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Serum creatinine, immunoreactive serum and urine β₂-microglobulin, plasma and urine thromboglobulin, plasma thromboxane-B₂ levels and daily protein excretion were determined in 61 insulin-treated diabetic patients, comparing the different patient groups (complication free, nephropathy without and with azotaemia) with control subjects. In the groups of diabetic patients, plasma and urine β-thromboglobulin (BTG) and plasma thromboxane-B₂ levels were higher than in the controls. There was a significant positive correlation between urine BTG and β₂-microglobulin in the group without complication, and between the plasma BTG and β₂-microglobulin, and plasma BTG and thromboxane levels in the diabetic group with azotaemia. In contrast to some previous assumptions, the increased level of plasma BTG reflects a real platelet hyperactivation in patients with diabetic nephropathy. At the same time, urine BTG also increases. Determination of urine BTG is more simple with less possibility of methodological error.

In vitro platelet aggregometry was performed in 201 patients with diabetes mellitus, and in 106 controls. The complication-free and retinopathic patients showed hyperaggregability to collagen and arachidonic acid, and also to epinephrine and adenosine diphosphate when neuropathy occurred. Patients with nephropathy, both with and without azotemia, had diminished in vitro platelet responses to each of the four stimuli as compared to age- and sex-matched controls. These characteristics were independent of the type of diabetes. It is concluded that diabetic nephropathy is characterized by reduced platelet in vitro reactivity. Further research is necessary to explain in vitro hypoaggregability in contrast to the numerous proofs of in vivo hyperfunction of platelets in diabetes.

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