Page 254 - Problem-Based Feline Medicine

246 PART 4 CAT WITH URINARY TRACT SIGNS

intestinal calcium uptake and calcium resorption from the GIT. Phosphate retention also reduces
from bone. extracellular calcium.
● Calcitonin acts to decrease high calcium concen- ● Chronic stimulation of the parathyroid glands to main-
trations, but does not appear to be important in tain serum calcium concentrations in renal failure
small day-to-day corrections of calcium concentra- leads to hyperplasia (renal secondary hyperparathy-
tion, which is the role of PTH and calcitriol. roidism). In some cats, autonomous function devel-
Calcitonin decreases osteoclast activity and forma- ops because some hyperplastic cell lines are very
tion of new osteoclasts. deficient in calcitriol receptors. Calcitriol regulates
synthesis of calcium receptors, so these cells are also
Hypercalcemia occurs when there is some derangement
poorly sensitive to calcium concentrations, and pro-
of the interaction between parathyroid hormone, vita-
duce large amounts of PTH. Uremia also reduces
min D and organs such as the gut, bone, kidneys and
formation of calcium receptors in parathyroid gland
parathyroid glands.
cells, leading to inappropriate PTH secretion.
Malignancy (lymphoma and squamous cell carci-
The diuretic phase of acute renal failure may also be
noma), renal failure and primary hyperparathy-
associated with hypercalcemia via other mechanisms.
roidism are the most common causes of hypercalcemia
in cats. In many cats, the cause of the hypercalcemia Primary hyperparathyroidism is a less common
is not identified, and is termed idiopathic hypercal- cause of hypercalcemia, and is the result of an
cemia. autonomous adenoma producing excess PTH. It is usu-
ally a solitary functional adenoma, although bilateral
Hypercalcemia of malignancy is the most common
cystadenomas and solitary or bilateral adenocarcino-
cause of hypercalcemia in cats. It results from secretion
mas have been reported.
of locally acting or humorally acting osteoclast-activat-
ing substances. Vitamin D toxicosis may be acute and associated with
● In cats, lymphoma and squamous cell carcinoma cholecalciferol (vitamin D) rodenticides, or chronic
are most often associated with hypercalcemia but due to excess supplementation or plant ingestion. In
multiple myeloma and adenocarcinoma have also some countries, cholecalciferol rodenticides have been
been reported. withdrawn from the market because of their potential
● In some tumors, for example lymphoma, there is for irreversible nephrotoxicity in children.
autonomous secretion of a humorally acting PTH- ● Acute toxicity occurs at 5 g of bait/kg body
related protein, which activates osteoclasts, increases weight and hypercalcemia occurs within 24 h of
intestinal absorption and increases renal tubular ingestion.
reabsorption of calcium and excretion of phospho- ● At lower doses of vitamin D, the maximal effect on
rus. Endogenous PTH secretion is suppressed. calcium and phosphorus may not be evident for 1–2
● Some neoplastic cells invade bone or bone marrow weeks after ingestion.
and secrete products that act locally to activate ● Cats requiring supplementation with vitamin D and
osteoclasts, such as prostaglandins, osteoclast-acti- calcium following thyroidectomy are at risk of vita-
vating factor, calcitriol, interleukin-1, and PTH- min D toxicity and nephrocalcinosis, if calcium and
related protein or PTH. phosphorus is not monitored carefully.
● Some plants contain active metabolites of vita-
Chronic renal failure is the second most common
min D such as the houseplant Cestrum diurnum
cause of hypercalcemia in cats. A number of mecha-
(day-blooming jasmine). Solanum malacoxylon
nisms associated with chronic renal failure lead initially
and Trisetum flavescen also contain vitamin D
to reduced extracellular calcium. In a few cats, com-
metabolites.
pensatory mechanisms eventually result in hypercal-
cemia. Fungal and bacterial granulomatous disease is a rare
● Extracellular calcium concentration is decreased in cause of hypercalcemia. The inflammatory process
renal failure because reduced renal mass and hyper- may or may not directly involve the bone. The mecha-
phosphatemia reduce formation of calcitriol (active nism may involve local osteolysis or secretion of fac-
vitamin D), leading to reduced calcium absorption tors from inflammatory cells such as prostaglandins