[Potentialities of non-invasive diagnosis of liver cirrhosis in children with the use of serological markers].

The study included 95 children with chronic hepatic disorders of different etiology. All of them underwent hepatic puncture biopsy for morphological studies and calculation of histological sclerosis index based on the Knoddel scale. Commercial enzyme immunoassay kits were used to measure hyaluronic acid (HA), type IV collagen (CIV), matrix metalloproteinase-1 (MMP-2), transforming growth factor-beta 1 (TGF), and leptin levels as non-invasive markers of fibrosis. It was shown that concentrations of TGF and MMP-2 at early stages of hepatic fibrosis, HA and CIV at its later stages are of diagnostic value.

[Biologically active compounds in the mechanism of formation of reflux-nephropathy in children].

A concept is proposed laying emphasis on the involvement of cytokines, growth factors, prostaglandins, and nitrogen oxides in the mechanism of formation of reflux-nephropathy in children. It is shown that enhanced production of mediators of inflammation and humoral growth factors in patients with vesico-ureter reflux depends on the degree of infiltrative and sclerotic changes in the kidneys. The accompanying dysbalance of pro- and anti-inflammatory cytokines due to increased endogeneous production of TNF-alpha and concomitant decrease of daily BL-10 excretion constitutes an unfavourable prognostic factor of reflux-nephropathy. There is evidence that inclusion of ACE inhibitors (Enap) in therapy of vesico-ureter reflux during 6 months leads to a marked improvement of the structural and functional state of the kidneys. It suggests high renoprotective potential of these preparations and the possibility of their use for prophylaxis of nephrosclerosis in children.

[Endothelial dysfunction in children's chronic glomerulonephritis].

Production of NO, sVCAM-1, Et-1, FV, PAI- 1 was measured in blood sera of children with different forms of chronic glomerulonephritis. Endothelial dysfunction (ED) occurred in the active phase of the disease and persisted during remission regardless of the clinical form of glomerulonephritis. Severity of ED and involvement of its markers depended on morphological type of the disease. Production of endothelin-1 was highest in patients with sclerotic glomerulonephritis and accompanying arterial hypertension. ED caused activation of hemostasis with the prevalence of prothrombotic condition. ED contributed to the progress of glomerulonephritis acting via sclerotization and cell proliferation. Selected markers ED are shown to be of prognostic value in children with chronic glomerulonephritis.

[Renal prostanoids in experimental diabetes mellitus]. / Pochechnye prostanoidy pri éksperimental'nom sakharnom diabete.

Participation of renal prostanoids in development of diabetes-induced nephropathy was studied in rats with streptozotocin diabetes. Development of diabetic nephropathy occurred with simultaneous decreases in production of intrarenal natriuretic, depressor prostaglandin and prostacyclin as well as with increases in content of antinatriuretic, pressor, prothrombogenic TxA2. The imbalance observed in the production of renal prostanoids contributed slightly to impairments of hemodynamics, osmo- and ion regulating functions of kidney, i.e. to formation of diabetic nephropathy in the experimental animals.

[The interaction of atrial natriuretic peptide with other bioregulators of kidney function in chronic glomerulonephritis in children]. / Vzaimodeistvie atrial'nogo natriiureticheskogo peptida s drugimi bioreguliatorami funktsii pochek pri khronicheskom glomerulonefrite u detei.

A study was made of renin-angiotensin-aldosterone system activity and plasmic concentrations of atrial natriuretic peptide (NUP) as well as antidiuretic hormone in children with primary glomerulonephritis. A close relationship was established of these parameters in regulation of water-salt homeostasis. The above systems are involved in pathogenesis of childhood glomerulonephritis. This finding should be considered in development of pathogenetically validated therapy of glomerulonephritis, including introduction of synthetic NUP.

[Endogenous vasoactive factors in children with nephrotic syndrome]. / Endogennye vazoaktivnye faktory pri nefroticheskom sindrome u detei.

In accordance with the results of examining 40 children with nephrotic and mixed glomerulonephritis, it has been established that in the pathogenesis of the nephrotic syndrome of paramount importance is imbalance of the output of renal prostanoids, manifesting in the predominance of the vasopressor and proaggregate fraction--thromboxane A2 and in the deficiency of its antagonist prostacyclin that exerts a protective action on glomerular filtration. Sodium and water retention in patients with the nephrotic syndrome favours an increase of the content of antidiuretic hormone and plasma renin activity.

[The urinary excretion of renal prostanoids in children with chronic obstructive pyelonephritis in vesicoureteral reflux before and after antireflux operations]. / Ekskretsiia pochechnykh prostanoidov s mochoi u detei s khronicheskim obstruktivnym pielonefritom pri puzyrno-mochetochnikovom refliukse do i posle antirefliuksnykh operatsii.

The excretion of renal prostaglandins (PGE, PGF2 alpha, 6-keto-PGE1 alpha and TKB2) was studied in 45 children with chronic obstructive pyelonephritis in the presence of vesicoureteral reflux with account for the disease stage (partial remission--group I; total clinical and laboratory remission--group II) in various periods of surgical corrections of the impaired urodynamics in the area of vesicoureteral segments (in the early postoperative period of 12-14 days after the surgery; in the follow-up period of 6-12 months after the surgery). Preoperative observation of Group I children revealed a significant decrease in urinary PGF2 alpha excretion in the presence of an increase in the circadian TKB2 and 6-keto-PGF1 alpha excretion, whereas the patients from Group II who had normal levels of TKB2 and 6-keto-PGF1 alpha excretion, the levels of PGE and PGF2 alpha were lowered. The retention of sodium was documented in both groups. There was a total recovery of renal sodium and water excretion 6-12 months after the surgery. Children without the urinary syndrome (group II) demonstrated normalization of all secreted prostanoids, whereas in those with pronounced severity of pyelonephritis (group I), the excretion of sodium and diuresis were likely to be provided by hyperproduction of vasodilating sodium and diuretic PGE.

[The effect of diabetes mellitus on the renal prostanoid system and on the arterial pressure level in spontaneously hypertensive rats]. / Vliianie sakharnogo diabeta na pochechnuiu sistemu prostanoidov i uroven' arterial'nogo davleniia u spontanno gipertenzivnykh krys.

The authors studied the effect of diabetes mellitus on the renal prostanoid (PN) system in rats with spontaneous hypertension. Marked changes of renal PN excretion, biosynthesis, and metabolism were revealed. The absence of signs of diabetic nephropathy in rats with hereditary determined hypertension may be attributed to increased production of prostaglandin E and prostacyclin. These PN augment the renal blood flow, prevent sodium retention in the organism, and inhibit the progress of arterial hypertension which is one of the signs characteristic of diabetic nephropathy.

[Renal prostaglandins in glomerulonephritis in children]. / Pochechnye prostaglandiny pri glomerulonefrite u detei.

Prostanoid excretion with urine in children suffering from glomerulonephritis indicates that in the kidneys the output of prostacycline decreases and that of thromboxan rises. In glomerulonephritis children prostacycline and prostaglandin E promote the maintenance of glomerular filtration, which is evidenced by the reduction of their output in the stage of chronic renal failure. The growth of renin and antidiuretic hormone synthesis in children suffering from nephrotic glomerulonephritis is not accompanied by the increase of the output of prostaglandin E, their renal antagonist, and may be one of the reasons of the development of the edematous syndrome.

[Effect of diets with various contents of linoleic acid on the prostaglandin system in the rat kidney]. / Vliianie diet s razlichnym soderzhaniem linolevoi kisloty na prostaglandinovuiu sistemu pochek krys.

Effect of diets containing various amount of linoleic acid on formation of prostaglandins in kidney as well as excretion of the substances with urine were studied in 45 normotensive rats of Wistar-Kyoto strain. Distinct alterations were observed in the kidney prostaglandin system, which directly or via other hormonal systems (renin-angiotensin, antidiuretic hormone of hypophysis) caused the corresponding shifts in the water-electrolyte balance.

[Renal prostaglandins of children and adolescents with nephrogenic arterial hypertension]. / Prostaglandiny pochek u detei i podrostkov s nefrogennoi arterial'noi gipertenziei.

Renal prostaglandin activity was assessed in children and adolescents with two forms of secondary (nephrogenic) arterial hypertension: vasorenal and chronic pyelonephritis-associated hypertension. Children with vasorenal hypertension showed renal PG changes, dependent on the duration of the disease. Positive correlation between arterial BP and PGF2 excretion, and negative correlation between PGE excretion and arterial BP are suggestive of the involvement of the renal PG system in vasorenal hypertension. Children and adolescents with arterial hypertension in the presence of chronic secondary pyelonephritis demonstrated a tendency to low excretion of both PG fractions, while their ratio remained unchanged. The absence of a correlation between urinary PG excretion and arterial BP indicates that renal prostaglandins make no significant pathogenetic contribution to this type of arterial hypertension.

[Age and features of prostanoid biosynthesis in the rat kidney]. / Vozrastnye osobennosti biosinteza prostoidov v pochkakh krys.

The biosynthesis of PgF2, 6-keto-PgF1 alpha and TxB2 from endogenous precursor in vitro by the rat kidney cortex and medulla in ontogenesis was found to be highest at young age reducing from papillae to kidney cortex. The main product of the biosynthesis in kidney medulla of young and adult rats was PgE.

[The renin-angiotensin-aldosterone system in children and adolescents with nephrogenic hypertension]. / Sistema renin-angiotenzin-al'dosteron pri nefrogennoi gipertenzii u detei i podrostkov.

Renin-angiotensin-aldosterone (RAA) function was studied in children with secondary hypertension of 2 varieties: vasorenal hypertension (VRH) and arterial hypertension (AH) associated with chronic pyelonephritis. Children with VRH showed RAA activation that depended on the duration of the disease for its markedness. A direct correlation found between ABP, on the one hand, and plasma renin activity and blood aldosterone level, on the other, is evidence of the latter's involvement in VRH pathogenesis. In AH that is due to chronic pyelonephritis, RAA activation was also demonstrated, however, its pathogenetic involvement was only documented in children with urinary passage disorders (vesico-renal reflux), whereas in the rest RAA activation was not a primary cause of BP elevation.

[Mineralocorticoid function of the adrenal glands in adolescents with primary arterial hypertension before and after treatment with beta-blocking agents]. / Sostoianie mineralokortikoidnoi funktsii nadpochechnikov u podrostkov s pervichnoi arterial'noi gipertoniei do i posle lecheniia beta-blokatorami.

A study of adrenal mineral corticoid function in adolescents with primary arterial hypertension, stage Ib, revealed hyperaldosteronism in more than half of the patients (57%). Treatment with beta-blocking agents (anaprilin and obsidan) was only effective (producing a drop in arterial pressure) in patients with initial high plasma aldosterone levels. beta-blocking agents administered to patients with normal blood aldosterone content did not result in arterial pressure change (failure of treatment). The results obtained suggest that the effect of beta-blocking agents on adrenal mineral corticoid activity in adolescent patients with primary arterial hypertension depends on its baseline level; they are also indicative of a dependence of the hypotensive effect of beta-adrenoreceptor blockers on the state of mineral corticoid function.

[Dynamics of the change in the prostaglandin content of brain tissue in upper cervical sympathectomy and circulatory hypoxia]. / Dinamika izmeneniia soderzhaniia prostaglandinov v tkani mozga pri verkhnesheinoi simpatéktomii i tsirkuliatornoi gipoksii.

A study was made of the effect of cervical sympathectomy (SE) on the time course in the content of prostaglandins (PG) (E + A) and F2 alpha under normoxia and circulatory hypoxia. The sympathectomized rats manifested a biphasic change in the content of PG (E + A). The content of PG (E + A) rose by days 1 and 7. It returned to normal by day 14 and increased again by day 40 after SE. The content of PG F2 alpha drastically increased 7 days after SE and then returned to normal. Brain ischemia induced by bilateral ligation of the common carotid arteries led to an increase in the content of PG (E + A) and in that of PGF2 alpha, in particular. Preliminary SE resulted in the absence of differences in the content of PG (E + A) caused by brain ischemia. It is assumed that PGF2 is largely implicated in the regulation of the tone of the bran vessels and in the regulation of metabolism during ischemia with disordered sympathetic control.