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The most significant complication of elevated parathyroid hormone (PTH) levels in uremia is the development of osteitis fibrosa cystica. The hormone also appears to play a role in soft-tissue and organ calcification, metabolic abnormalities (glucose, lipids), and electroencephalographic changes seen in uremic patients. Its role in the hematological abnormalities of uremia (anemia, bleeding) is controversial. A role for PTH in heart and skeletal muscle dysfunction in uremia has not been clearly established. Further studies are required to establish PTH as a "universal" toxin in uremia. INTRODUCTION The pathogenesis of the uremic syndrome has been variously attributed to (a) retention of nitrogenous waste products, (b) excessive accumulation of several peptide hormones, including parathyroid hormone (PTH), and (c) deficiencies of essential compounds that may not be produced in adequate amounts in uremia. Numerous attempts to identify substances that accumulate in renal failure and ultimately reach levels that are toxic to vital functions have yielded disappointing results. In recent years a role for PTH as a "uremic toxin" has been proposed (1-4). This manuscript reviews the evidence of PTH as a uremic toxin. Parathyroid hormone is an 84-amino-acid peptide secreted by the parathyroid glands in response to changes in ionized serum
Annual Review of Medicine – Annual Reviews
Published: Feb 1, 1986
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