Elevated Levels of Plasma and Urine Beta-Thromboglobulin or Thromboxane-B₂ as Markers of Real Platelet Hyperactivation in Diabetic Nephropathy

Abstract

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.

Combination of Pentoxifylline with Angiotensin Converting Enzyme Inhibitors Produces an Additional Reduction in Microalbuminuria in Hypertensive Type 2 Diabetic Patients

“…The reduction of thromboxane levels has been associated with a decrease in UAE. [5][6][7][8] Diabetic hyperviscosity syndrome causes a reduction in peritubular vascular circulation, which leads to an increase in glomerular filtration pressure. Peritubular hemoconcentration causes glomerular injury by hyperfiltration and hyperviscosity.…”

Narushenie sistemy gemostaza u bol'nykh sakharnym diabetom

“…Тромбоциты больных сахарным диабетом сенсибилизированы к активации адгезии и агрегации [27], что обусловлено снижением чувстви тельности к действию простациклина и оксида азота, вырабатываемых эндотелием. В норме инсулин сенситизирует мембрану тромбоцита к действию выше указанных агентов, при диабете имеет место дефект этого его действия [54]. У больных СД 2 обнаружено повышение коллагензависимой агрегации тромбоци тов, что свидетельствует о том, что больные диабетом нуждаются в более тщательной антиагрегационной терапии, особенно перед проведением различных кардиологических манипуляций [44].…”