*Review* **Parathyroid Hormone: A Uremic Toxin**

### **Eduardo J. Duque 1, Rosilene M. Elias 1,2 and Rosa M. A. Moysés 1,\***


Received: 31 January 2020; Accepted: 8 March 2020; Published: 17 March 2020

**Abstract:** Parathyroid hormone (PTH) has an important role in the maintenance of serum calcium levels. It activates renal 1 α-hydroxylase and increases the synthesis of the active form of vitamin D (1,25[OH]2D3). PTH promotes calcium release from the bone and enhances tubular calcium resorption through direct action on these sites. Hallmarks of secondary hyperparathyroidism associated with chronic kidney disease (CKD) include increase in serum fibroblast growth factor 23 (FGF-23), reduction in renal 1,25[OH]2D3 production with a decline in its serum levels, decrease in intestinal calcium absorption, and, at later stages, hyperphosphatemia and high levels of PTH. In this paper, we aim to critically discuss severe CKD-related hyperparathyroidism, in which PTH, through calcium-dependent and -independent mechanisms, leads to harmful e ffects and manifestations of the uremic syndrome, such as bone loss, skin and soft tissue calcification, cardiomyopathy, immunodeficiency, impairment of erythropoiesis, increase of energy expenditure, and muscle weakness.

**Keywords:** parathyroid hormone; secondary hyperparathyroidism; uremic toxin

**Key Contribution:** Secondary hyperparathyroidism is a serious and common complication of CKD; with a negative impact on morbidity and mortality of patients on dialysis. Persistent high levels of PTH cause abnormalities in the cellular function of di fferent target organs; contributing to several findings of the uremic syndrome.
