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 of fibronectin, endothelin -1,2, 6-keto-PGF(1a)(,) thromboxane B-2(TxB(2)) 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, TxB(2) and beta-thromboglobulin in blood plasm, aggregation with ADP in CGN pregnant women were higher than in healthy pregnant women and nonpregnaant CGN patients. Plasmic 6-keto-PGF(1a) was low. Preeclampsia was accompanied with elevated fibronectin, TxB(2) 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-thrombocytic 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.

Aim. To evaluate platelet dysfunctions and pregnancy outcomes in females with gestational exacerbation of chronic glomerulonephritis (CGN) and the disease remission. Materials and methods, Platelet metabolism was studied by activity of intraplatelet LDG, platelet secretory activity by plasm beta-TG and ADP-aggregation in 75 gravidae. Of them 16 had exacerbation of CGN, 40 females were in remission of CGN and 19 healthy pregnant women sewed control Results. Enhanced LDG activity and intensity of maximal ADP aggregation, high beta-TG levels compared to control were recorded in gravidae with CGN both in exacerbation and remission. The frequency of preterm deliveries, intrauterine growth retardation, neonatal hypotrophy was greater in women with gestational exacerbation of nephritis compared to pregnant women with stable nephritis. Conclusion. Metabolic and functional platelet hyperactivity with platelet intravascular activation in pregnancy in aggravated CGN suggest contribution of platelets to onset of the disease gestational exacerbation. Pregnancy-induced overactivation of platelets in CGN exacerbation stimulates intravascular coagulation in placental circulation with resultant microthrombi in placental vessels responsible for high rare of unfavorable pregnancy outcomes in relevant patients.

Cryoglobulins were measured spectrophotometrically in the sera of 40 patients with renal diseases. 18 of them had chronic glomerulonephritis, 14 lupus nephritis and 8 nephritis. 20 patients with high concentration of cryoglobulins (100-600 mu g/ml) exhibited high incidence of nephrotic syndrome (80%), arterial hypertension (90%), creatininemia (70%) and, respectively, 25, 25 and 15% of patients free of cryoglobulinemia. There was a correlation between cryoglobulins level and creatininemia (r = 0.468), proteinuria (r = 0.478), ESR (r = 0,393), systolic and dyastolic arterial pressure (r = 0.393 and r = 342, respectively). An inverse relation existed with serum albumins (r = -0.526). Progression of renal failure was associated with high cryoglobulinemia. In decline of cryoglobulins content there was clinical improvement, lowering or normalization of blood creatinin levels.

To assess platelet changes in pregnant women with chronic glomerulonephritis (CGN) and essential hypertension (EH) we estimated platelet lactic dehydrogenase activity (LDH), beta-thromboglobulin and thromboxane B-2 (TxB(2)) plasma levels and ADP-stimulated platelet aggregability. Five groups of gravidae (26-40 weeks of gestation) were studied: with EH (n=20), with CGN and hypertension (n=31), with CGN without hypertension (n=29), with late toxemia (n=11), nonpregnant CGN women (n=10) and healthy pregnant women (n=20). Activation of platelet function was found in gravidae with CGN and EH. Platelet disorders were especially pronounced in pregnant women with CGN and with EH, but they were less pronounced than in control group with late toxemia. We believe that hypertension is more important stimulating factor for platelet activation than renal disease. We suggest that platelet disorders in outpatients are brought about by endothelium damage caused by elevated blood pressure.

Pregnancy complications have been analyzed in 124 females suffering from essential hypertension (EH) and chronic glomerulonephritis (CGN). Such complications, as late gestosis (8.9%), ablation placentae (1.6%), premature delivery (14.5%), intrauterine growth retardation (14.5%) occurred more frequently than in population. Pre- and perinatal deaths were encountered with the same frequency as in the population. Morphologically, the placentas had in many cases histological evidence of moderate placental insufficiency (PI). In more than 60% of the patients there were uteroplacental and fetoplacental hemodynamic defects. Placental circulatory disorders and PI ran subclinically in most of the cases as they were compensated. In EH and CGN pregnant women, compared to healthy controls, red cells acquired abnormal forms more frequently, serum thromboxane B2 levels got elevated, lactate hydrogenase activity became enhanced. Erythrocytic damage and platelet activation in EH and CGN pregnant women may indirectly confirm the existence of systemic angiopathy. It is suggested that ischemic placenta may produce endothelial toxin, that systemic endothelial damage in EH, CGN, PI may be synergetic which potentiates its clinical appearance in the form of the above pregnancy complications.

To determine feasibility of using quantitative histochemical assessment of platelet anaerobic metabolism in lupus nephritis (LN) prognostication and elucidation of its activity, the authors examined 23 SLE patients. 20 of them developed renal lesions. Anaerobic metabolism of platelets was measured according to lactate dehydrogenase levels. All the SLE patients had significantly higher levels of the enzyme than healthy controls showed. Maximal LDG activity was registered in rapidly progressive LN with thrombocytopenia. The findings support activation of platelet hemostatic component in SLE patients and valid utilization of a new quantitative histochemical technique for determination of intracellular metabolism enzymes content.

As many as 47 patients with amyloidosis and 31 with chronic glomerulonephritis (CGN) were examined for the blood serum content of R proteins, chemotaxic activity of blood leukocytes and the degree of the inhibitory influence of the autologous serum on chemotaxis. Amyloidosis and CGN were marked by an increase of the level of receptor proteins. A reverse correlation was established between the rise of the content of R-proteins and the chemotaxic properties of leukocytes. In CGN, the rate of demonstration of the high titers of R-proteins and the magnitude of the chemotaxis decline depended on the disease phase (the degree of activity) whereas in amyloidosis, these reactions differed insignificantly in patients with various clinical patterns and stages of renal amyloidosis.