Secondary hyperparathyroidism is a well known complication of chronic renal insufficency. It is not only a state of increased parathyroid hormone secre-tion but also a state of parathyroid gland hyperplasia. Prevention and treatment of secondary hyperpara-thyroidism is a huge challenge for the nephrologist, despite new agents for the treatment of hyperphos-phataemia, new vitamin D analogues and calci-mimetics. The importance of parathyroid gland hyperplasia and the possibility of its reduction frequently are neglected issues. Ultrasonography could be very useful in detection of parathyroid gland size and shape and in the management of secondary hyperparathyroidism.

A 24-year-old female patient with parathyroid carcinoma, the rarest endocrine malignancy, had two pregnancies. In the first pregnancy, she had severe nausea and fatigue. Hypercalcemia and hyperparathyroidism were diagnosed in the postpartum period. Hyperemesis gravidarum masked a diagnosis of hypercalcemia. Neck ultrasound and Tc-99m sestamibi found an enlarged lower right parathyroid gland. The gland was surgically removed, and an initial pathology report described atypical adenoma. Shortly afterward, she became pregnant again. During the second pregnancy, her calcium level was frequently controlled but was always in the normal range. Normocalcemia is explained by the specific physiology of pregnancy accompanied by hemodilution, hypoalbuminemia and maternal hypercalciuria (mediated by increased glomerular filtration). During lactation, calcium levels rose, and a new neck ultrasound showed a solitary mass in the area of prior surgery and an enlarged pretracheal lymph node. Fine needle aspiration of the solitary mass and node showed parathyroid carcinoma cells. The tumor mass was resected en bloc with the contiguous tissues and surrounding lymph nodes (pathology report; parathyroid carcinoma with metastases). Over the next five years, four consecutive surgeries were performed to remove malignant parathyroid tissue, lymph nodes and local metastases. Following the surgical procedures, no hypocalcemia was observed. More serious hypercalcemia recurred; the calcium level was difficult to control with a combination of pamidronate, cinacalcet and loop diuretic. No elements of multiple endocrine neoplasia were present.

Secondary hyperparathyroidism (SHPT) is one of the most common complications in patients with chronic kidney disease (CKD). Bone and mineral disorders, increased morbidity and mortality are the consequences of SHPT. Therefore, prevention and control of hyperparathyroidism is one of the main objectives in the management of patients with CKD, particularly in dialysis patients.It is well known that SHPT in CKD is not only a state of increased parathyroid hormone (PTH) synthesis and secretion, but more importantly, it is a state of parathyroid gland (PTG) hyperplasia. The serum concentration of intact PTH is the main method used to assess PTG overactivity. Unfortunately, estimating the size and shape of the PTG in SHPT diagnosis, i.e., parathyroid hyperplasia, is still neglected. Among the various procedures, ultrasonography could be the method of choice to detect PTG size and shape because of its simplicity and noninvasiveness. This method can be sufficiently sensitive to distinguish diffuse and nodular hyperplasia.

Criteria for calcimimetic agent ulonephritis). The other seven patients were clinically diagnosed with chronic renal failure. Twelve urine and branous glomerulonephritis.

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