Nephrotic edema syndrome

Nephrotic syndrome - Clinico-laboratory symptom complex,(more than 3.5 g protein per day), a violation of protein-lipid metabolism (hypoproteinemia is a total protein less than 60 g / l), dysproteinemia (albumin-globulin coefficient less than 1.0), hyperlipidemia and edema, often cavitary.

NA develops in many diseasesimmunoinflammatory, autoimmune, metabolic and hereditary nature. Most often occurs with glomerulonephritis with minimal changes (lipoid nephrosis), membranous nephropathy, amyloidosis, systemic connective tissue diseases (lupus nephritis), diabetes mellitus, bacterial, parasitic, viral origin, tumors of various localizations (paraneoplastic nephropathies), allergic diseases pollinosis, food idiosyncrasy, insect bites), drug disease, nephropathy of pregnant women, thrombosis of renal veins, may be of an innate nature ( microcystosis of the kidneys).

The causes of the development of nephrotic syndrome.

1. Primary kidney disease:

- the disease of minimal changes;

- mesangial proliferative glomerulonephritis;

- focal and segmental glomerular sclerosis;

- rare types of lesions (crescent glomerulonephritis, focal and segmental proliferative glomerulonephritis), unclassified lesions.

2. Secondary to other diseases:

- infectious diseases (post-streptococcal glomerulonephritis, endocarditis, secondary syphilis, leprosy, hepatitis B, mononucleosis, malaria, schistosomiasis;

- medicines: organic and inorganic compounds of mercury, neoncillamine, heroin, captopril, radiocontrast agents;

- tumors: lymphogranulomatosis, lymphoma, leukemia, carcinoma, melanoma. Wilms tumor;

- polysystemic diseases: systemic lupus erythematosus, Shenlaine-Henoch disease, vasculitis, Goodpasture's syndrome, amyloidosis, sarcoidosis, Sjogren's syndrome, rheumatoid arthritis;

- Family-inherited diseases: diabetes, Alport syndrome, sickle cell disease, Fabry's disease, lipodystrophy, congenital nephrotic syndrome;

- mixed: preeclampsia, myxedema, malignant obesity, thyroiditis, vasorenal hypertension, chronic interstitial nephritis with vesico-urethral reflux, chronic rejection of renal transplant.

The development of large proteinuria, and "trigger"mechanism in nephrotic syndrome) is associated with a change in the structures of the glomerular vascular filter with a decrease in the constant electric charge of the wall of the capillary loop. Nephrotic edema is the result of hypoproteinemia due to the irreplaceable loss of protein in the urine and its passage into edematous fluids, activation of the reninangiotensin-aldosterone system, increased secretion of antidiuretic hormone.

Patients pay attention to swelling, poorappetite, weakness. Swelling sometimes spreads throughout the body, fluid accumulates in the pleural cavity (hydrothorax), abdominal cavity (ascites). A blistering test can detect fluid retention before the onset of edema: the time of resorption of the intradermal papule after the injection of 0.2 ml of isotonic sodium chloride solution is reduced from 30-40 minutes to several minutes. With large edema, striae (strips of skin stretch) appear on the hips, the lateral surface of the chest, abdomen. The skin becomes dystrophic, dry, nails and hair are brittle. Heart sounds are muffled, tachycardia, systolic murmur, on ECG - signs of a change in the heart muscle. The functions of the pancreas, thyroid gland, adrenal glands have been disrupted, the basic metabolism is decreased.

Laboratory signs. The main symptom of HC is massive proteinuria. With urine, a beige can lose 20-50 g per day; In the urine, mainly there is albumin, but large-molecule proteins may also appear. Depending on the composition of excreted proteins, selective and nonselective proteinuria are isolated, the urinary sediment can be scarce (amyloidosis), contain a large number of erythrocytes (hemorrhagic vasculitis) or leukocytes. In the sediment of urine, hyaline, less often granular and waxy cylinders are found.

A characteristic feature of NS-hypoalbuminization,reaching 20-10 g / l and lower values. Causes of hypoalbuminemia in nephrotic syndrome: increased filtration through the glomerular filter, its passage into edematous fluid, enhanced catabolism of albumin in the epithelium of the tubules and its loss through the intestine.

Hypoalbuminemia determines the levelhypoproteinemia: the level of total protein in the serum of the nephrotic syndrome can be reduced to 30-25 g / l. Along with hypoproteinemia, marked dysproteinemia with a decrease in blood albumin, immunoglobulins, an increase in a-2-globulins. The parameters of the blood coagulation system are changed toward hypercoagulability: the concentration of fibrinogen is increased, there is a tendency to increase platelets, the content of prothrombin is increased. Hypercoagulation can achieve a degree of thrombosis (local thrombosis, or disseminated intravascular coagulation). Lipidemia is one of the permanent clinical manifestations of the National Assembly. The expressed edematic syndrome is accompanied by the greatest maintenance in a blood of the general lipids, cholesterol, b-lipoproteins, triglycerides.

Violations of the functional state of the kidneysDifferent for different versions of HC. For the period of pronounced edema, a certain decrease in glomerular filtration is characteristic, as the edematous syndrome disappears, it may increase. The most characteristic for HC is a violation of the processes of concentration and dilution. Usually urine before the decrease in kidney function has a high relative density (up to 1030-1050 mmol / l).

According to the nature of the course, the following variants of the nephrotic syndrome are distinguished:

Complications of nephrotic syndrome: edema of the brain, retina, hypovolemic shock, peripheral phlebothrombosis. Of the infectious complications most common are pneumonia, pleurisy with a possible pleural empyema, bacterial peritonitis, which must be differentiated from the abdominal nephrotic crisis - one of the manifestations of developing hypovolemic edema. Other possible complications of UA: ischemic heart disease, pulmonary thromboembolism, kidney artery thrombosis, renal vein thrombosis, strokes, phlebothrombosis. Signs suggesting the development of thrombosis of renal veins include unilateral or bilateral pains in the side or lower back, expressed hematuria, left varicocele, asymmetry in the size of the kidneys and the degree of preservation of their function, signs of pulmonary embolism or infarction.

Differential diagnosis of nephrotic syndromeis carried out for the detection of nephrotic syndrome, establishing the nature of nephropathy, the underlying disease. Diagnosis of difficulties does not cause. The most informative in diagnosis is a biopsy of the kidney and sometimes other organs (skin, bone marrow, rectal mucosa, gums).

Early hospitalization is needed, clarificationnosological form, the nature of nephropathy, the functional state of the kidneys. Patient's dosing regimen, showing exercise therapy, observance of body hygiene, sanitation of the oral cavity. The diet is salt-free, animal protein 1 g / kg body weight. With a significant hypoproteinemia, infusion introduction of protein preparations, with hypovolemia - plazmozameschayuschie solutions.

In a number of cases, an appointmentglucocorticoids, cytostatics, nonsteroidal anti-inflammatory drugs, anticoagulants. With significant swelling appoint diuretics - saluretics (hypothiazide, furosemide, triampur, brinaldix), sometimes in combination with an aldosterone antagonist - veroshpiron. Doses of diuretics are individual, blood potassium levels are mandatory. Excessive diuresis may cause a sharp decrease in the effective volume of blood plasma and lead to a further decrease in the rate of glomerular filtration, increased azotemia.

Euphyllin, antiplatelet drugs improve kidney circulation.

Sanatorium treatment at nephroticsyndrome depends on the nature of the disease and kidney function. During the remission of the nephrotic syndrome, climatic treatment on the southern coast of the Crimea. Treatment in Bukhara with glomerulonephritis without signs of renal failure and severe arterial hypertension.

Prognosis: nephrotic syndrome is reversible.