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Platelet adhesiveness, ADP-aetivated platelet a.ggregation and the activity of the ADP-splitting enzymes m blood and plasma have been studied in 22 diabetics with severe retinopathy, 22 long-duration diabetics with minimal or no retinopathy and 28 control subjects. The rate of platelet aggregation under the influence of 5, 3, 2 and t txM ADP, the maximum aggregation attained and the rate of disaggregation of these aggregates were measured. The platelets from actively deteriorating retinopaths were found to be more sensitive to the effect of low concentrations of ADP; a significant increase in the extent of aggregation and a decrease in the rate of disaggregation of platelet aggregates formed under the experimental conditions, in vitro were observed. If this should occur in vivo, then capillary occlusion might ensue. This increased sensitivity to ADP and inability to disaggregate, was not due to any differences in the activity of the ADP-splitting enzyme systems in blood. Significant differences in the parameters were not observed when the large diabetic groups were compared with the control subjects. Contrary to some reports, an increase in platelet adhesiveness was not apparent in either diabetic group.

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and the Renal Uniit, Royal Infirmary, Cardiff SYNOPSIS Coagulation and platelet function studies were performed on 24 normal subjects and 29 patients with chronic renal failure due to various causes. Thrombocytopenia was uncommon in the uraemic patients but there was reduced platelet retention in glass bead columns and platelet aggregation with adenosine diphosphate (ADP) and thrombin was slower and less complete than normal. The rate of platelet disaggregation in uraemic patients was significantly reduced. The abnormalities tended to be more severe in more uraemic subjects. In normal subjects no interrelationships were observed between the various measurements of platelet activity. In patients there were significant interrelationships between the measurements of platelet aggregation with ADP and thrombin and between the measurements of aggregation and retention in glass bead columns. It is suggested that if a common pathway is involved in these reactions it is adversely affected in uraemia.Plasma coagulation defects were uncommon and present in only five of the uraemic subjects. Impaired prothrombin consumption apparently due to defective platelet function was present in half the patients but was not detected by a kaolin aotivation method. Although platelet coagulation function was activated during ADP aggregation and disaggregation in normal and uraemic subjects, it did not correlate in the latter with impairment of aggregation. It is suggested that aggregation and activation of platelet coagulant activity are not necessarily related aspects of platelet function. An effect of uraemic plasma on normal platelets was demonstrated by mixing experiments consistent with a humoral cause for the uraemic platelet defects.An abnormal bleeding tendency in patients with renal failure has been recognized for many years and has been attributed to several causes. Increased capillary fragility and thrombocytopenia have been described but recent work suggests that in uraemia the platelets do not function properly. In this condition they have been found to adhere abnormally to glass and to aggregate poorly with adenosine diphosphate (ADP) (Castaldi, Rozenberg, and Stewart, 1966) and thrombin Received for publication 31 May 1972. are due to the production of abnormal platelets or to the direct effect of humoral or other factors.In this paper we describe the results of a study of platelet function in chronic renal failure. The platelets of these patients were retained abnormally in glass bead columns and they aggregated poorly with ADP, and especially with tbrombin. Incubation of normal platelets with uraemic plasma resulted in an altered pattern of aggregation with ADP.