Abstract
Fourteen patients with chronic renal failure underwent parathyroidectomy. Postoperatively, seven patients exhibited a rise in hematocrit reading, but seven others did not. Responders had more severe bone disease and lower initial hematocrit values than did nonresponders. Marrow fibrosis was slightly more prominent in responders. Current concepts of marrow erythropoietic inhibition in renal failure suggest a toxic serum factor as the cause. This report fails to support parathyroid hormone as the toxic agent directly responsible for marrow inhibition. Rather, parathyroid hormone may contribute to anemia in renal failure by causing marrow fibrosis, a process sometimes reversible by successful therapy of hyperparathyroidism.
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