Endothelium and platelets in pregnant women with chronicglomerulonephritis and therapeutic efficacy of acetylsalicylicacid and dipiridamol


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Aim. To estimate platelet and endothelial condition in pregnant women with chronic glomerulonephritis (CGN),
prognostic value of these changes and efficacy of acetylsalicylic acid (ASA) and dipiridamol
in prevention of unfavourable outcomes of pregnancy in CGN.
Material and methods. The examination covered 74 CGN pregnant patients, 14 non-pregnant CGN
patients, 11 pregnant women with preeclampsia, 19 healthy pregnant women. The levels offlbronectin,
endothelin -1,2, 6-keto-PGFla, thromboxane B/TxB^ secretory beta-thromboglobulin in the blood,
activity of intrathrombocytic lactatedehydrogenase (LHG), platelet aggregation. ASA (125 mg/day)
was given to 33 CGN pregnant women in combination with dipiridamol (150-225 mg/day). Control
group consisted of 32 CGN pregnant women.
Results. Content of fibronectin, endothelin, TxB2 and beta-thromboglobulin in blood plasm, aggregation
with ADP in CGN pregnant women were higher than in healthy pregnant women and nonpregnant
CGN patients. Plasmic 6-keto-PGFla was low. Preeclampsia was accompanied with elevated fibronectin,
TxB2 and beta-thromboglobulin, hyperactive LDH. Platelet aggregation was suppressed.
Blood beta-thromboglobulin directly correlated with systolic and diastolic arterial pressure, 24-h proteinuria
and blood creatinine. Reverse Correlation was seen in blood beta-thromboglobulin with albuminemia,
glomerular filtration rate, body mass of the newborn and term of labor. A direct correlation
was found between the activity of intrathrombocytic LDH and systolic and diastolic arterial pressure,
a weak reverse correlation - between platelet count in capillary blood and systolic pressure, platelet
aggregation with ADP and terms of labor. Of the highest prognostic value were the level of beta-thromboglobulin
and fibronectin, the activity of intrathrombocytic LDH and platelet aggregation in response
to ADP. ASA and dipiridamol reduced the risk of fetal retardation and fetal loss.
Conclusion. Pregnant women with CGN have endothelial-thronbocytic dysfunction because of unidirectional
influence of both CGN and pregnancy. We think that endothelial-platelet dysfunction connects
renal impairment and placental failure in pregnant women with CGN deteriorating a gestational
CGN and pregnancy complications. Correction of endothelial-platelet state with ASA and dipiridamol
is effective in prevention of fetal retardation and fetal loss in pregnant women with CGN.

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