Suppression of Secondary Hyperparathyroidism by Propranolol in Renal Failure Patients
- 1 January 1981
- journal article
- research article
- Published by S. Karger AG in Nephron
- Vol. 27 (3), 127-133
- https://doi.org/10.1159/000182038
Abstract
Renal osteodystrophy, in part due to secondary hyperparathyroidism, is one of the major unresolved problems affecting patients on chronic hemodialysis. In addition, evidence has shown that parathyroid hormone (PTH) is toxic to other organ systems besides bone. The results of a prospective study on the effect of propranolol in reducing PTH levels in chronic renal failure patients on hemodialysis are reported. Propranolol administration reduced PTH levels by over 50–75%. The levels of calcium, phosphorus, alkaline phosphatase and hematocrit were variable, but patients with severe derangements in these measurements also seemed to benefit from propranolol. It should now be determined by larger and longer studies whether these biochemical improvements can be translated into clinical benefits.Keywords
This publication has 12 references indexed in Scilit:
- Neurodiagnostic Abnormalities in Patients with Acute Renal FailureJournal of Clinical Investigation, 1978
- 1,25 Dihydroxycholecalciferol Effects in Chronic DialysisAnnals of Internal Medicine, 1978
- Search for the Uremic ToxinNew England Journal of Medicine, 1978
- Parathyroid Hormone Responses to Catecholamines and to Changes of Extracellular Calcium in CowsJournal of Clinical Investigation, 1978
- Comparative Effect of Calcium and of the Adrenergic System on Calcitonin Secretion in Man*Journal of Clinical Endocrinology & Metabolism, 1978
- Propranolol Effects in Long-Term Hemodialysis Patients with Renin-Dependent HypertensionAnnals of Internal Medicine, 1978
- Iron Balance in Hemodialysis PatientsAnnals of Internal Medicine, 1977
- The Renal Handling of Parathyroid HormoneJournal of Clinical Investigation, 1977
- Is Parathyroid Hormone a Uremic Toxin?Nephron, 1977
- Study of the effect of uremic metabolites on erythrocyte glycolysisMetabolism, 1964