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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Lack of evidence for the role of secondary hyperparathyroidism in the pathogenesis of uremic thrombocytopathy.

The possible relationship between platelet dysfunction and secondary hyperparathyroidism ( HPT) in chronic renal failure was examined in 23 uremic patients on conservative therapy (group I) and in 27 patients on maintenance hemodialysis (group II). Platelet function was assessed by measuring the degree of aggregation in response to various concentrations of adenosine diphosphate. 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 impaired platelet aggregation in group I patients, compared to either group II patients or controls. There were no significant differences when group II patients were compared to controls. No significant correlations between platelet aggregation and the hematochemical changes associated with secondary HPT were found. No differences in platelet aggregation were found with regard to the activity (alkaline phosphatase) and the severity (x-ray findings) of secondary HPT. Effective treatment of secondary HPT with 1,25-dihydroxycholecalciferol in both group I and group II patients was not associated with consequent changes in platelet aggregation. It is concluded that secondary HPT is probably not a major factor in the pathogenesis of platelet dysfunction in chronic renal failure.[1]


  1. Lack of evidence for the role of secondary hyperparathyroidism in the pathogenesis of uremic thrombocytopathy. Docci, D., Turci, F., Delvecchio, C., Gollini, C., Baldrati, L., Pistocchi, E. Nephron (1986) [Pubmed]
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