascorbic acid supplementation. 558 cemia was detected in 93% of affected dogs, and tCa
Hypothermia has caused hypercalcemia in one cat. 429 ranged from 8 to 26 mg/dL. 169,230 Of 40 dogs, 23
One cat with pancreatitis and hypercalcemia has been (57.5%) survived, and 17 (42.5%) failed to survive; 15
described, even though hypocalcemia is more common of 23 underwent complete resolution of azotemia. Initial
in cases of pancreatitis. 247 In one report, a dog receiving and peak serum tCa concentrations and initial and peak
intermittent calcium therapy for hypocalcemia developed calcium X phosphorus products were significantly higher
hypercalcemia and acute pancreatic hemorrhage that may in those that did not survive as compared with those that
have been related to excessive calcium therapy. 409 Dehy- did survive. Hypercalcemia was documented in 1 of 3
dration may cause mild and reversible hypercalcemia, dogs evaluated within 24 hours of ingestion, in 2 of
especially with normal kidney function. Disuse osteopo- 8 dogs within 24 to 48 hours, and in 12 of 13 dogs
rosis after prolonged immobilization can rarely contrib- evaluated for the first time 48 to 72 hours after ingestion.
ute to the development of mild hypercalcemia because Total calcium concentration returned to the normal
weight bearing is necessary to maintain the balance range in a median of 11 days (range, 2 to 51 days). Unfor-
between new bone formation and resorption of old bone. tunately, iCa measurements have yet to be reported for
Serum total hypercalcemia has been noted in a small per- any dogs with raisin toxicity, AIRF, and hypercalcemia
centage of hyperthyroid cats, 28,511 but iCa concentration based on serum tCa. Because many dogs with severe
is normal. In cats with untreated hyperthyroidism, mild AIRF have hyperphosphatemia, some of the increased
ionized hypercalcemia that resolved following conversion serum tCa may be because of complex formation with
to euthyroidism with treatment has been uncommonly phosphate. The observation that serum tCa