Serum C-reactive protein (CRP) levels were measured by nephelometry in 30 healthy subjects (controls) and in 99 patients with uncomplicated terminal uremia on conservative therapy (group 1, n = 30) or chronic hemodialysis (group 2, n = 69). Whereas there was no difference between controls and group 1, both the mean concentration of CRP and the incidence of elevated levels were significantly higher in group 2 in comparison with both controls and group 1. Moreover, the degree of increase in these patients was directly correlated with the duration of hemodialysis. The abnormality, therefore, is somehow related to chronic hemodialysis per se. From a practical standpoint, we concluded that this test cannot be recommended as an acute-phase reactant in this clinical setting.
The possible relationship between red blood cell (RBC) deformability and secondary hyperparathyroidism (HPT) in 23 patients on maintenance hemodialysis was examined. Secondary HPT was evaluated by means of serum biochemistry (parathyroid hormone, calcium, phosphorus, and alkaline phosphatase) and radiographic examinations. This study showed that RBC deformability is markedly reduced in hemodialyzed patients when compared with normal controls. No significant correlation between RBC deformability and the hematochemical changes associated with secondary HPT was found. No difference in RBC deformability was observed as far as the activity (alkaline phosphatase) and the severity (radiographic findings) of secondary HPT are concerned. Effective treatment of secondary HPT by either pharmacological means (1 alpha, 25-dihydroxycholecalciferol therapy) or surgical removal was not associated with consequent improvement in RBC deformability. It is concluded that secondary HPT is probably not a major factor influencing RBC deformability in uremic patients on maintenance hemodialysis.
Red blood cell volume distribution width (RDW) was obtained with the Coulter counter in 60 haemodialysis patients and 55 normal individuals. RDW tended to be higher in the former and the degree of increase was to some extent correlated with the underlying nephropathy. Although RDW failed to correlate with conventional tests of iron status, it was observed that iron administration could produce a decrease toward normal in RDW and a parallel increase in haemoglobin when the initial RDW was increased. In contrast, the response to iron was negligible in the patients with normal RDW basally. It was concluded that high RDW is an acceptable indicator of iron deficiency in haemodialysis patients.
To evaluate the relative contribution that dialyzer membrane composition and geometry make to hemodialysis-associated platelet loss, the effect of a single dialysis with three different types of dialyzers on platelet count was examined on a cross-over basis in 19 uremic patients on maintenance hemodialysis. Also, the plasma levels of antithrombin-iii before and after dialysis were measured, but no significant variations were found regardless of which dialyzer was in use. Our patients suffered significant platelet loss during cuprophan dialysis, but not polyacrylonitrile dialysis. More than 99% of initial circulating platelets were recovered at the end of polyacrylonitrile dialysis, whereas cuprophan dialysis did leave a significantly lower percentage of circulating platelets (p less than 0.05). The internal comparison of results obtained with the two cuprophan dialyzers used shows no difference as to the dialyzer geometry (flat plate or hollow fiber). This indicates that the membrane composition is the major factor influencing hemodialysis-associated platelet loss. We suggest that patients with low platelet count and/or with risk of bleeding may benefit from polyacrylonitrile dialysis.
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.
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