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Galloway memorial lecture. Platelet injury and antithrombin III in clinical nephrology
Plasma Antithrombin III (AT III) has been shown to be elevated in certain conditions like diabetes mellitus and coronary artery disease as well as in situations where there is increased platelet turnover. This study attempts to define the role of platelet injury in Clinical Nephrology and assesses the clinical value of ATT III. In IgA Nephritis, plasma AT III levels (105 +/- 10%) in 97 patients were higher than those of normal controls (96 +/- 5%) (p less than 0.0005). AT III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.01), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised AT III had more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA on IMG (p less than 0.02) when compared to patients with normal AT III levels. The data suggest that plasma AT III may serve as a marker of disease activity in IgA nephritis. Plasma AT III levels in hemodialysis patients, low prior to dialysis, improved after dialysis (p less than 0.01). Pre and post hemodialysis platelet counts however did not change significantly. In peritoneal dialysis patients, AT III levels which were normal before dialysis, increased significantly after peritoneal dialysis (p less than 0.01). The platelet counts before and after peritoneal dialysis also improved (p less than 0.005). No correlation was found between AT III levels and platelet counts. Although platelet damage has a contributory role in increasing AT III levels during hemodialysis, the data on peritoneal dialysis suggest that there may be other factors affecting platelets and AT III during dialysis.
Plasma Antithrombin III (AT III) has been shown to be elevated in certain conditions like diabetes mellitus and coronary artery disease as well as in situations where there is increased platelet turnover. This study attempts to define the role of platelet injury in Clinical Nephrology and assesses the clinical value of ATT III. In IgA Nephritis, plasma AT III levels (105 +/- 10%) in 97 patients were higher than those of normal controls (96 +/- 5%) (p less than 0.0005). AT III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.01), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised AT III had more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA on IMG (p less than 0.02) when compared to patients with normal AT III levels. The data suggest that plasma AT III may serve as a marker of disease activity in IgA nephritis. Plasma AT III levels in hemodialysis patients, low prior to dialysis, improved after dialysis (p less than 0.01). Pre and post hemodialysis platelet counts however did not change significantly. In peritoneal dialysis patients, AT III levels which were normal before dialysis, increased significantly after peritoneal dialysis (p less than 0.01). The platelet counts before and after peritoneal dialysis also improved (p less than 0.005). No correlation was found between AT III levels and platelet counts. Although platelet damage has a contributory role in increasing AT III levels during hemodialysis, the data on peritoneal dialysis suggest that there may be other factors affecting platelets and AT III during dialysis.