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Biomedical subjects

N L Kozlovskaia

Publications and source records attributed to N L Kozlovskaia.

At least 19 recordsLinked to original sources
PubMed2006

[Clinical significance of myocardial lesion in antiphospholipid syndrome].

Antiphospholipin syndrome (APLS) is one of the most frequent reasons for arterial and venous thromboses. Primary and secondary APLS can lead to thrombotic process in coronary arteries. The biggest diagnostic difficulties appear in cases of small coronary vasal involvement leading to diffuse myocardial lesion. Perfusion myocardial scintigraphy (MS) allows specification of the character of myocardial changes. Revealing of myocardial changes by means of MS makes it possible to start timely anticoagulative therapy, which significantly improves prognosis and life quality.

Adult↗
PubMed2006

[Clinical and morphological characteristics of lupus nephritis in systemic lupus erythematosus with antiphospholipid syndrome].

AIM: To ascertain clinical and morphological features of lupus nephritis (LN) in systemic lupus erythematosus (SLE) associated with antiphospholipid syndrome (APS). MATERIAL AND METHODS: Immunological markers of SLE and APS, clinical picture, urine indices were examined in 138 patients with SLE, APS and renal dysfunction. RESULTS: LN associated with APS is characterized with marked arterial hypertension, such patients had arterial thromboses more frequently than patients with isolated LN. Patients with anticardiolipin antibodies have arteriolosclerosis, in APS - diffuse interstitial sclerosis. CONCLUSION: Renal impairment in SLE may run not only with LN but also with thrombotic microangiopathy modifying clinical symptoms and course of the disease.

Adolescent↗
PubMed2004

[Chronic glomerulonephritis and pregnancy].

AIM: To clarify factors of risk for unfavourable variants of gestational chronic glomerulonephritis (CGN) and poor pregnancy outcomes in CGN; to determine prognostic implications of changes in some renal and uteroplacental indices. MATERIAL AND METHODS: Variants of CGN gestational course and pregnancy outcomes have been analysed for 156 CGN patients. The women were examined before pregnancy, in the course of pregnancy and 3-24 months after the delivery. Measurements were made of 24 h proteinuria, glomerular filtration rate, blood transaminases activity, functional renal reserve (FRR), uricemia, blood level of alpha-phetoprotein. Placentas were studied morphologically, uterine and umbilical artery circulation was assessed by dopplerometry. RESULTS: The following abnormalities were registered: high proteinuria (34.6%), progression of hypertension (29.5%), renal function deterioration (15.4%), fetal and neonatal losses (15.4%), fetal underdevelopment (25%), preterm delivery (17.3%), preeclampsia (7.7%), preterm placental detachment (1.9%). There is morphological, dopplerometric and biochemical evidence for placental insufficiency in CGN pregnant women. CONCLUSION: Activity of CGN (nephritic or acute nephritic syndromes), hypertension, renal failure, disorders of renal hemodynamics are factors of risk for unfavourable gestational course of CGN and pregnancy complications. Placental insufficiency deteriorates pregnancy outcomes in CGN, but changes in uterine and umbilical circulation as well as blood levels of alpha-fetoprotein are not prognostically significant.

Adolescent↗
PubMed2004

[Low-molecular heparins in the treatment of APS-nephropathy in primary and secondary antiphospholipid syndrome].

AIM: To evaluate efficacy of low-molecular heparin enoxaparin in the treatment of nephropathy in patients with primary and secondary antiphospholipid syndrome (APS). MATERIAL AND METHODS: A total of 11 APS-nephropathy patients participated in the study. Of them 8 patients had primary APS and 3 patients had secondary APS. Biopsy of the kidney was made in 5 patients, ultrasonic dopplerography of renal vessels was performed in all 11 patients. Enoxaparin was given as monotherapy to primary APS and combined treatment to secondary APS patients. RESULTS: Enoxaparin decreased proteinuria, arterial pressure, glomerular filtration rate in all the patients. It also promoted normalization of creatinin. Before the anticoagulant treatment a reduction of maximal systolic and diastolic velocities of blood flow have been registered in segmental and interlobar arteries in all APS nephropathy patients compared to healthy subjects. The depletion of renal cortex blood flow beginning with the level of arcuate arteries was also observed in all the patients. Enoxaparin enhanced blood flow in segmental and interlobar arteries. The recovery of blood flow in the arcuate arteries was registered in 6 of 9 patients. CONCLUSION: Low molecular heparin may be used in the treatment of nephropathy in patients with primary and secondary APS.

Adult↗
PubMed2004

[Endothelium and platelets in pregnant women with chronic glomerulonephritis and therapeutic efficacy of acetylsalicylic acid and dipiridamol].

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-PGF1a, thromboxane B2 (TxB2) secretory beta-thromboglobulin in the blood, activity of intrathrombocytic lactate dehydrogenase (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-PGF1a 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-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.

Administration, Oral↗
PubMed2003

[Clinical manifestations of APS-nephropathy in primary antiphospholipid syndrome].

AIM: To elicit clinical features of nephropathy associated with antiphospholipid syndrome (APSN) in patients with primary antiphospholipid syndrome (PAPS). MATERIAL AND METHODS: The analysis of clinical characteristics and course of APSN has covered 24 patients with PAPS (16 females and 8 males, mean age 34.3 years). Renal damage was represented by arterial hypertension (AH), urinary syndrome, functional decline. All the patients were tested for anticardiolipin antibodies and/or lupus anticoagulant. Renal biopsy was made in 7 patients. RESULTS: PAPS patients developed renal affection in the onset of APS or within the first 5 years of its course. In the majority of patients APSN combined with abnormalities of CNS, heart and skin. Arterial/arteriolar thromboses prevailed. APSN manifested with: AH (n = 23, severe AH in 11), abnormal renal filtration (n = 17, creatinine rise in 8), urinary syndrome with proteinuria (n = 23, in 14 with hematuria). The following clinical variants of APSN were proposed: urinary syndrome with AH (n = 16; 67%), acute nephritic syndrome (n = 7; 29%), nephrotic syndrome (n = 1). Morphological studies of biopsies from APSN patients have revealed sclerotic changes, thrombotic microangiopathy, nonspecific alterations in the glomeruli. CONCLUSION: APSN is a variant of microvascular renal affection caused by thrombotic processes in intra-organ microcirculation. It is an early clinical marker of APS. Clinically, APSN manifests with vascular renal affection, the earliest symptom being inhibition of glomerular filtration. Clinical combinations of the symptoms allow to distinguish variant of APSN suggesting the existence of acute and chronic APSN. Combination of APSN with affection of the CNS, heart and skin points to a special PAPS subtype characterized by generalized ischemic damage to the organs as a result of intraorganic arterial and/or arteriolar thromboses.

Adult↗
PubMed2001

[Kidney damage in primary antiphospholipid syndrome].

AIM: To characterize clinical manifestations, course and laboratory signs of nephropathy in primary antiphospholipid syndrome (PAS). MATERIAL AND METHODS: 6 patients with PAS and renal affection were observed for 10 years since 1991. They were examined for anticardiolipin antibodies and/or lupus anticoagulant. Renal tissue was studied morphologically in one patient. RESULTS: In all the patients renal damage manifested with arterial hypertension associated with isolated proteinuria. The majority of the patients had renal dysfunction. All of them had elevated level of antibodies to cardiolipin primarily in combination with lupus anticoagulant. Histological changes of renal tissue presented with thrombotic microangiopathy of glomerular and extraglomerular vessels, intimal proliferation and vascular wall thickening with occlusion of their lumen which combined with morphological indicators of focal segmental glomerulosclerosis. CONCLUSION: The thrombotic process in the intrarenal vessels in PAS dictates the necessity to develop novel approaches to treatment of such patients. In addition to immunodepressants the treatment should include indirect anticoagulants and antiaggregants.

Adult↗
PubMed2001

[Experience in the use of valsartan with the aim to inhibit progression of kidney failure in patients with chronic glomerulonephritis].

AIM: To assess the effect of valsartan, angiotensin-II receptor blocker type 1, on key factors of progression of chronic renal failure (CRF)--arterial hypertension (AH), proteinuria (PU), sodium excretion (SE)--in patients with chronic glomerulonephritis (CGN) and initial affection of renal function. MATERIAL AND METHODS: 11 patients (mean age 33.7 +/- 13.3 years, mean duration of nephritis 8.6 +/- 6.4 years, male to female ratio 8:3) with AH (AP > 140/90 mm Hg) and marked PU (> 1 g/day) who had not received immunosuppressive drugs for at least 6 months before the trial were given valsartan. It was administered after the period of "washing out" at the initial dose 80 mg/day with further addition of diuretics or raising the dose twice (in hyperuricemia) to decrease AP under 140/90 mm Hg. The duration of the treatment was 3 months. RESULTS: After 3 months of valsartan therapy systolic arterial pressure fell from 162 +/- 18 to 138 +/- 20 mm Hg (p < 0.05), diastolic pressure from 100 +/- 8 to 92 +/- 15 mm Hg (single measurements). 24-h monitoring of AP showed a significant lowering of mean 24-h and night systolic and diastolic AP, day-time diastolic AP, 24-h time index of systolic and diastolic AP. Initial antiproteinuric effect was observed after 1 month of the treatment and after 3 months of therapy PU reduced significantly (from 5.7 +/- 6.0 g/day to 3.3 +/- 3.3 g/day). After 3 months sodium excretion significantly rose, while creatinine level and glomerular filtration rate did not. Potassium rose in one patient. CONCLUSION: In CGN with initial CRF valsartan in a dose 80-160 mg/day produces a pronounced antihypertensive and antiproteinuric actions, stimulates sodium excretion. No serious side effects were noted. It is necessary to continue studies on the ability of valsartan to inhibit progression of CRF.

Adult↗
PubMed1999

[Platelet dysfunction and pregnancy in gestational exacerbation of chronic glomerulonephritis].

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 served 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 rate of unfavorable pregnancy outcomes in relevant patients.

Blood Platelets↗
PubMed1997

[Kidney involvement in hereditary osteo-onychodysplasia].

Review of the literature and case report concern renal damage in hereditary osteo-onychodysplasia (nail-patella syndrome). This syndrome is a rare genetic disease inherited by the autosome-dominant type. It arises because of underdevelopment of tissues of mesodermal and ectodermal origin and is characterized by hypoplasia or absence of patella, ulnar dysplasia, nail plate dystrophy, growths on the iliac bones, renal affection. The disease was detected in early childhood. Renal affection presented with urinary syndrome with a concurrent nephrotic syndrome later on followed by moderate arterial hypertension and progression to renal failure. Renal biopsy revealed the picture of focal segmentary glomerular hyalinosis typical for this disorder. Because immunodepressants were thought inadequate, the treatment included lovastatin and inhibitors of angiotensin-converting enzyme to inhibit non-immune mechanisms of the disease progression.

Adult↗