Calcium plays an essential role in numerous biochemical pathways, and adequate amounts are required for optimal cell growth,
neuromuscular function, blood coagulation, and cell membrane stability. Consequently, the serum concentration of ionized (active)
calcium is tightly controlled through complex interplay among parathyroid hormone (PTH), calcitonin, and vitamin D metabolites.
In healthy individuals, calcium absorption from the intestinal tract, calcium release from bone, and calcium conservation
or excretion by the kidneys are all carefully regulated to optimize ionized calcium (iCa) concentrations.
Illustration by Paul Petersen
Hypercalcemia is a fairly uncommon disorder in cats, but it can cause substantial patient morbidity and is associated with
serious medical disorders such as neoplasia and renal failure.1 In this article, I review the definition of hypercalcemia and the steps to take when clinically evaluating a hypercalcemic
DEFINING AND CONFIRMING HYPERCALCEMIA
Circulating calcium exists in three distinct forms: bound to serum proteins (40%); complexed with citrate, phosphate, and other anions (8%); or ionized (52%).2 The ionized fraction is the biologically active form, and an elevated iCa concentration defines true hypercalcemia. The
calcium reported on standard serum chemistry profiles is a total calcium value (tCa; i.e. bound, complexed, and ionized), so changes in acid-base status and serum protein concentrations frequently affect this result.
In dogs, the effect of serum proteins may be mitigated by calculating the corrected or adjusted total calcium value. This
formula has not been validated in cats and should not be used.3 Instead, measure serum iCa concentrations in cats with elevated tCa concentrations, with tCa concentrations at the upper
end of the normal range, or exhibiting risk factors associated with hypercalcemia (e.g. calcium oxalate urolithiasis, chronic renal failure).2 Several commercially available in-house machines can accurately measure iCa concentrations, or a reference laboratory may
be used. Samples must be collected anaerobically, handled correctly, and shipped appropriately, as changes in pH can substantially
alter the percentage of calcium bound to protein and, thus, the iCa concentration.
Total calcium concentrations can be spuriously elevated. Lipemia and hemolysis can affect colorimetric measurements. Before
considering additional diagnostic tests, always verify hypercalcemia, either by repeating a tCa measurement in a fasted patient
or by determining the iCa concentration.
SIGNS OF HYPERCALCEMIA
Cats appear to be more resistant to the clinical consequences of hypercalcemia than are dogs, and it is not unusual to document
substantial hypercalcemia in an apparently normal patient.2 The most prevalent clinical signs reported in hypercalcemic cats are vague and nonspecific, such as lethargy, depression,
and anorexia.2 Other changes include an increase in thirst and urination due to antidiuretic hormone antagonism at the renal collecting
ducts, or dysuria and abdominal pain secondary to calcium-containing uroliths (Table 1).
As serum calcium concentrations continue to rise, gastrointestinal disturbances (vomiting and constipation) or neuromuscular
dysfunction (twitching and seizures) may be noted. If the serum calcium-phosphorus product exceeds 70, tissue mineralization
and secondary organ damage—primarily renal—are expected. Precipitous increases in serum calcium concentrations are often fatal.2