The sensitivity of parathyroid glands to a low calcium level in plasma results in parathyroid hormone (PTH) release in order to restore the normal Ca²+ concentration. Hyperparathyroidism is a common endocrinopathy, caused by uncontrolled growth of parathyroid cells. In primary hyperparathyroidism, hypercalcemia develops due to extensive autonomous secretion of PTH. Secondary hyperparathyroidism is a well-established complication of chronic renal insufficiency, where marked parathyroid hyperplasia occurs, especially in patients with long dialysis vintage. The elevated PTH level in the circulation is a direct result of renal function disturbances, vitamin D deficiency, and impaired calcium/phosphate metabolism. After successful kidney transplantation, the normalization of kidney function fails to normalize the secretion of PTH by parathyroid glands, which have become relatively autonomous and unresponsive to hypercalcemic conditions in the plasma. The development of tertiary hyperparathyroidism occurs in these conditions. The aim of our report is to present current views on the clinical, pathological and biochemical features of primary, secondary and tertiary hyperparathyroidism. The diagnostics of calcium/phosphate abnormalities in parathyroid gland disorders, as well as some aspects of hyperparathyroidism treatment, are briefly summarized.