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Renal Secondary Hyperparathyroidism in Dogs

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Renal Secondary Hyperparathyroidism in Dogs 3 CE CREDITS CE Article Renal Secondary Hyperparathyroidism in Dogs ❯❯ Jenefer R. Stillion, DVM Abstract: The parathyroid glands secrete parathyroid hormone (PTH), which is important for main- Cornell University Hospital taining calcium homeostasis. Parathyroid gland hyperplasia and subsequent hyperparathyroid- for Animals ism can occur secondary to chronic renal failure in dogs, resulting in significant alterations in ❯❯ Michelle G. Ritt, DVM, calcium metabolism. Renal secondary hyperparathyroidism is a complex, multifactorial syndrome DACVIM that involves changes in circulating levels of calcium, PTH, phosphorus, and 1,25-dihydroxychole- University of Minnesota calciferol (calcitriol). An increased PTH level can have deleterious effects, including soft tissue College of Veterinary Medicine mineralization, fibrous osteodystrophy, bone marrow suppression, urolithiasis, and neuropathy. Dietary phosphorus restriction, intestinal phosphate binders, and calcitriol supplementation may slow the progression of renal disease and decrease PTH concentrations in animals with secondary hyperparathyroidism; however, the prognosis for these animals is guarded to poor. he four canine parathyroid glands Importance of Calcium are embedded in the poles of the two The control of calcium metabolism is Tlobes of the thyroid gland, although important because calcium plays an inte- they share no anatomic or physiologic gral role in many physiologic processes. At a Glance connections with the thyroid gland. The Serum calcium must be maintained in main function of the parathyroid glands a narrow range for normal nerve and Importance of Calcium is to maintain calcium metabolism in the muscle function, heart muscle contrac- Page E1 body. In response to decreasing levels of tion, cell membrane stability and linkage, Renal Secondary serum ionized calcium (iCa), chief cells in coagulation, and, to a small degree, struc- Hyperparathyroidism the parathyroid gland secrete parathyroid tural integrity of bones and teeth. Calcium Page E3 hormone (PTH). PTH acts on the bones, in the extracellular fluid helps regulate Causes of Hypercalcemia kidneys, and, indirectly, intestinal mucosa the cellular functions of several organs, in Dogs to elevate the serum calcium level.1,2 including the kidneys, thyroid C cells, Page E5 Patients with parathyroid hyperplasia and parathyroid glands. Calcium ions also Clinical Signs of Chronic and hyperparathyroidism secondary to serve as messengers, conveying signals Renal Failure and Primary chronic renal failure (CRF) have significant from cell surfaces into cells.3 Hyperparathyroidism in Dogs alterations in calcium metabolism2,3 as well Page E6 as changes in circulating levels of PTH, Calcium Distribution Expected Diagnostic Test phosphorus, and 1,25-dihydroxycholecal- Most calcium (99%) is found in bone in Results for the Most Common ciferol (calcitriol). The diagnosis, treatment, the form of hydroxyapatite crystals, which Causes of Hypercalcemia and prevention of renal secondary hyper- contain phosphate, water, and calcium.1,2 Page E7 parathyroidism are important because Intracellular calcium accounts for most Available Oral Phosphate excess PTH may complicate treatment and of the remaining calcium in the body. In Binders and Recommended cause progression of renal disease in dogs. inactive cells, the intracellular iCa level Dosages for Use in Dogs This article reviews the normal physiology is low because most calcium is bound to Page E8 and metabolism of calcium as they relate to protein or contained in the mitochondria the pathogenesis, diagnosis, and treatment or endoplasmic reticulum. As cell activ- of renal secondary hyperparathyroidism. ity increases, so does the intracellular iCa CompendiumVet.com | July 2009 | Compendium: Continuing Education for Veterinarians® E1 ©Copyright 2009 Veterinary Learning Systems. This document is for internal purposes only. Reprinting or posting on an external website without written permission from VLS is a violation of copyright laws. FREE CE Renal Secondary Hyperparathyroidism in Dogs level. The smallest pool of calcium in the body cells in response to a low serum iCa level. is the extracellular fluid component, which Increased PTH secretion leads to an increase comprises complexed calcium (bound to phos- in serum concentrations of total calcium and phate, sulfate, bicarbonate, citrate, and lactate), iCa and a decrease in the serum phosphate iCa, and protein-bound calcium. Extracellular concentration. If the serum calcium level is iCa is the most important factor in controlling chronically decreased, such as in animals with QuickNotes the calcium serum concentration.1,2 renal failure or those that are pregnant or lac- tating, hyperplasia of the parathyroid glands Serum ionized Regulation of Calcium in the Body occurs.3 The enlarged glands are more sensi- calcium, not total Normal calcium homeostasis is maintained tive to small reductions in the calcium level calcium, should be principally by the actions of three hormones: and secrete PTH more efficiently. measured in dogs PTH, calcitriol, and calcitonin (FIGURE 1). These PTH acts on the kidneys to increase with chronic renal hormones control the movement of calcium the serum calcium level by increasing cal- failure to diag- between the extracellular fluid, gastrointestinal cium reabsorption from the renal proximal nose and monitor tract, kidneys, and bones. Phosphorus is also tubules.1,2 It acts on bone tissue to increase changes in the an important regulator of calcium. calcium resorption from the bone matrix to elevate the serum calcium level, principally calcium level. Parathyroid Hormone by stimulating osteoclasts, which digest bone The serum calcium level is monitored by spe- matrix and increase the calcium ion level in cific membrane calcium receptors on the sur- the matrix fluid. Calcium ions are then trans- face of the chief cells of the parathyroid gland. ported from the bone fluid to the extracellu- PTH is synthesized and secreted by these lar fluid via an extensive membrane system formed by the processes of osteocytes and FIGURE 1 osteoblasts.1,3 PTH indirectly increases intes- tinal absorption of calcium and phosphorus Increased calcium through the conversion of calcidiol to calcitriol 2 resorption Increased in the proximal renal tubules. calcium absorption Bone Calcitriol Dogs ingest vitamin D (calciferol) in their Intestines food, and it is absorbed from the intestines. Calciferol is hydroxylated in the liver to pro- Calcitonin duce 25-hydroxyvitamin D (calcidiol), which PTH is further hydroxylated to calcitriol in the kidneys.2 In response to hypocalcemia, PTH is secreted from the parathyroid glands and stimulates the synthesis and secretion of calcit- riol by the kidneys. Calcitriol acts directly on Kidneys Calcitriol enterocytes to increase intestinal absorption of calcium and phosphorus. In the kidneys, calcitriol increases reabsorption of phospho- rus and calcium from the glomerular filtrate. Increased It also exerts negative feedback on the kid- calcium neys to inhibit the production of more calcit- reabsorption riol and on the parathyroid glands to decrease PTH synthesis and secretion when the serum Hormonal regulation of calcium homeostasis. Normal calcium homeosta- calcium level is high.1–3 sis is maintained principally by the actions of parathyroid hormone (PTH), calcit- riol, and calcitonin. These hormones control the movement of calcium between Calcitonin the extracellular fluid, gastrointestinal tract, kidneys, and bones. Positive feedback Calcitonin is secreted by the parafollicular (+) is indicated by the solid lines; negative feedback (–) is indicated by the dashed C cells of the thyroid gland in response to line. (Adapted from Polzin DJ, Osborne CA, Ross S. Chronic renal failure. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine Diseases of increases in serum calcium. It acts on bone the Dog and Cat. 6th ed. St Louis: Elsevier; 2005:1756-1785.) tissue to decrease the serum calcium level by E2 Compendium: Continuing Education for Veterinarians® | July 2009 | CompendiumVet.com FREE Renal Secondary Hyperparathyroidism in Dogs CE stimulating osteoblasts to increase calcium mal tubules. This deficit precedes the increase absorption and deposition in the skeleton in the serum phosphate level. Extracellular iCa and inhibiting osteoclasts to decrease bone subsequently decreases due to reduced intesti- resorption of calcium.1 In a healthy animal, nal absorption of calcium, which is mediated by the action of calcitonin is less important than calcitriol. Because calcitriol acts directly on the that of PTH for minute-to-minute regulation parathyroid glands to regulate PTH secretion, of serum calcium. However, it is important in a decrease in calcitriol also leads to a lack of growing, pregnant, and lactating animals, in negative feedback and a further increase in the which it protects the bones from excess cal- PTH level. This mechanism may coexist with cium loss.1 decreased renal phosphorus excretion. Other factors that may contribute to the Phosphorus development of hyperparathyroidism in CRF In a healthy animal, PTH acts on the kidneys include alterations in the set point for the to increase renal excretion of phosphate ions response of the parathyroid glands to calcium and reabsorption of serum calcium, thereby and decreased breakdown of PTH by the dis- increasing the serum calcium level.1,2 Decreases eased kidneys.2 in serum phosphate lead to an increase in extracellular calcium.3 Sudden
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