1995 Fiscal Year Final Research Report Summary
PTHmRNA and vitamin D_3 receptor RNA in primary hyperparathyroidism.
Project/Area Number |
06671573
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Urology
|
Research Institution | KYORIN UNIVERSITY |
Principal Investigator |
NUTAHARA Kikuo Kyorin Univ., School of Med., Dept.of Urology, Associate Professor, 医学部, 助教授 (00143470)
|
Co-Investigator(Kenkyū-buntansha) |
HIGASHIHARA Eiji Kyorin Univ., School of Med., Dept.of Urology, Professor, 医学部, 教授 (00092312)
|
Project Period (FY) |
1994 – 1995
|
Keywords | PRIMARY HIPERPARATHYROIDISM. / ACID-BASE BALANCE. / BONE MINERAL DENSITY. / PTHmRNA. / VITAMIN D_3 RECEPTOR RNA |
Research Abstract |
1. Renal bicarbonate metabolism in patients with primary hyperparathyroidism This study evaluated the acid-base balance and renal handling of bicarbonate in ten patients with primary hyperparathyroidism before and after parathyroidectomy. Renal tubular threshold of bicarbonate increased and fractional urinary bicarbonate excretion of the filtered load decreased after parathyroidectomy. However, no disturbances or changes in acid-base balance were observed before and after surgery. 2. Bone mineral density in patients with primary hyperparathyroidism This study evaluated the bone mineral density in 15 patients with primary hyperparathyroidism before and after parathyroidectomy. Bone mineral density decreased in the patient, with primary hyperparathyroidism of chemical and renal stone types. After surgery, bone mineral density of the skull and lumbar spine increased immediately. However, no changes in bone mineral density of the lower limbs were observed before and after surgery. 3. PTHmRNA and vitamin D_3 receptor RNA in primary hyperparathyroidism Total RNA of the parathyroid gland could be measured in five patients with primary hyperparathyroidism (parathyroid adenomas). However, the measurement of the PTHmRNA and vitamin D_3 receptor RNA in parathyroid adenomas using Northern bolt methods were failed. We conclude that primary hyperparathyroidism does not induce an acid-base disturbance, although the renal tubular threshold of bicarbonate is suppressed and fractional urinary bicarbonate excretion of filtered load is increased by excessiv endogenous PTH.Normal acid-base balance in primary hyperparathyroidism might be due to enhancement of extrarenal acid buffering capacyty (probably, bone).
|