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The Role of Parathyroid Hormone as a Uremic Toxin: Current Concepts

Uremia affects nearly all organ systems. Although effective methods of treating uremia have become available during the past four decades, our understanding of the pathophysiology of this disorder is still limited. The classical conception of uremia (“urine in the blood”) is that of an intoxication of the body by substances normally removed by the kidneys. Despite the fact that there is no absolute relationship between the blood level of these “toxins” and the findings of uremia (1, 2), elevated blood levels of many substances are invariably found in uremic patients. Dialysis was devised as a means of removing these toxic substances from the blood. In formulating his “trade-off hypothesis” of the pathogenesis of uremia, Bricker (3) extended the idea of uremic toxins to include endogenous humoral substances such as parathyroid hormone (PTH), the blood levels of which increase to pathological concentrations due to the metabolic derangements of renal failure. In the case of PTH, its adverse effects can be compared to those in patients with primary hyperparathyroidism. In considering PTH as a uremic toxin, there are a number of caveats. In the first place, uremia is a complex syndrome, and it is usually simplistic to attribute any one uremic manifestation to a single metabolic abnormality. Some substances may exhibit synergistic toxicity (4). Second, the mere correlation of the blood level of a proposed toxin with a uremic finding does not by itself prove causality. In reviewing the possible role of PTH in uremia, Klahr and Slatopolsky ( 5 ) pointed out that it is difficult to attribute the dysfunction of an organ to PTH if the organ has no known receptors for the hormone. Third, many uremic symptoms improve with dialysis, which does not remove PTH from the plasma. Fourth, there may be a discrepancy between the acute effect and the chronic effect of a purported toxin (see below). Finally, it is now clear that uremia must be considered a deficiency state, as well as an