Lack of Relation between Secondary Hyperparathyroidism and Red Blood Cell Osmotic Fragility in Chronic Renal Failure

Abstract

The possible relationship between red blood cell (RBC) osmotic fragility and secondary hyperparathyroidism (HPT) in chronic renal failure was examined in 23 uremic patients on conservative therapy and in 42 patients on maintenance hemodialysis. Secondary HPT was evaluated by means of serum biochemistry (parathyroid hormone, calcium, phosphorus, and alkaline phosphatase) and radiographic examinations (X-ray films of the hand skeleton). This study showed increased RBC osmotic fragility in uremic patients when compared with controls, with no difference between those on conservative therapy and those on maintenance hemodialysis. No correlation between RBC osmotic fragility and the hematochemical changes associated with secondary HPT was found. No difference in RBC osmotic fragility was observed with regard to the activity (alkaline phosphatase) and the severity (X-ray findings) of secondary HPT. Effective treatment of secondary HPT by either pharmacological means (1,25-dihydroxycholecalciferol) or surgical removal was not associated with consequent improvement in RBC osmotic fragility. It is concluded that secondary HPT is probably not a major factor influencing RBC osmotic fragility in chronic renal failure.

Osmotic Fragility of Erythrocytes and Secondary Hyperparathyroidism in Chronic Renal Failure

“…Again, this observation reflects undue haste in the reading of our papers. On the contrary, as clearly stated in the 'Results' sections [2,3], we found that the fall in the mean serum PTH concentration after treatment did not achieve statis tical significance because of the wide variation in the individual changes in the patients. Yet, according to Massry et al [6], we think that such a treatment was all the same effective in controlling secondary HPT in our pa tients in view of the normalization or near normalization of serum alkaline phosphatase levels in them.…”

“…The patients studied indeed had serum PTH levels by be tween 1.4and 50.7 ng/ml (i.e., 0.56-56.6 times higherthan normal). It is in such patients that we failed to find a significant correlation between RBC osmotic fragility and serum PTH [2,3] [2,3], we found that the fall in the mean serum PTH concentration after treatment did not achieve statis tical significance because of the wide variation in the individual changes in the patients. Yet, according to Massry et al…”

“…Moreover, it should be remarked that in such patients the individual changes in RBC osmotic fragility in response to treat ment with l,25-(OH)2D3 did not correlate with the respec tive changes in serum PTH [2,3] and that no improvement in RBC osmotic fragility was observed in 2 patients after parathyroidectomy in the face of the substantial decrease in serum PTH in both [2].…”

“…

The letter of Massry and Akmal, published in Nephron 43:70 (1986) [1], attacks harshly our previous papers [2,3] on the relation, if any, between red blood cell (RBC) osmotic fragility and secondary hyperparathyroidism (H PT) in chronic renal failure. We would like to have had a reply printed simultaneously; nevertheless, let us make some comments now.

Firstly, Massry and Akmal [1] state that in the study of Bogin et al

[4] amounts of parathyroid hormone (PTH) only Vito 1 times higherthan normal were found to induce the maximum increase in the osmotic fragility of human RBC in vitro.

…”

Red Blood Cell Osmotic Fragility in Chronically Hemodialyzed Patients

“…These authors examined the osmotic fragility of human red blood cells exposed to PTH and found that exposure to intact PTH (1 U/ml) increased calcium influx into these cells. However, this finding is still controversial [7]. Hemolysis in the context of chronic hemodialysis is a multifactorial problem which is further complicated by the multiple mechanisms of RBC injury which can be induced by the dialysis procedure itself [8].…”