Erythrocyte survival in chronic renal failure. Role of secondary hyperparathyroidism.
Erythrocyte survival in chronic renal failure. Role of secondary hyperparathyroidism.
复制标题
慢性肾功能衰竭中的红细胞存活。
DOI:
10.1172/jci112157
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发表时间:
1985
期刊:
影响因子:
--
通讯作者:
Massry,SG
中科院分区:
文献类型:
--
作者:
Akmal,M;Telfer,N;Ansari,AN;Massry,SG
The human erythrocyte (RBC) is a target organ for parathyroid hormone (PTH) and the hormone increases RBC osmotic fragility and induces their hemolysis. The present study was undertaken to examine whether elevated blood levels of PTH affect RBC survival, and therefore whether PTH, being an extracorpuscular factor, is responsible for the shortened RBC survival in chronic renal failure. 51Cr-labeled RBC survival was elevated in six normal dogs, in six animals with chronic renal failure and secondary hyperparathyroidism (NPX), and in six thyroparathyroidectomized dogs (NPX-TPTX) with comparable degree and duration of chronic renal failure. In the normal dogs, 51Cr-labeled RBC survival ranged between 22 and 35 (25.6 +/- 1.9) d. In the NPX dogs, 51Cr-labeled RBC survival was shortened and the values ranged between 16 and 20 (18.4 +/- 0.6) d, a value significantly (P less than 0.01) lower than normal dogs. In NPX-TPTX dogs, 51Cr-labeled RBC survival ranged between 20 and 33 (25.2 +/- 1.8) d, a value not different from that in normal dogs but significantly higher (P less than 0.01) than that in NPX animals. Our data demonstrate that excess blood levels of PTH and not other consequences of the uremic state are responsible for the shortened RBC survival in chronic renal failure.
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影响因子:
3.3
作者:
J. Eaton;M. N. Leida
通讯作者:
M. N. Leida
影响因子:
1.1
作者:
J. Hefti;A. Blumberg;H. Marti
通讯作者:
H. Marti
影响因子:
--
作者:
S. Massry
通讯作者:
S. Massry
DOI:
10.1001/archinte.1958.00260140158024
发表时间:
1958
期刊:
A.M.A. archives of internal medicine
影响因子:
--
作者:
J. Desforges;J. P. Dawson
通讯作者:
J. P. Dawson
DOI:
--
发表时间:
1972
期刊:
Transactions - American Society for Artificial Internal Organs
影响因子:
--
作者:
S. Massry;J. Coburn;M. Peacock;C. Kleeman
通讯作者:
C. Kleeman