Nephropathy of pregnant women

Nephropathy of pregnant women is a complication of the second half of pregnancy, manifested by arterial hypertension, proteinuria, often in combination with edema, which can have a progressive nature with the development of critical conditions in the mother and fetus (eclampsia, HELLP syndrome, DVS syndrome, intrauterine growth retardation and fetal death) .

[1], [2], [3], [4]

Causes of the nephropathy of pregnant women

The cause of nephropathy of pregnant women is still unclear, whereas its pathophysiological mechanisms have been fairly well studied. According to modern ideas, nephropathy of pregnant women should be considered as a systemic complication of pregnancy, in which almost all vital organs are affected, and arterial hypertension is only one aspect of the problem. The main pathogenetic feature of preeclampsia is the damage and dysfunction of the vascular endothelium, especially expressed in the placental and renal microcirculatory bed.

As a result of endothelial pathology, the synthesis of vasodilating, antiaggregant and anticoagulant factors (prostacyclin, nitric oxide, antithrombin III), which ensure natural endothelial embolism, is reduced, and vasoconstrictor and procoagulant release (endothelium, thromboxane, von Willebrand factor, fibronectin, plasminogen activator inhibitor ). These changes lead to the following violations:

• Increased sensitivity of the vascular wall to pressor effects and vasoconstriction.
• Increase in permeability of the vessel wall with propotovaniya part of the plasma in the interstitial space, which is accompanied by the development of edema, a decrease in the volume of circulating fluid and thickening of the blood.
• Activation of platelet and plasma links of hemostasis with the development of intravascular coagulation of blood.

The combination of vasoconstriction, a decrease in the volume of circulating fluid and thrombosis leads to a violation of the perfusion of organs and tissues with the development of ischemia of the organs, mainly the placenta, kidneys, brain and liver.

The trigger mechanism that initiates the described processes is not clearly established. However, according to the most widely accepted hypothesis of CJM de Groot and RN Taylor, the impaired adaptation of the spiral arteries of the uterus to a developing pregnancy is considered to be primary, which leads to the development of circulatory placental insufficiency. The result is the development of ischemic placenta factors that have the properties of endothelial toxins and cause systemic damage to the endothelium in nephropathy of pregnant women. As other factors inducing endothelial damage in preeclampsia, activation of neutrophils mediated by cytokines, lipid peroxidation and oxidative stress are considered.

[5], [6], [7], [8], [9], [10]

Risk factors

The main risk factor for nephropathy in pregnant women is the first pregnancy, in which the probability of developing nephropathy is 15 times higher than with repeated pregnancies. Gestational arterial hypertension is also more common during the first pregnancy.

Another important risk factor for nephropathy in pregnant women is considered somatic pathology: diseases of the cardiovascular system (primarily arterial hypertension), kidneys, systemic connective tissue diseases, diabetes, obesity.

Additional risk factors for nephropathy in pregnant women are considered to be the age of the mother (over 35 and younger than 19 years), smoking, hereditary complications in nephropathy of pregnant women on the maternal line, as well as multiple pregnancies.

[11], [12], [13], [14]

Pathogenesis

The main changes in nephropathy of pregnant women occur in the vascular bed of the placenta and kidneys. They are noted constantly, regardless of involvement in the process of other organs and systems.

Pathology of the utero-placental bed

In normal pregnancy, the formation of the vascular system of the placenta occurs when the trophoblast interacts (the outer layer of the embryo cells) with the spiral arteries of the uterus. Trophoblast has the capacity for invasive growth deep into the uterus and the formation of villi. Gradually the naps grow, forming their own vascular system, connected through the umbilical cord with the circulatory system of the fetus. Simultaneously, when the trophoblast invades the spiral arteries of the uterus, the structural changes of these vessels develop, manifested in the loss of their endothelial and muscular layers, the internal elastic membrane, as a result of which they are practically transformed from muscle-type arteries into yawning sinusoids. In the process of such transformation spiral arteries are shortened, expanded and straightened, losing the ability to respond to pressor effects. These changes, which each spiral artery undergoes, are an adaptive mechanism that ensures the inflow of maternal blood into the intervillar space in accordance with the needs of the fetus. Transformation of the spiral arteries of the uterus and the formation of the vascular system of the placenta and fetus are completed by 18-22 weeks of pregnancy. It is from this time that development of pre-eclampsia (eclampsia) is possible.

In nephropathy of pregnant women, from half to two thirds of the spiral arteries undergo adaptive changes, and structural adjustment is not completed in them, since the muscular layer is partially or completely preserved in the vessels. This qualitative and quantitative inferiority of physiological restructuring leads to a decrease in placental blood flow, which increases with the development of pregnancy. In addition, the muscle layer remaining in the vessels retains their sensitivity to the vasomotor stimuli and, consequently, the capacity for vasoconstriction.

Another typical, albeit nonspecific, sign of the vascular pathology of the placental bed with nephropathy of pregnant women is "acute atherosis." This term is called necrotizing arteriopathy, characterized by fibrinoid necrosis of the vessel wall, accumulation of foam cells (macrophages containing lipids) in the damaged vascular wall, proliferation of fibroblasts and perivascular infiltration with mononuclear cells.

These changes contribute to increased placental ischemia, leading in most severe cases to her heart attacks and fetal damage: the probability of intrauterine growth retardation and fetal death during preeclampsia increases by 2-10 times.

[15], [16], [17], [18], [19]

Pathomorphology of the kidneys

A typical morphological sign of nephropathy in pregnant women is glomerular capillary endotheliosis - glomerular changes due to endothelial pathology. The glomeruli are enlarged in size, the lumen of the capillary loops is sharply narrowed due to the swelling of the endothelial cells. In most cases, an increase in the mesangial matrix is also noted, an interposition of the mesangiocyte processes between the basal membrane and the endothelium with the accumulation of a matrix in this zone, which may be taken as a thickening of the basal membrane. Sometimes in the glomeruli, deposits of fibrin and IgM are found. The severity of morphological changes correlates with the severity of clinical manifestations of nephropathy in pregnant women. Glomerular-capillary endotheliosis is completely reversible and disappears within a few weeks after delivery.

A rare morphological sign of pre-eclampsia (characteristic for cases with early onset and severe course) is considered focal segmental glomerular hyalinosis, which is detected with kidney biopsy in the postpartum period. Its development is associated with glomerular endotheliosis and intraglular clotting of blood, leading to kidney ischemia. Another rare morphological sign of severe nephropathy in pregnant women is fibrinoid necrosis and sclerosis of the intervertebral arteries, which develops as a result of the direct damaging effect of acute and high arterial hypertension. In women with focal segmental glomerular hyalinosis and sclerosis of the intrarenal vessels, hypertension is subsequently maintained, sometimes with malignant course.

Anatomical and functional changes in the urinary system

During normal pregnancy, the size of the kidneys increases: their length increases by 1.5-2 cm. The basic anatomical changes affect the cup-and-pelvis system: the enlargement of renal pelvis, calyx, and ureter caused by hyperprogestinemia is noted early in gestation. As a rule, dilatation of the calyx-pelvis system is more pronounced on the right. In the second half of pregnancy, changes in the urinary tract are retained due not only to hormonal factors, but also to the mechanical action of the enlarged uterus. These changes, leading to a violation of urodynamics and urine stasis, are a risk factor for urinary tract infection (from asymptomatic bacteriuria to acute pyelonephritis) in pregnant women.

[20]

Changes in renal hemodynamics and renal function

Physiological pregnancy is characterized by a significant systemic vasodilatation, which develops with the onset of gestation. In pregnancy, kidney blood flow and GFR increase: the maximum values of these indicators are registered already in the first trimester and on average exceed by 35-50% those of non-pregnant. The increase in renal blood flow and GFR is associated with renal vessel dilatation and increased glomerular plasmacy, which was established by micro-puncture on experimental models of pregnancy in rats.

• During pregnancy, there is no increase in creatinine production, therefore increased GFR leads to a decrease in the concentration in the blood of creatinine, as well as other products of nitrogen metabolism. The normal level of creatinine during pregnancy does not exceed 1 mg / dL, uric acid 4.5 mg / dL, urea nitrogen 12 mg / dl.
• Increased GFR with tubular reabsorption, which has not changed during pregnancy, is the reason for the increased urinary excretion of glucose, uric acid, calcium, amino acids, bicarbonate. Bicarbonaturia is considered as a compensatory reaction in response to the development of hypocapnia (respiratory alkalosis develops in pregnant women due to physiological hyperventilation). A persistent alkaline urine reaction, characteristic of pregnancy, is another risk factor for developing a urinary infection.
• As a result of the increase in GFR, physiological proteinuria of pregnant women also develops. Daily excretion of protein during pregnancy is 150-300 mg.

[21], [22], [23], [24], [25], [26], [27], [28]

Changes in the water-salt balance

During physiological pregnancy, significant changes in the water-salt balance are observed. As a result of hyperproduction of mineralocorticoids, a significant retention of sodium and water ions occurs. By the end of pregnancy, about 900 mEq of sodium accumulate in the pregnant body, which corresponds to 6-8 L of fluid, which leads to an increase in the volume of circulating plasma during gestation by 40-50%, with the maximum increase occurring in the second half of pregnancy. About two thirds of the accumulated sodium (or its volumetric equivalent) is contained in the tissues of the fetus, one-third - in the mother's body, evenly distributed between the vascular bed and the interstitium. As a result of this, along with the increase of intravascular volume of blood, the hydrophilicity of tissues increases and physiological edema is developed, which are detected at different terms of pregnancy in 80% of women. These edemas are unstable, do not combine with proteinuria and / or increased blood pressure and do not require treatment in this connection.

Because of the delay of sodium and water ions, the phenomenon of blood dilution develops. It can be diagnosed on the basis of a decrease in hematocrit to 35-36%, hemoglobin concentration to 120-100 g / l and a decrease in the concentration of total protein and albumin in the blood on average by 10 g / l.

[29], [30], [31], [32], [33]

Regulation of blood pressure during pregnancy

During pregnancy, there is a decrease in blood pressure, which reaches the minimum values by the end of the first trimester. In pregnant women systolic blood pressure averages 10-15 mm Hg, and diastolic blood pressure by 5-15 mm Hg. Lower than before pregnancy. Since the beginning of the second trimester, blood pressure is gradually increasing very slowly and by the end of pregnancy it can reach the level observed before conception. Reduction of blood pressure occurs, despite the increase in the volume of circulating blood and the minute volume of blood circulation, characteristic of pregnancy. The main reason for lowering blood pressure is the development of vasodilation, which, in turn, results in the action of placental hormones on the vascular endothelium. In the physiological course of pregnancy, the placenta produces significant amounts of prostacyclin 1 ₂ and endothelial relaxing factor (nitric oxide), which have vasodilating and antiplatelet properties. With the action of prostacyclin and nitric oxide in pregnancy, in addition to vasodilation, the vascular wall is also refractory to the action of pressor factors, which ultimately leads to a decrease in blood pressure. In response to vasodilation and reduction in blood pressure during gestation, activation of RAAS occurs.

From the very beginning of pregnancy, there is a distinct increase in renin plasma activity, reaching a maximum (on average 4 times more than before pregnancy) values for the second half of gestation.

• An increase in the level of renin in the blood is accompanied by an increase in the secretion of aldosterone.
• The state of the production of angiotensin II in pregnant women has not been studied enough, but apparently its level is also elevated, since pregnant women with normal arterial pressure are diagnosed with an excessive response to acute ACE blockade.

Thus, it can be assumed that the activation of RAAS in pregnancy is an important mechanism for preventing hypotension, since blood pressure remains normal.

Symptoms of the nephropathy of pregnant women

Nephropathy of pregnant women always develops in the second half of pregnancy. Symptoms of nephropathy in pregnant women are presented below.

• The main symptom of nephropathy of pregnant women is proteinuria, exceeding 0.3 g / day, the severity of which serves as an indicator of the severity of the disease. A distinctive feature of proteinuria in preeclampsia is considered to be the rate of its growth: sometimes from the time of the appearance of protein in the urine to the development of massive proteinuria (5-10 or even 15-30 g / l) is only a few hours. In this regard, with timely delivery, nephrotic syndrome may not form. With a relatively long existence (1 week or more) of proteinuria exceeding 3 g / day, the development of a nephrotic syndrome is possible, the index of which in pregnant women is the concentration of albumin of blood less than 25 g / l. As a rule, proteinuria is combined with severe arterial hypertension. However, in a number of cases the arterial pressure rises slightly, which does not exclude the development of preeclampsia / eclampsia, which manifests itself as isolated proteinuria.
• Arterial hypertension is another important symptom of nephropathy in pregnant women. The criterion for hypertension in pregnant women is the repeated increase in arterial pressure to 140/90 mm Hg.
  • A steady increase in diastolic blood pressure to 90 mm Hg. And more, recorded after 20 weeks gestation, indicates the development of pregnancy-induced hypertension and has unfavorable prognostic value, since it was found that the excess of this level of diastolic blood pressure in a pregnant woman is accompanied by an increase in perinatal mortality. The diastolic blood pressure is 110 mm Hg. And more, are considered a sign of pre-eclampsia.
  • When nephropathy is pregnant, the systolic blood pressure value has no diagnostic or prognostic significance.
  • Arterial hypertension can have a progressive or a crisis current. Characteristic of the night increase in blood pressure. With blood pressure exceeding 180/110 mm Hg, hypertensive encephalopathy, hemorrhagic stroke, acute left ventricular failure with pulmonary edema, retinal detachment can develop.
• In most women with nephropathy, pregnant women are marked by swelling, which is accompanied by a rapid increase in body weight, however, even with severe pre-eclampsia / eclampsia, swelling may be absent. At present, edemas are excluded from the diagnostic criteria of nephropathy due to their nonspecificity.
• An important symptom of nephropathy in pregnant women is hyperuricemia (more than 357 μmol / L), which, as a rule, precedes the appearance of proteinuria. The value of hyperuricemia allows to differentiate preeclampsia, in which the uric acid content in the blood can reach 595 μmol / l, from transient arterial hypertension, which is characterized by lower concentrations of uric acid in the blood. Hyperuricemia, apparently, is due to impaired renal perfusion.
• Pregnant women with nephropathy are noted to have decreased renal blood flow and GFR. Despite the decrease in creatinine clearance, the level of creatinine in the blood, as a rule, remains normal.
• The complications of nephropathy of pregnant women include acute tubular necrosis and, in rare cases, acute cortical necrosis, manifested by a clinical picture of acute renal failure.

The defeat of the central nervous system (eclampsia)

The defeat of the CNS (eclampsia) in most cases develops as a result of the progression of nephropathy in pregnant women, but in 15-20% of cases eclampsia may occur without previous proteinuria and hypertension. Eclampsia is considered a sign of ischemic involvement of the central nervous system, apparently due to spasm of cerebral vessels and thrombotic microangiopathy due to intravascular hypercoagulation. Eclampsia develops in the second half of pregnancy, usually before giving birth or within a week of them (in some patients directly in childbirth), manifests as seizures reminiscent of epileptic seizures, and is usually accompanied by hypertension, although not necessarily severe. The development of convulsive syndrome can be preceded by a short period of prodromas in the form of headaches, visual disturbances, epigastric pains, nausea, or vomiting. There may be an increase in the activity of liver enzymes in the blood, hyperuricemia, thrombocytopenia and blood clotting disorders. Given the possibility of developing eclampsia in the absence of proteinuria and hypertension, it is recommended that women in the second half of pregnancy consider the described prodromal symptoms of nephropathy in pregnant women as early manifestations of preeclampsia, until their other cause is established.

Lesion of the liver

The defeat of the liver develops with the most severe progression of nephropathy in pregnant women and is caused by thrombotic microangiopathy of the intrahepatic vessels leading to ischemic organ damage.

Morphologically, this type of lesions is marked by intrahepatic hemorrhages, periportal deposition of fibrin, foci of necrosis of the hepatic tissue.

The combination of liver damage with microangiopathic hemolytic anemia in patients with preeclampsia (eclampsia) is called HELLP-syndrome (Hemolysis, Elevated Liver enzymes, Low Platelet - hemolysis, increased activity of liver enzymes, thrombocytopenia) developing in 0.2-0.9% of pregnant women . This syndrome occurs in 2 times more often with repeated pregnancies, especially in the case of an unfavorable outcome of the first, and is accompanied by high perinatal (30-60%) and maternal (24-30%) mortality, and almost 50% of newborns are showing signs of intrauterine growth retardation. In 70% of cases, HELLP-syndrome develops immediately before childbirth, although it may occur within 24-48 hours after them. The clinical picture of HELLP syndrome includes symptoms of liver damage (increased activity of transaminases and y-glutamyltransferase in the blood), hemolytic anemia (the presence of hemolysis is judged by increasing the percentage of fragmented erythrocytes in the smear of peripheral blood and by lactate dehydrogenase activity above 600 IU / L), thrombocytopenia less than 100,000 in 1 μl) followed by acute renal failure or, more rarely, multiple organ failure. In 25% of patients this pathology is complicated by the development of the DIC syndrome. In rare cases, HELLP-syndrome develops life-threatening complications of women: subcapsular hematomas, hemorrhages in the parenchyma and liver ruptures. The only means of effective treatment of HELLP syndrome is urgent delivery.

Pathology of the coagulating system of blood

Patients with nephropathy of pregnant women are marked by activation of intravascular coagulation, caused by damage to the vascular endothelium. As a result, platelets are activated, as evidenced by a decrease in their number (due to their "consumption" in the foci of endothelial damage), a rise in the blood concentrations of substances contained in thromboglobulin platelets, thromboxane A1, cepotonin), a decrease in aggregation properties of these cells in samples in vitro. Along with the activation of platelets, activation of the plasma clotting and fibrinolysis unit occurs, the laboratory features of which are the increased concentration of degradation products of fibrinogen and soluble fibrin-monomer complexes. In the most severe cases, the progression of nephropathy in pregnant women is complicated by the development of an acute DIC syndrome, manifested by generalized bleeding and symptoms of multiple organ failure. In acute ICE in patients noted severe thrombocytopenia (less than 50,000 in 1 μl) and severe hypofibrinogenemia, a high percentage of fragmented erythrocytes.

The course of nephropathy in pregnant women

Nephropathy of pregnant women always develops in the second half of pregnancy. In most cases, it occurs after 34 weeks of gestation. Early development (up to 34 weeks) and severe course of nephropathy of pregnant women are characteristic of patients with antiphospholipid syndrome. Pre-eclampsia is characterized by a progressive course, which is manifested in the steady increase of proteinuria and arterial hypertension or the emergence of new clinical signs, resulting in the development of critical conditions such as eclampsia, acute DVS, hepatic or renal insufficiency, premature detachment of the normally located placenta, fetal death. The period of time from the first clinical manifestations of nephropathy to the development of these conditions varies from 2 days to 3 weeks, not exceeding the majority of patients 12 days. The duration of the precritical stage of nephropathy in pregnant women is usually 4-5 weeks, but it is possible that the fulminant pre-eclampsia course takes place in just a few hours from the appearance of the first symptoms of nephropathy in pregnant women until the patient dies.

Forms

The domestic term "nephropathy of pregnant women" according to clinical criteria is close to the international terms "pre-eclampsia" or "proteinuric hypertension". However, different classifications of this syndrome have been adopted in Russia and abroad. In Russia, nephropathy of pregnant women is one of the stages of gestosis (shortened from the German term Gestationstoxicose - toxicosis of pregnant women), which is divided into dropsy (isolated edema), nephropathy of pregnant women (combination of proteinuria and arterial hypertension), preeclampsia (combination of nephropathy with moderate CNS lesion) and eclampsia (nephropathy and severe CNS involvement with convulsions and often coma). Abroad, according to the WHO classification (1996), preeclampsia is considered as one of the forms of hypertension in pregnant women.

There are 4 forms of hypertension in pregnant women.

1. Preeclampsia / eclampsia.
2. Chronic arterial hypertension.
3. Chronic arterial hypertension with associated preeclampsia / eclampsia.
4. Gestational arterial hypertension.

• Pre-eclampsia (proteinuric hypertension, nephropathy of pregnant women) is a specific syndrome that develops in the second half of pregnancy and is characterized by hypertension and proteinuria. Edema is not currently considered as a diagnostic sign of preeclampsia due to their non-specificity. Eclampsia is a CNS lesion that develops as a result of the progression of preeclampsia.
• Chronic arterial hypertension is an arterial hypertension that existed before pregnancy (hypertension, secondary arterial hypertension, including renal etiology). Its criteria are listed below.
  • Registration of blood pressure equal to 140/90 mm Hg. And more, at least 2 times before the onset of pregnancy.
  • Detection of high blood pressure in the first half of pregnancy.
  • Preservation of high blood pressure for more than 12 weeks after childbirth if it was first registered in the second half of pregnancy.
• Gestational arterial hypertension is an uncomplicated (without proteinuria) uncomplicated increase in arterial pressure, first detected in the second half of pregnancy. Women with gestational arterial hypertension should be observed at least 12 weeks after birth before clarifying the diagnosis, which may have the following formulations.
  • Transient arterial hypertension (in case of normalization of arterial pressure).
  • Chronic arterial hypertension (with a persistent increase in blood pressure).

Abroad, the term "arterial hypertension induced by pregnancy" is often used, which combines preeclampsia and transient arterial hypertension. In this case, transient arterial hypertension is called mild arterial hypertension, induced by pregnancy, and pre-eclampsia - of severe arterial hypertension induced by pregnancy, conducting this division based on the severity of arterial hypertension and the presence of proteinuria.

Arterial hypertension in pregnant women is one of the most important and widespread complications of pregnancy of a therapeutic nature. In different countries of the world it is detected in 8-15% of pregnant women. The prevalence of preeclampsia (nephropathy of pregnant women) is about 3%, and eclampsia - 0.1%. In Russia, according to an epidemiological study conducted in 1998, hypertension was registered in 20% of pregnant women. The diagnosis of "gestosis" was established in 13.5% of all pregnant women. Such variability of epidemiological data is due to the difference in classifications and diagnostic criteria adopted in Russia and abroad.

[34], [35], [36]

Treatment of the nephropathy of pregnant women

Conservative treatment of nephropathy in pregnant women is ineffective. Attempt to save pregnancy, lowering blood pressure, can be dangerous for the mother and fetus, since correction of hypertension does not affect the progression of gestosis and does not exclude the development of eclampsia and severe placental insufficiency. In this regard, the established diagnosis of nephropathy of pregnant women is an indication for delivery, which is considered the only effective method of treatment. After giving birth, a rapid reverse development of all clinical manifestations occurs.

The patient with nephropathy of pregnant women should be immediately hospitalized in the intensive care unit. Bed rest (which promotes improvement of uteroplacental blood flow), monitoring of mother and fetal condition, eclampsia prevention, sedative and antihypertensive therapy, correction of hypovolemia, hemodynamic and coagulation disorders are shown. A dynamic assessment of the severity of the condition of a woman and a fetus is necessary to make a timely decision on delivery. For this purpose, a thorough control of blood pressure, daily (sometimes hourly) determination of proteinuria and diuresis is carried out. Every day, a biochemical blood test is performed, including the determination of the concentration of total protein, creatinine, uric acid, liver transaminase activity, control hemoglobin, hematocrit, platelet count, coagulogram parameters. Fetal examination includes ultrasonic and biophysical methods.

• The drug of choice for the prevention of eclampsia is magnesium sulfate, which reduces the excitability of the central nervous system more than neuroleptic drugs and tranquilizers, and surpasses their safety for the mother and fetus. Although magnesium sulfate is not currently considered an antihypertensive drug, in most patients its use leads to a reduction in blood pressure. Magnesium sulphate is recommended to be administered immediately after delivery, as convulsions tend to develop in the early postpartum period. The use of drugs before birth is undesirable, because it can worsen labor activities or lead to complications of anesthesia during cesarean delivery.
• The purpose of infusion therapy is to correct the rheological state of blood and hypovolemia to ensure adequate perfusion of organs, primarily the utero-placental complex and kidneys. To avoid hyperhydration and pulmonary edema, careful monitoring of diuresis, blood pressure, hematocrit is necessary. Applied as solutions of low-molecular substances (glucose, dextran), and blood products (albumin, fresh frozen plasma).
• With the development of the DIC syndrome, a freshly frozen plasma is prescribed, which serves as a natural source of antithrombin III, which has the property of blocking intravascular coagulation of blood. The dose of fresh frozen plasma is 6-12 ml / kg of body weight per day. With the development of HELLP-syndrome, infusion of fresh frozen plasma is advisable to combine with the conduct of plasmapheresis. The use of freshly frozen plasma in severe hypercoagulable disorders is combined with the appointment of heparin at a dose of 10 000-20 000 units / day. With developed bleeding, the dose of heparin should not exceed 5000 units / day, and drugs should be injected directly into fresh frozen plasma for faster activation of antithrombin III, the cofactor of which is heparin.
• Correction of arterial hypertension is necessary for nephropathy of pregnant women to prevent acute complications - cerebral hemorrhages, pulmonary edema, retinal detachment. Antihypertensive treatment of nephropathy in pregnant women should be prescribed at arterial pressure above 160/100 mm Hg, nevertheless a rapid decrease in blood pressure can lead to a sharp deterioration in perfusion of the placenta, brain and kidneys, which will lead to deterioration of the mother and fetus, eclampsia and intrauterine fetal death. For this reason, antihypertensive therapy in pregnant women with pre-eclampsia should be carried out with caution, and the target level of blood pressure for nephropathy in pregnant women should be considered 130-140 / 85-90 mm Hg.
  • If the delivery is scheduled within the next 24 hours, antihypertensive drugs should be given parenterally. In this case, the appointment of beta-adrenoblocker labetalol (intravenously) or hydralazine (intravenously or implantally) is indicated. Sublingual administration of slow calcium channel blockers is also possible. If blood pressure control with these drugs was not achieved, intravenous sodium nitroprusside is justified, despite its toxicity to the fetus.
  • In cases where the delivery can be delayed, the drugs are prescribed inside.
    • A safe and effective antihypertensive drug in pregnancy is a-methyldopa, which should be prescribed in doses exceeding the conventional 2-3 times because of the characteristics of liver metabolism of the drug in pregnant women. The appointment of beta-blockers: atenolol in a dose of 50-100 mg / day in 2 doses, metoprolol in a dose of 100-200 mg / day in 2 doses, betaxolol 5-20 mg / day in 1 reception. In addition to these drugs, it is possible to use blockers of slow calcium channels, usually nifedipine series.
    • Do not show the appointment of pregnant thiazide and other diuretics as antihypertensive drugs, because they can reduce the volume of circulating blood, which can contribute to the development of perfusion disorders in the organs. The appointment of diuretics can be shown only in the presence of resistant to other drugs of hypertension and the risk of hypertensive complications.
    • Pregnancy is an absolute contraindication to the appointment of ACE inhibitors, which can cause fetal death, acute renal failure, and non-infarction of the ductus arteriosus in a newborn.

Prevention

Preventive maintenance of a nephropathy of pregnant women till now is not finally solved. Women who have risk factors for nephropathy, taking into account the pathogenetic value of endothelial-platelet disorders, are recommended to administer small doses of acetylsalicylic acid (60-125 mg / day), inhibiting the synthesis of thromboxane in platelets and not affecting the production of prostacyclin by vascular endothelium. However, in large placebo-controlled studies involving high-risk pregnant women, the effectiveness of this drug in preventing nephropathy in pregnant women has not been proven. The exception was women with antiphospholipid syndrome, in whom the appointment of acetylsalicylic acid prevented the early development of nephropathy in pregnant women. It has also been shown that in patients with antiphospholipid syndrome, the risk of developing pre-eclampsia decreases with the use of anticoagulant drugs (heparin).

[37], [38], [39], [40],

Forecast

[41], [42], [43],

Exodus for mother

Until now, nephropathy of pregnant women remains one of the main causes of maternal mortality in developed countries. Its share in the structure of maternal mortality is 20-33%. Annually from this difficult complication of pregnancy in the world 50 000 women die. The main causes of death in preeclampsia (eclampsia) are CNS damage (hemorrhagic and ischemic stroke, edema of the brain), pulmonary edema, liver necrosis, acute DVS syndrome. In women who undergone nephropathy of pregnant women, the incidence of hypertension subsequently does not exceed that in the general population. However, with the early onset of nephropathy (before 34 weeks of pregnancy) or its relapse during the next pregnancy, the risk of developing hypertension in the future increases.

[44], [45], [46]

Outcome for the fetus

Preeclampsia is associated with a high perinatal mortality rate of 33.7 cases per 1000 newborns (in women with normal blood pressure this figure is 19.2 cases per 1000 newborns). In addition, with pre-eclampsia, a high incidence of premature birth and perinatal morbidity due to intrauterine growth retardation and asphyxia is noted.