Nephropathy of pregnancy

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

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Causes maternal nephropathies

The cause of nephropathy of pregnancy is still unclear, while its pathophysiological mechanisms are fairly well studied. According to modern concepts, nephropathy of pregnancy 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 damage and dysfunction of the vascular endothelium, especially pronounced in the placental and renal microcirculatory bed.

As a result of endothelial pathology, the synthesis of vasodilators, antiplatelet and anticoagulant factors (prostacyclin, nitric oxide, antithrombin III), which provide natural athrombogenicity of the endothelium, decreases, and, on the contrary, the release of vasoconstrictors and procoagulants (endothelin, thromboxane, von Willebrand factor, fibronectin, plasminogen activator inhibitor) increases. These changes lead to the following disorders:

• Increased sensitivity of the vascular wall to pressor effects and vasoconstriction.
• Increased permeability of the vascular wall with the leakage of part of the plasma into 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 blood coagulation.

The combination of vasoconstriction, a decrease in the volume of circulating fluid and thrombus formation leads to a disruption of organ and tissue perfusion with the development of organ ischemia, mainly the placenta, kidneys, brain and liver.

The trigger mechanism initiating the described processes has not been clearly established. However, according to the currently most common hypothesis of CJM de Groot and RN Taylor, the primary mechanism is considered to be a violation of the adaptation of the uterine spiral arteries to the developing pregnancy, which leads to the development of circulatory placental insufficiency. This results in the production by the ischemic placenta of factors that have the properties of endothelial toxins and cause systemic damage to the endothelium in nephropathy of pregnancy. Other factors inducing endothelial damage in preeclampsia include cytokine-mediated neutrophil activation, lipid peroxidation, and oxidative stress.

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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 in repeated pregnancies. Gestational hypertension also develops more often during the first pregnancy.

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

Additional risk factors for nephropathy of pregnancy include maternal age (over 35 and under 19 years), smoking, a family history of nephropathy of pregnancy on the maternal side, and multiple pregnancies.

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Pathogenesis

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

Pathomorphology of the uteroplacental bed

During normal pregnancy, the formation of the vascular system of the placenta occurs through the interaction of the trophoblast (the outer layer of embryonic cells) with the spiral arteries of the uterus. The trophoblast has the ability to invasively grow deep into the uterus and form villi. Gradually, the villi grow, forming their own vascular system connected through the umbilical cord to the circulatory system of the fetus. At the same time, with the invasion of the trophoblast into the spiral arteries of the uterus, structural changes in these vessels develop, expressed in the loss of the endothelial and muscular layers, the internal elastic membrane, as a result of which they are practically transformed from muscular arteries into gaping sinusoids. In the process of such transformation, the spiral arteries shorten, expand and straighten, losing the ability to respond to pressor effects. These changes, to which each spiral artery is subjected, represent an adaptive mechanism that ensures the influx of maternal blood into the intervillous space in accordance with the needs of the fetus. The 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 period that preeclampsia (eclampsia) can develop.

In nephropathy of pregnancy, adaptive changes are experienced by half to two thirds of the spiral arteries, and structural reorganization is not completed in them, since the muscular layer is partially or completely preserved in the vessels. Such qualitative and quantitative inadequacy of physiological reorganization leads to a decrease in placental blood flow, which increases as pregnancy progresses. In addition, the muscular layer remaining in the vessels maintains their sensitivity to vasomotor stimuli and, therefore, the ability to vasoconstrict.

Another typical, although non-specific, sign of vascular pathology of the placental bed in nephropathy of pregnancy is "acute atherosis." This term refers to necrotizing arteriopathy characterized by fibrinoid necrosis of the vessel wall, accumulation of foam cells (lipid-containing macrophages) in the damaged vessel wall, proliferation of fibroblasts, and perivascular infiltration of mononuclear cells.

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

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Pathomorphology of the kidneys

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

A rare morphological sign of preeclampsia (typical for cases with early onset and severe course) is considered to be focal segmental glomerular hyalinosis, detected during kidney biopsy in the postpartum period. Its development is associated with glomerular endotheliosis and intraglomerular blood coagulation, leading to renal ischemia. Another rare morphological sign of severe nephropathy of pregnancy is fibrinoid necrosis and sclerosis of interlobar 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 intrarenal vessels, arterial hypertension subsequently persists, sometimes with a malignant course.

Anatomical and functional changes in the urinary system

During normal pregnancy, the kidneys increase in size: their length increases by 1.5-2 cm. The main anatomical changes affect the renal pelvis: dilation of the renal pelvis, calyces, and ureters, caused by hyperprogestinemia, is noted already in the early stages of gestation. As a rule, dilation of the renal pelvis is more pronounced on the right. In the second half of pregnancy, changes in the urinary tract persist due to not only hormonal factors, but also the mechanical effect of the enlarging uterus. These changes, leading to impaired urodynamics and urine stasis, serve as a risk factor for the development of urinary tract infection (from asymptomatic bacteriuria to acute pyelonephritis) in pregnant women.

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Changes in renal hemodynamics and renal function

Physiological pregnancy is characterized by significant systemic vasodilation, which develops from the beginning of gestation. In pregnant women, renal blood flow and SCF increase: the maximum values of these indicators are recorded already in the first trimester and, on average, exceed those in non-pregnant women by 35-50%. The increase in renal blood flow and SCF is associated with dilation of renal vessels and increased glomerular plasma flow, which was established by the micropuncture method on experimental models of pregnancy in rats.

• During pregnancy, creatinine production does not increase, so the increased SCF leads to a decrease in the concentration of creatinine in the blood, 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 SCF with unchanged tubular reabsorption during pregnancy is the cause of increased urinary excretion of glucose, uric acid, calcium, amino acids, and bicarbonate. Bicarbonaturia is considered a compensatory reaction in response to the development of hypocapnia (respiratory alkalosis develops in pregnant women due to physiological hyperventilation). Persistent alkaline urine reaction, characteristic of pregnancy, is another risk factor for the development of urinary infection.
• Due to the increase in SCF, physiological proteinuria of pregnant women also develops. Daily protein excretion during pregnancy is 150-300 mg.

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Changes in 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 ions and water occurs. By the end of pregnancy, about 900 mEq of sodium accumulates in the pregnant woman's body, which corresponds to 6-8 liters 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 volume 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, along with an increase in the intravascular blood volume, tissue hydrophilicity increases and physiological edema develops, detected at different stages of pregnancy in 80% of women. These edemas are unstable, are not combined with proteinuria and / or increased blood pressure and do not require treatment in this regard.

Due to the retention of sodium ions and water, the phenomenon of blood dilution develops. It can be diagnosed based on 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 by an average of 10 g/l.

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Regulation of blood pressure during pregnancy

During pregnancy, there is a decrease in blood pressure, which reaches its minimum values by the end of the first trimester. In pregnant women, systolic blood pressure is on average 10-15 mm Hg, and diastolic blood pressure is 5-15 mm Hg lower than before pregnancy. From the beginning of the second trimester, blood pressure gradually increases very slowly and by the end of pregnancy can reach the level observed before conception. A decrease in 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 the decrease in blood pressure is the development of vasodilation, which, in turn, results from the effect of placental hormones on the vascular endothelium. During 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. In addition to vasodilation, the action of prostacyclin and nitric oxide during pregnancy is associated with the refractoriness of the vascular wall to the action of pressor factors, which ultimately leads to a decrease in blood pressure. In response to vasodilation and a decrease in blood pressure during gestation, RAAS is activated.

From the very beginning of pregnancy, a clear increase in plasma renin activity is noted, reaching its maximum (on average 4 times more than before pregnancy) value by 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 angiotensin II production in pregnant women has not been sufficiently studied, but its level is apparently also elevated, since an excessive response to acute ACE blockade is detected in pregnant women with normal blood pressure.

Thus, it can be assumed that activation of RAAS during pregnancy serves as an important mechanism for preventing hypotension, since blood pressure remains normal.

Symptoms maternal nephropathies

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

• The main symptom of nephropathy of pregnancy 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 the rate of its increase: sometimes only a few hours pass from the moment protein appears in the urine to the development of massive proteinuria (5-10 or even 15-30 g/l). In this regard, with timely delivery, nephrotic syndrome may not develop. With a relatively long existence (1 week or more) of proteinuria exceeding 3 g/day, the development of nephrotic syndrome is possible, an indicator of which in pregnant women is the concentration of blood albumin less than 25 g/l. As a rule, proteinuria is combined with severe arterial hypertension. However, in some cases, blood pressure increases 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 arterial hypertension in pregnant women is a repeated increase in blood pressure to 140/90 mm Hg.
  • A persistent increase in diastolic blood pressure to 90 mm Hg or more, recorded after 20 weeks of pregnancy, indicates the development of pregnancy-induced arterial hypertension and has an unfavorable prognostic value, since it has been established that exceeding this level of diastolic blood pressure in a pregnant woman is accompanied by an increase in perinatal mortality. Diastolic blood pressure equal to 110 mm Hg or more is considered a sign of preeclampsia.
  • In nephropathy of pregnancy, the value of systolic blood pressure has no diagnostic or prognostic value.
  • Arterial hypertension may have a progressive or crisis course. Nocturnal increase in blood pressure is typical. With blood pressure exceeding 180/110 mm Hg, hypertensive encephalopathy, hemorrhagic stroke, acute left ventricular failure with pulmonary edema, and retinal detachment may develop.
• Most women with nephropathy of pregnancy experience edema, which is accompanied by rapid weight gain, but even in severe preeclampsia/eclampsia edema may be absent. Edema is currently excluded from the diagnostic criteria for nephropathy due to its nonspecificity.
• An important symptom of nephropathy of pregnancy is hyperuricemia (more than 357 μmol/l), which usually precedes the appearance of proteinuria. The magnitude of hyperuricemia allows one 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 is apparently caused by impaired renal perfusion.
• In pregnant women with nephropathy, decreased renal blood flow and SCF are observed. Despite the decrease in creatinine clearance, the creatinine level in the blood usually remains normal.
• Complications of nephropathy in pregnancy include acute tubular necrosis and, in rare cases, acute cortical necrosis, which manifest as a clinical picture of acute renal failure.

Central nervous system damage (eclampsia)

CNS damage (eclampsia) in most cases develops as a result of progression of nephropathy of pregnancy, however, in 15-20% of cases, eclampsia may develop without preceding proteinuria and arterial hypertension. Eclampsia is considered a sign of ischemic CNS damage, apparently caused by spasm of cerebral vessels and thrombotic microangiopathy due to intravascular hypercoagulation. Eclampsia develops in the second half of pregnancy, usually before labor or within a week after it (in some patients directly during labor), manifests itself as convulsions resembling an epileptic seizure, and, as a rule, is accompanied by arterial hypertension, although not necessarily severe. The development of convulsive syndrome may be preceded by a short prodrome in the form of headaches, visual impairment, epigastric pain, nausea or vomiting. Increased activity of liver enzymes in the blood, hyperuricemia, thrombocytopenia and blood clotting disorders are possible. Taking into account the possibility of developing eclampsia in the absence of proteinuria and arterial hypertension, it is recommended that women in the second half of pregnancy consider the described prodromal symptoms of nephropathy of pregnancy as early manifestations of preeclampsia until another cause is established.

Liver damage

Liver damage develops in the most severe progressive course of nephropathy of pregnancy and is caused by thrombotic microangiopathy of the intrahepatic vessels, leading to ischemic damage to the organ.

Morphologically, this type of lesion is characterized by intrahepatic hemorrhages, periportal fibrin deposition, and foci of liver tissue necrosis.

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 2 times more often in repeated pregnancies, especially with an unfavorable outcome of the first, and is accompanied by high perinatal (30-60%) and maternal (24-30%) mortality, and almost 50% of newborns show signs of intrauterine growth retardation. In 70% of cases, HELLP syndrome develops immediately before childbirth, although it can also occur 24-48 hours after. The clinical picture of HELLP syndrome includes symptoms of liver damage (increased activity of transaminases and γ-glutamyl transferase in the blood), hemolytic anemia (the presence of hemolysis is judged by the increase in the percentage of fragmented erythrocytes in a peripheral blood smear and by lactate dehydrogenase activity over 600 IU/l), thrombocytopenia (less than 100,000 in 1 μl) followed by acute renal failure or, less often, multiple organ failure. In 25% of patients, this pathology is complicated by the development of DIC syndrome. In rare cases, HELLP syndrome can cause life-threatening complications for a woman: subcapsular hematomas, hemorrhages into the parenchyma, and liver ruptures. The only effective treatment for HELLP syndrome is emergency delivery.

Pathology of the blood coagulation system

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

The course of nephropathy in pregnant women

Nephropathy of pregnancy always develops in the second half of pregnancy. In most cases, it occurs after 34 weeks of gestation. Early development (before 34 weeks) and severe course of nephropathy of pregnancy are typical for patients with antiphospholipid syndrome. Preeclampsia is characterized by a progressive course, which is expressed in a steady increase in proteinuria and arterial hypertension or the appearance of new clinical signs, which may result in the development of such critical conditions as eclampsia, acute DIC syndrome, liver or kidney failure, premature detachment of a 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 12 days in most patients. The duration of the pre-critical stage of nephropathy of pregnancy is usually 4-5 weeks, however, a fulminant course of preeclampsia is possible, in which only a few hours pass from the appearance of the first symptoms of nephropathy of pregnancy to the death of the patient.

Forms

The domestic term "nephropathy of pregnancy" is close in clinical criteria to the international terms "preeclampsia" or "proteinuric hypertension". However, different classifications of this syndrome are accepted in Russia and abroad. In Russia, nephropathy of pregnancy is one of the stages of gestosis (short for the German term Gestationstoxicose - toxicosis of pregnancy), which is divided into dropsy (isolated edema), nephropathy of pregnancy (a combination of proteinuria and arterial hypertension), preeclampsia (a combination of nephropathy with moderate damage to the central nervous system) and eclampsia (nephropathy and severe damage to the central nervous system with convulsions and often coma). Abroad, according to the WHO classification (1996), preeclampsia is considered one of the forms of arterial hypertension of pregnancy.

There are 4 forms of arterial hypertension in pregnant women.

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

• Preeclampsia (proteinuric hypertension, nephropathy of pregnancy) is a specific syndrome that develops in the second half of pregnancy and is characterized by arterial hypertension and proteinuria. Edema is currently not considered a diagnostic sign of preeclampsia due to its non-specificity. Eclampsia is a CNS lesion that develops as a result of the progression of preeclampsia.
• Chronic arterial hypertension is 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 or more, at least 2 times before pregnancy.
  • Detection of high blood pressure in the first half of pregnancy.
  • Persistence of elevated blood pressure for more than 12 weeks after delivery if it was first recorded in the second half of pregnancy.
• Gestational hypertension is an isolated (without proteinuria) uncomplicated increase in blood pressure, first detected in the second half of pregnancy. Women with gestational hypertension should be observed for at least 12 weeks after delivery before refining the diagnosis, which may have the following formulations.
  • Transient arterial hypertension (in case of normalization of blood pressure).
  • Chronic arterial hypertension (with persistent increase in blood pressure).

Abroad, the term "pregnancy-induced arterial hypertension" is often used, which combines preeclampsia and transient arterial hypertension. In this case, transient arterial hypertension is called moderate pregnancy-induced arterial hypertension, and preeclampsia is called severe pregnancy-induced arterial hypertension, making this distinction 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, arterial hypertension is 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.

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Treatment maternal nephropathies

Conservative treatment of nephropathy of pregnancy is ineffective. An attempt to maintain pregnancy by reducing blood pressure may be dangerous for the mother and fetus, since correction of arterial 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 pregnancy serves as an indication for delivery, which is considered the only effective method of treatment. After delivery, there is a rapid reverse development of all clinical manifestations.

A patient with nephropathy of pregnancy should be immediately hospitalized in the intensive care unit. Bed rest (which improves uteroplacental blood flow), monitoring of the mother and fetus, prevention of eclampsia, sedative and antihypertensive therapy, correction of hypovolemia, hemodynamic and coagulation disorders are indicated. Dynamic assessment of the severity of the woman and fetus is necessary to make a timely decision on delivery. For this purpose, careful monitoring of blood pressure, daily (sometimes hourly) determination of proteinuria and diuresis are carried out. Biochemical blood tests are performed daily, including determination of the concentration of total protein, creatinine, uric acid, liver transaminase activity, hemoglobin content, hematocrit, platelet count in the blood, coagulogram parameters are monitored. Fetal examination includes ultrasound and biophysical methods.

• Magnesium sulfate is considered the drug of choice for the prevention of eclampsia, as it reduces CNS excitability to a greater extent than neuroleptic drugs and tranquilizers, and is superior to them in terms of safety for the mother and fetus. Although magnesium sulfate is not currently considered an antihypertensive drug, its use leads to a decrease in blood pressure in most patients. Magnesium sulfate is recommended to be administered immediately after delivery, since convulsions usually develop in the early postpartum period. The use of drugs before delivery is undesirable, since it can worsen labor or lead to complications of anesthesia during cesarean section.
• The goal of infusion therapy is to correct the rheological state of the blood and hypovolemia to ensure adequate perfusion of organs, primarily the uteroplacental complex and kidneys. To avoid hyperhydration and pulmonary edema, careful monitoring of diuresis, arterial pressure, and hematocrit is necessary. Both solutions of low-molecular substances (glucose, dextran) and blood products (albumin, fresh frozen plasma) are used.
• In the development of DIC syndrome, fresh frozen plasma is prescribed, which serves as a natural source of antithrombin III, which has the property of blocking intravascular blood coagulation. The dose of fresh frozen plasma is 6-12 ml/kg of body weight per day. In the development of HELLP syndrome, it is advisable to combine infusions of fresh frozen plasma with plasmapheresis. The use of fresh frozen plasma in severe hypercoagulation disorders is combined with the administration of heparin at a dose of 10,000-20,000 U/day. In the event of bleeding, the dose of heparin should not exceed 5000 U/day, and the drugs should be administered directly into fresh frozen plasma for faster activation of antithrombin III, the cofactor of which is heparin.
• Correction of arterial hypertension is necessary in case of nephropathy of pregnancy to prevent acute complications - cerebral hemorrhage, pulmonary edema, retinal detachment. Antihypertensive treatment of nephropathy of pregnancy should be prescribed at blood pressure above 160/100 mm Hg, however, a rapid decrease in blood pressure can lead to a sharp deterioration in the perfusion of the placenta, brain and kidneys, which will lead to deterioration of the condition of the mother and fetus up to the development of eclampsia and intrauterine fetal death. For this reason, antihypertensive therapy in pregnant women with preeclampsia should be carried out with caution, and the target blood pressure level for nephropathy of pregnancy should be considered 130-140/85-90 mm Hg.
  • If delivery is scheduled within the next 24 hours, antihypertensive drugs should be administered parenterally. In this case, the beta-blocker labetalol (intravenously) or hydralazine (intravenously or intramuscularly) are indicated. Sublingual calcium channel blockers are also possible. If blood pressure control with these drugs is not achieved, intravenous sodium nitroprusside is justified, despite its toxicity to the fetus.
  • In cases where delivery can be delayed, medications are administered orally.
    • A safe and effective antihypertensive drug during pregnancy is a-methyldopa, which should be prescribed in doses 2-3 times higher than the generally accepted ones due to the peculiarities of the liver metabolism of the drug in pregnant women. The use of beta-blockers is also indicated: atenolol at a dose of 50-100 mg / day in 2 doses, metoprolol at a dose of 100-200 mg / day in 2 doses, betaxolol at 5-20 mg / day in 1 dose. In addition to these drugs, it is possible to use slow calcium channel blockers, usually nifedipine series.
    • Prescription of thiazide and other diuretics as antihypertensive drugs is not indicated for pregnant women, since their use may reduce the volume of circulating blood, which may contribute to the development of perfusion disorders in organs. Prescription of diuretics may be indicated only in the presence of arterial hypertension resistant to other drugs and the risk of hypertensive complications.
    • Pregnancy is an absolute contraindication to the use of ACE inhibitors, which can cause intrauterine fetal death, acute renal failure and patent ductus arteriosus in the newborn.

Prevention

Prevention of nephropathy in pregnant women has not yet been fully resolved. Women with risk factors for nephropathy, taking into account the pathogenetic significance of endothelial-platelet disorders, are recommended to prescribe small doses of acetylsalicylic acid (60-125 mg/day), which inhibits the synthesis of thromboxane in platelets and does not affect the production of prostacyclin by the vascular endothelium. However, in large placebo-controlled studies involving high-risk pregnant women, the effectiveness of this drug in preventing nephropathy in pregnant women was not proven. The exception was women with antiphospholipid syndrome, in whom the administration of acetylsalicylic acid prevented the early development of nephropathy in pregnant women. It was also shown that in patients with antiphospholipid syndrome, the risk of preeclampsia is reduced by the use of anticoagulant drugs (heparin).

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Forecast

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Exodus for the mother

To date, nephropathy of pregnancy remains one of the main causes of maternal mortality in developed countries. Its share in the structure of maternal mortality is 20-33%. Every year, 50,000 women die from this severe pregnancy complication worldwide. The main causes of death in preeclampsia (eclampsia) are CNS damage (hemorrhagic and ischemic stroke, cerebral edema), pulmonary edema, liver necrosis, and acute DIC syndrome. In women who have had nephropathy of pregnancy, the incidence of arterial hypertension in the future does not exceed that in the general population. However, with early onset of nephropathy (before 34 weeks of pregnancy) or its recurrence during the next pregnancy, the risk of developing arterial hypertension in the future increases.

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Outcome for the fetus

Preeclampsia is associated with high perinatal mortality, amounting to 33.7 cases per 1000 newborns (in women with normal blood pressure, this figure is 19.2 cases per 1000 newborns). In addition, preeclampsia is associated with a high incidence of premature birth and perinatal morbidity caused by intrauterine growth retardation and asphyxia.