**1. Introduction**

Hyperparathyroidism (HPT) is a pathology caused by the increased synthesis of parathyroid hormone (PTH) by the parathyroid glands. This process can be a consequence of an intrinsic parathyroid disorder or secondary to an imbalance of calcium metabolism in patients with systemic diseases, such as chronic kidney disease (CKD) [1]. PTH plays a central and fundamental role in homeostasis of the control of calcium and phosphorus in the body. Its action on the renal, bone, and, indirectly, intestinal cells implies a rapid increase in the extracellular flow of calcium. This hormone has a short half-life (2–3 min) that quickly mobilizes calcium to the intravascular. It binds to specific membrane receptors on the kidney and bone cells, fibroblasts, chondrocytes, vascular smooth muscle, adipocytes, and placental trophoblasts [2].

## **2. History**

The parathyroid glands were initially discovered in the eighteenth century by Richard Owen, who dissected the parathyroid glands of an approximately 2260 kg rhino, being reported as "a small, compact yellow glandular body attached to the thyroid at the point where the veins emerge" [3, 4]. However, the definitive discovery of the parathyroid glands in humans was made in 1877 by Swede Ivar Sandström, a medical student at Uppsala University, Sweden, publishing his work in which he wrote: "Almost three years ago I found on the thyroid gland of a dog a small organ, hardly as big as a hemp seed, which was enclosed in the same connective tissue as the thyroid, but could be distinguished therefrom by the light color. Microscopically the examination revealed glandular tissue completely different from that of the thyroid" [4]. After identification in dogs, he finally dissected such structures in human cadavers, calling them *glandulae parathyroidae* (**Figure 1**).

Later, in 1891, Eugene Gley reported symptoms of tetany when these glands were removed during thyroidectomies [5]. At the beginning of the twentieth century, the theory described by Jacob Erdheim emerged, which related hypertrophy of parathyroid tissue as a response to bone disease (osteomalacia and/or cystic fibrous osteitis). This theory was rejected by Felix Mandl in 1925, who performed the first parathyroid surgery in Vienna. Initially, it was believed that bone lesions were a consequence of a parathyroid deficiency, and to prove it, transplantation of cadaveric parathyroid tissues was performed in patients with cystic bone lesions and hypercalciuria. With the procedure unsuccessful, Mandl proceeded with cervical exploration and identified a 21 × 12 × 12 mm parathyroid "tumor," which was resected, observing the patient's improvement [6]. Still in 1925, Collip brought a breakthrough in studying the function of PTH, by treating patients with tetany due to parathyroidectomy with relative PTH extract with relative success [4].

The term tertiary HPT came up with Dr. Walter St. Goar, when describing a case report in the New England Journal of Medicine, number 268, in 1963, of a patient with CKD and functional parathyroid autonomy [7]. McPhaul, in 1964, published

**71**

**Figure 2.**

*Mechanisms of action of parathyroid hormone.*

*Parathyroid Glands and Hyperparathyroidism: A General Overview*

the first surgical success in patients with this clinical condition [8]. Later, in 1968, Davies and colleagues also studied 200 cases of HPT and, of these, obtained 14

PTH plays a central and fundamental role in homeostasis of the control of calcium and phosphorus in the body. It is produced by the parathyroid glands, composed mainly of main cells, and, to a lesser extent, by oxyphil cells [1, 4]. Studies show that, over time, the main cells are replaced by oxyphil cells, which are more sensitive to PTH production, especially in cases of CKD [9, 10]. Its action on renal, bone, and, indirectly, intestinal cells implies a rapid increase in the extracellular flow of calcium (**Figure 2**). This hormone is a peptide with 84 amino acids and a molecular weight of 9500 Da. It has a short half-life (2–3 min) and is broken down into the amino-terminal and carboxy-terminal portions. Only the amino-terminal portion has biological effects on the body, while the carboxy-terminal portion remains inactive. PTH binds to specific membrane receptors in renal and bone cells, fibroblasts, chondrocytes, vascular smooth muscle, adipocytes, and placental trophoblasts [11].

PTH causes an increase in the calcium reabsorption of the glomerular filtrate. This is mainly due to some factors. First, it acts in the loop of Henle, increasing the voltage gradient to allow the passive transport of ionized calcium. Then, it acts on the granular portion of the distal contorted tubules, inducing translocation of preformed calcium channels on the cell surface, increasing the entry of calcium into the vascular lumen. Finally, it also acts on the collecting tubules by changing

kidney cells, such as an increase in phosphate excretion, with increased phosphaturia and decreased serum phosphate; increased bicarbonate clearance with urine

/Ca2+ pump [11–13]. In addition, PTH has other effects on

*DOI: http://dx.doi.org/10.5772/intechopen.92785*

cases of tertiary HPT [7].

**3.1 Effect of PTH on the kidneys**

the activation of the Na+

**3. Physiology**

the first surgical success in patients with this clinical condition [8]. Later, in 1968, Davies and colleagues also studied 200 cases of HPT and, of these, obtained 14 cases of tertiary HPT [7].
