Calcitonin response in cats with chronic kidney disease

Abstract

Background Chronic kidney disease (CKD) is the 7th most frequently encountered disorder in cats in general practice in England, with a disease prevalence of 30 to 80% in cats over 10 years old, and is commonly associated with hypercalcemia. The kidneys play an important role in calcium regulation, but the etiology of hypercalcemia in cats with CKD is not completely understood. Derangements in hormones involved in calcium homeostasis, such as secondary renal hyperparathyroidism, are common and occur early in cats as part of CKDmineral and bone disorder. Although it is traditionally stated that secondary renal hyperparathyroidism could cause ionized hypercalcemia in cats with CKD, hypercalcemia often appears parathyroid-independent, with secondary suppression of parathyroid hormone (PTH) secretion. Calcitonin is released by C-cells of the thyroid in response to an increased serum ionized calcium concentration. It protects against hypercalcemia by inhibition of bone turnover and renal reabsorption of calcium, but it does not appear to have an important physiologic role in all species. The kidneys are the most important site for calcitonin degradation. Calcitonin concentrations are increased in human CKD patients from stage 3 onwards, which may be caused by C-cell hyperplasia rather than reduced metabolism. Healthy and azotemic normocalcemic cats generally appear to have undetectable plasma calcitonin concentrations.