Three cases of renal hyperparathyroidism detected by ultrasound.
CASE A:
A woman with hypercalcinosis, renal stones and increasing PTH value but 2 times ultrasound misdiagnosed.
A parathyroid tumor at the upper pole of the left lobe of thyroid later reviewed by ultrasound.
CASE B:
A 36 year-old man with renal insufficiency on stage 5, PTH high value. Ultrasound detected secondary parathyroid tumors both 2 sides.
CASE C:
A 46 year-old man with RI and PTH high value due to renal hyperparathyroidism. Ultrasound detected 2 side parathyroid tumors.
Sizes, numbers and structures of renal hyperparathyroidism seem to be not influenced by the blood phosphat and PTH value.
REFERENCE:
Pathogenesis of secondary hyperparathyroidism in CKD. Progressive loss of renal mass impairs renal phosphate excretion, which causes an increase in serum phosphorus. Abnormalities in serum phosphorus homeostasis stimulate FGF23 from bone. Higher serum FGF23 levels in addition to decreased renal mass cause a quantitative decrease in synthesis of 1,25(OH) 2 D. High serum FGF23 levels decrease the activity of the 1a-hydroxylase enzyme. 1,25 (OH) 2 D deficiency decreases intestinal absorption of calcium, leading to hypocalcemia, which is augmented by the direct effect of hyperphosphatemia. Hypocalcemia and hyperphosphatemia stimulate PTH release and synthesis. The lack of 1,25(OH) 2 D, which would ordinarily feed back to inhibit the transcription of prepro-PTH and exert an antiproliferative effect on parathyroid cells, allows the increased PTH production to continue. Current therapeutic methods used to decrease PTH release in CKD include correction of hyperphosphatemia, maintenance of normal serum calcium levels, administration of 1,25(OH) 2 D analogs orally or intravenously, and administration of a CaSR agonist (e.g., cinacalcet).
